A   TEXT-BOOK   OF   MEDICINE 


VOL.   I 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons- 


http://www.archive.org/details/textbookofmedic01dieu 


A    TEXT- BOOK    OF 
MEDICINE 


BY 


G.    DIEULAFOY 


PROFESSOB   OF    CLINIC.UL   MEDICINE    AT    THE    FACULTE    DE    MEDECINE   DE   PABIS ;   PHYSICIAN 
TO    THE    HOTEL   DIEU  ;    MF.MBRE    DE    l'aCADEMIE    DE   MEDECINE 


AUTHORIZED    ENGLISH   TRANSLATION    FROM   THE 

FIFTEENTH   EDITION   OF   "MANUEL  DE 

PATHOLOGIE   INTERNE" 

BY 

V.  E.   COLLINS,    M.D.   Lond.,    M.R.C.S.,    L.R.G.P. 

AM) 

J.  A.   LIEBMANN,    PhD,   M.A.,    LL.D. 


IN  TWO  VOLUMES 
VOL.  I 


NEW  YORK 

D.    APPLETON  AND   COMPANY 

1911 


\  I-    IIS"  7/    ^ 


LT^ 


s>l 


AUTHOR'S  PREFACE  TO  THE  ENGLISH  EDITION. 

Having  been  asked  for  a  preface  to  tlie  English  translation  of  my  "  Text- 
Book  of  Medicine,"  my  first  desire  is  to  express  tlie  great  satisfaction  I 
feel  at  seeing  my  work  translated  into  English,  for  that  language  is  so 
widespread  over  both  hemispheres  that  no  other  translation  which  has 
yet  been  made  would  have  contributed  to  the  same  extent  to  the  recognition 
abroad  of  this  work  of  French  origin. 

I  must  add  that  in  writing  my  "  Text-Book  of  Medicine,"  which  has  now 
reached  its  fifteenth  edition,  I  have  given  much  space  to  the  works  of  my 
eminent  English  colleagues,  since  a  number  of  them  are  of  the  very  first 
importance.  Thus  will  be  found  the  illustrious  names  of  Sydenham,  Graves, 
Basedow,  Corrigan,  Addison,  Bright,  Stokes,  Paget,  etc.,  whose  scientific 
researches  are  known  and  appreciated  by  everyone. 

Long  ago  my  venerated  master,  the  great  Trousseau,  popularized  in  his 
"Clinical  Lectures"  the  valuable  discoveries  of  English  practitioners,  and 
gave  the  names  of  their  authors  to  the  newly  diagnosed  diseases.  I  have 
followed  the  example  of  Trousseau,  and  have  often  dipped  into  English 
medical  literature,  so  rich  in  precious  documents.  I  shall  lie  satisfied  if 
the  medical  profession  in  England  will  on  their  side  give  a  good  reception 
to  the  work  which  I  am  now  presenting  to  them. 

G.  DIKULAFOY. 
Paris, 
April  17,  1910. 


TRANSLATORS'  PREFACE 

The  "  Manuel  de  Pathologie  Interne,"  by  Professor  Dieulafoy,  has  passed 
through  fifteen  editions  in  France,  and  has  been  also  translated  into  several 
European  languages.  The  translators  of  the  English  edition  have  undertaken 
the  work  in  the  hope  that  English-speaking  physicians  may  be  afforded  an 
opportunity  of  reading  one  of  the  most  complete  and  helpful  works  on  the 
practice  of  medicine  that  has  appeared  within  recent  times.  The  author's 
association  with  the  late  Professor  Trousseau,  combined  with  his  own  pro- 
found clinical  knowledge,  certainly  makes  his  manual  a  safe  guide  to  the 
practice  of  medicine.  The  author  has  throughout  confined  himself  to 
established  facts,  avoiding  useless  discussions  and  sterile  hypotheses.  We 
have  to  thank  Dr.  A.  N.  Sinclair,  for  much  kindly  help  in  reading  the  proof- 
sheets. 

V.  E    COLLINS. 

J.  A.  LIEBMANN. 
April,  19J0. 


CONTENTS   OF   VOL.   I 


u/ 


PART  I 


DISEASES  OP  THE  RESPIRATORY  SYSTEM 

CHAPTER  PAGE 

I.  DISEASES  OF  THE  NASAL  FOSS^    --....  1 

I.  CORYZA     ........  1 

n.    NASAL   DIPHTHERIA    -.-....  4 

in.    NASAL    SYPHILIS — SYPHILITIC    RHINITIS            ....  5 

n.   DISEASES   OF   THE   LARYNX     -                 -                                  -                 -                 -                 -  23 

I.    GENERAL    SURVEY     OP    THE    ANATOMY   AND     PHYSIOLOGY    OF    THE 

LARYNX                  -------  23 

II.    ACUTE   CATARRHAL   LuVRYNGITIS          -                 -                 -                 -                 -  27 

III.  CHRONIC   LARYNGITIS                 -••---  29 

IV.  SYPHILIS  OF  THE  LARYNX  (SECONDAl^  LARYNGOPATHIES — TERTIARY 

LARYNGOPATHIES)             -                 -                 -                 -                 -                 -  31 

V.    TUBERCULOSIS  OF  THE  L.4RYNX — LARYNGEAL  PHTHISIS          -                 -  40 

VI,    LARYNGEAL   DIPHTHERIA — CROUP      -                 -                 -                 -                 -  47 

VII.    STRIDULOUS    LARYNGITIS — FALSE   CROUP        -  -  -  -56 

VUI.    (EDEMA   OF   THE   LARYNX — (EDEMA   IN    BRIGHT's   DISEASE     -                 -  57 

IX.    SPASM   OF   THE   GLOTTIS           ------  C9 

X.    PARALYSIS   OF   THE   MUSCLES   OF   THE   LARYNX            -                 -                 -  71 

in.    DISEASES    OF   THE    BRONCHI    --.-..-  76 

-'l.    ACUTE   BRONCHITIS    ----..-  76 

_n.    CAPILLARY     BRONCHITIS — BRONCHO-PNEUMONIA — LOBULAR     PNEU- 
MONIA   .-..-.--  79 
-III.    CHRONIC   BRONCHITIS                ......  91 

-IV.    DILATATION    OF   THE    BRONCHI — BROXCHIECTTASIS       -                  -                  -  94 

-V.    PSEUDO-MEMBRANOUS    BRONCHITIS    -                  -                  -                  .                  -  KX) 

VL    TRA(rHEO-BRONCHIAL   SYPHILIS             .....  102 

VII.    WHOOPING-COUGH       .......  104 

VIII.    ASTHMA            ........  109 

IX.    SUMMER  ASTHMA — HAY-FEVER             -                 -                 -                 -                 -  115 

IV.    DISEASES   OF   THE   LUNG           -                 -                 -                 -                 -                 -                 -  117 

I.    GENERAL   SURVEY   OF   THE   ANATOMY   OF   THE   LUNG                -                 -  117 

—  n.    PULMONARY   CONGESTION       -                 -                 -                 -                 -                 -  118 

Iir.    INFLAMMATION   OF   THE    CHEST             -                 -                 -                 -                 -  119 

IV.    ACUTE    LOBAR   OR   FIBRINOUS    PNEUMONIA — PNEUMOCOCCIO    INFEC- 
TION— PNEUMOCOCCIA     -                 -                 -                 -                 -                 -  121 

-V.    CHRONIC   PNEUMONIA — FIBROSIS   OF   THK    LUNG          -                 -                 -  139 

-VL    OCCUPATION   PNEUMONIA — PNEUMOKONIOSI3                 -                 -                 -  142 

-VII.    THROMBOSIS   AND    EMBOLISM   OF   THE   PULMONARY   ARTERY                  -  144 
-VIU.    GANGRENE     OF     THE     LUNG — GANGRENE      OF      E.MBOLIO      ORIGIN — 

GANGRENE    OF   AEKIAL    OltlGIN  ....                  -  149 

ix 


CONTENTS  OF  VOL.  I 


CHAPTER  PAGE 

IV.  DISEASES  OF  THE  LUNG — Continued : 

IX.    BRONCHO-PULMONARY   HEMORRHAGE — HEMOPTYSIS                -                .  154 
X.    PULMONARY   EMPHYSEMA        ---...  I59 
XL    CEDEMA  OF  THE  LUNG — SUPERACUTE  CEDEMA  IN  BRIQHT's  DISEASE  161 
XII.    ON   TUBERCULOSIS   IN   GENERAL — BACILLUS   TOXINES              -                .  169 
XIIL    PULMONARY   PHTHISIS — COMMON   CHRONIC   TUBERCULOSIS    -                -  176 
Xn^    FIBROID    PHTHISIS       ---.-..  195 
XV.    PNEUMONIC    PHTHISIS — TUBERCULAR   PNEUMONIA — CASEOUS   PNEU- 
MONIA     --------  198 

XVI.   ACUTE     GRANULAR     TUBERCULOSIS — ACUTE     GENERALIZED     TUBER- 
CULIZATION        .......  203 

XVII.    FALSE   TUBERCULOSIS   OF   THE   LUNG                 -                -                -                -  207 

■    XVni.    CANCER   OF   THE   LUNG             --....  213 

XrX.    BRONCHO-PULMONARY   HTHIASIS        -                .                .                .                .  216 

XX.   HYDATID    CYSTS   OF   THE   LUNG   AND   OF   THE   PLEURA             -                -  219 

XXI.    SYPHILIS   OF   THE   LUNG          -                -                -                -                •                -  231 

V.    DISEASES   OF   THE   PLEURA      ---....  248 

I.   ACUTE    SERO-FIBRINOUS    PLEURISY — TUBERCULAR    SERO-FIBRINOUS 

PLEURISY              ..---..  248 
II.    HOW  TO  TELL  IF  AN  ACUTE  SERO-FIB«INOUS  PLEURISY  IS  OR  IS  NOT 

TUBERCULAR — CYTO-DIAGNOSIS — SERO-DIAGNOSIS            "               •  268 

III.    HEMORRHAGIC   PLEURISY        ......  284 

rv.    TRAUMATIC  HEMOTHORAX     ---...  295 

V.    PURULENT   PLEURISIES   OF   THE   GENERAL   PLEURAL   CAVITY                •  305 
VI.   ASEPTIC  PURIFORM  EFFUSIONS    IIs'TO    THE    PLEURA — INTEGRITY  OP 

THE   POLYNUCLEAR   CELLS            .....  314 

VII.    PULSATING    EMPYEMA                 -                 -                 -                 -                 -                  -  317 

VIII.    INTERLOBAR   PLEURISY — VOMICE — INTERLOBAR   HEMOPTYSIS             -  325 

IX.    MEDIASTINAL   PLEURISY — MEDIASTINAL   SYNDROME                  -                ■  337 

X.    DIAPHRAGMATIC   PLEURISY     ---...  343 

XL    LOCULATED,   AREOLAR,    OR   POLYMORPHOUS   PLEURISY                              -  344 

XII.    SYPHILITIC   PLEURISIES            ......  346 

XIIL    APPENDICULAR  PLEURISIES — PYOPNEUMOTHORAX  AND  SUBPHRENIC 

EMPYEMA              -.-....  348 

XrV.    FCETID,   PUTRID,    AND   GANGRENOUS   PLEURISY            -                -                -  357 

XV.    VOMICE           -.-.-..-  367 

XVI.    CHYLIFORM  AND    CHYLOUS   EFFUSIONS   OF   THE   PLEURA        .                -  369 

XVn.    HYDROTHORAX              .......  372 

XVIII.    PNEUMOTHORAX — HYDROPNEUMOTHORAX      ....  373 

VI.    DISEASES   OP   THE   MEDIASTINUM         ......  377 

I.    TUMOURS    OF   THE   MEDIASTINUM        .....  377 

11.    CANCER   OF   THE   THORACIC   DUCT      .....  382 


PAET  II 
DISEASES  OF  THE  CIRCULATORY  SYSTEM 

DISEASES   OP   THE   PERICARDIUM  .  .  .  - 

I.    ACUTE   PERICARDITIS  .... 

n.    CHRONIC   PERICARDITIS — ADHERENT   PERICARDIUM  - 
III.    HYDROPERICARDIUM — HYDROPNEUMOPERICARDIUM 


385 

385 
391 
392 


CONTENTS  OF  VOL.  I 


XI 


CHAPTER  PAOK 

II.    DISEASES   OF   THE    ENDOCAKDITM        --....  393 

I.    ACUTE    ENDOCARDITIS                ......  393 

n.    CHRONIC   ENDOCARDITIS          ......  404 

in.    VAL\njLAR   LESIONS   OF   THE   HEART                   ....  40.5 

IV.    MITRAL   ORIFICE — INSUFFICIENCY   AND    STENOSIS       .                 •                 -  410 

V.    AORTIC   ORIFICE — INSUFFICIENCY   AND    STENOSIS       -                 •                 •  425 

VI.    THE   TRICUSPID    ORIFICE — INSUFFICIENCY   AND    STENOSIS      .                 .  427 

VII.    PULMONARY   ARTERY — INSUFFICIENCY   AND    STENOSIS             .                 .  429 

VIII.    MORBUS    C.ERULEUS — CYANOSIS           .....  430 

III.    DISEASES   OF   THE   MYOCARDIUM           ......  433 

I.    ACUTE   MYOCARDITIS —FATTY    DEGENERATION    OF    THE   HEART           •  433 

II.    FIBROSIS    OF    THE    HEART         --..-.  436 

III.  ANEURYSMS  OF  THE  HEART — INFARCTS  AND  FIBROUS  PATCHES,  ETC. 

— RUPTURE    OF    THE    HEART         .....  438 

IV.  SYPHILIS   OF   THE   HEART         ......  441 

V.    TUMOURS   OF  THE  HEART  AND  TUBERCULOSIS  OF  THE  MYOCARDIUM  442 

VI.    HYPERTROPHY   AND    DILATATION    OF   THE   HEART       .                 -                 -  442 

Vn.    ASYSTOLE        -...-...  446 

nr.    NEUROSES   OP   THE   HEART      .......  447 

I.    PALPITATION                   .......  447 

n.    PAROXYSMAL   TACHYCARDIA                     .....  449 

III.  PERMANENT    BRADYCARDIA    ---...  450 
rV'.    EXOPHTHALMIC   GOITRE — BASEDOW'S   DISEASE             -                 .                 -  453 

V.   DISEASES   OF   THE   VESSELS     -        "         -                 .                 -                 -                 .                 .  470 

I.    PHXEBITIS — PHLEGMASIA    ALBA    DOLENS           ....  470 

II.    SYPHILITIC   PHLEBITIS               ......  47n 

in.    ARTERITIS — ATHEROMA — ARTERIO-SCLEROSIS                 -                 •                 -  478 

IV.  SYPHILITIC    ARTERITIS — ARTERITIS    OBLITERANS — SYPHILITIC    GAN- 

GRENE— ARTERITIS   ECTASIANS — SYPHILITIC   ANEURYSM                -  486 

V.    ACUTE   AND    CHRONIC   AORTITIS           .....  488 

VI.    ANEURYSMS   OF   THE   THORACIC   AORTA             .                 •                 .                 -  491 

VII.    SYPHILIS   OF   THE   AORTA — SYPHILITIC   AORTIC   ANEURYSMS                  -  502 
VIIL    DIAGNOSIS  BETWEEN  ANEURYSM  AND  NERVOUS  PULSATION  OF  THE 

ABDOMINAL   AORTA           ......  518 

IX.    CARDIO-AORTIC   LESIONS   VS  TABES — TABETIC    ANGINA     PECTORIS     -  519 

X.    ANGINA   PECTORIS       .......  525 

XI.   ARTERIAL  TENSION — HYPERTENSION — HYPOTENSION                •                -  530 


PART  III 
\/^DISEASES  OF  THE  DIGESTIVE  SYSTEM 


L   DISEASES   OF   THE   MOUTH 

I.  ERYTHEMATOUS   STOMATITIS 

11.  MERCURIAL   STOMATITIS 

lU.  ULCERO-MEMBRANOUS   STO.AUTITIS 

IV.  THRUSH  ... 

V.  APHTHA 

VI.  GANGRENE   OP   THE   MOUTH — NOMA 

VII.  SYPHILIS   OF   THE    LIPS 


534 
53  t 
535 
.537 
539 
543 
.541 
545 


xii  CONTENTS  OF  VOL.  I 

CHAPTER  PAQX 

I.  DISEASES  OF  THE  MOUTH — Continued  : 

VIII.    SYPHILIS   OP   THE   TONGUE     -..---  546 

IX.    SYPHILITIC  PERFORATION   OF   THE   ROOF   OF   THE   PALATE      -                 •  551 

X.  TUBERCULOSIS    OF   THE   MOUTH             .                 .                 .                  -                 .  556 

n.    DISEASES   OF   THE    THROAT   AND    PHARYNX     -----  559 
I.    ACUTE    CATARRHAL   ANGINA — ACUTE    ERYTHEMATOUS    ANGINA            -  559 
n.    ACUTE     TONSILLITIS — SIMPLE     TONSILLITIS — SUPPURATIVE     TONSIL- 
LITIS— ULCERO-MEMBRANOUS    TONSILLITIS — VINCENT'S  ANGINA  560 
in.    RETROPHARYNGEAL   ABSCESS                  .....  566 
IV.    CHRONIC  ANGINAL  CATARRH — GRANULAR  ANGINA — CHRONIC  TONSIL- 
LITIS     ..-.----  567 

V.    DIPHTHERIA                     -                 -                 -                 -                 -                 -                 -  569 

VI.    DIPHTHERITIC   ANGINA              ..----  574 

VII.    PSEUDO-DIPHTHERITIC   MEMBRANOUS   ANGINA               -                 .                 -  602 

VIII.    DIPHTHERITIC    PARALYSIS        -                 -                 -                 -     '            -                 -  607 

IX.    HERPETIC   ANGINA      -.--.--  612 
X.    GANGRENOUS    ANGINA                -                 -                 -                 -                 -                 -61.3 

XI.    CHANCRE   OP   THE   TONSIL       -                 -                 -                 -                 -                 -  614 

Xn.    SYPHILIS   OP   THE   SOFT   PALATE,    THROAT,    AND    PHARYNX    -                 -  020 

XIII.    TUBERCULOSIS  OP  THE  BACK  OP  THE  MOUTH  AND  OP  THE  PHARYNX  625 

XrV.    MASKED    TUBERCULOSIS    OF   THE    THREE    TONSILS       -                 -                 -  628 

III.    DISEASES   OP   THE   CESOPHAGUS              ..--.-  636 

I.    OESOPHAGITIS                  .......  636 

11.    SPASM   OP   THE    (ESOPHAGUS                    ....                 -  637 

III.    CANCER  AND    STRICTURES   OF   THE   CESOPHAGUS          ...  838 

rV.    DISEASES    OF   THE    STOMACH   -------  644 

I.  GASTRIC   DISTRESS — ACUTE    CATARRHAL   GASTRITIS    -'               -                 -  644 
n.    ACUTE    GASTRITIS        -------  646 

III.  CHRONIC   GASTRITIS   -------  647 

IV.  DYSPEPSIA      --------  649 

V.    GASTRALGIA  --------  654 

VI.   ULCERATION   OP   THE   STOMACH — GENERAL   CONSIDERATIONS                -  656 

VII.    PNEUMOCOCCAL   GASTRITIS   WITH   ULCERATION             -                 -                 -  658 

Vin.    APPENDICULAR   VOMITO   NEGRO            -----  661 

IX.    EXULCERATIO    SIMPLEX   OP    THE   STOMACH     -                 -                 -                 -  666 

X.    SIMPLE   ULCER   OP   THE    STOMACH    (CRUVEILHIER's    DISEASE)                  -  680 

XI.  PERFORATION    OF    SIMPLE    ULCER    OP    THE    STOMACH — SUPERACUTE 

PERITONITIS          -                 -                 -                 -                 -                 -                 -  691 

XII.    PERFORATING     ULCERS     OF     THE     STOMACH     AND     DUODENUM     CON- 
SECUTIVE   TO    APPENDICITIS         -                 ...                 -  695 
Xin.    TRANSFORMATION  OP  SIMPLE  ULCER  OP  THE  STOMACH  INTO  CANCER  699 
XrV.    GASTRIC   POLYADENOMA           ------  705 

XV.    CANCER   OP   THE    STOMACH     ------  706 

XVI.    SYPHILIS    OF   THE    STOMACH                     .                  .                 -                 -                 .  716 

XVII.    DILATATION    OF   THE    STOMACH              ...                 -                 -  720 

XVIU.    GASTRORRHAGIA — H^^MATEMESIS         ....                 -  722 

XIX.    VISCERAL   PTOSES        ..-----  724 

V.    DISEASES   OF   THE   INTESTINE                  -...--  726 

I.    ACUTE   ENTERITIS        -.-----  726 

II.  INFANTILE    GASTRO-ENTERITIS    (INFANTILE    CHOLERA)              -                 -  728 


CONTENTS  OF  VOL.  I  xiii 

CHAPTER  PAGE 

V.   DISEASES  OF  THE  INTESTIJfE — Continued  : 

III.  APPENDICITIS — APPENDICULAR       PERITONITIS— APPENDICULAR      IN- 

TOXICATION— APPENDIC^MLA      -  -  -  .  .  735 

IV.  MUCOUS,  MEMBRANOUS,    AND    SABULOUS    ENTERO-TYPHLOCOLITIS^ 

INTESTINAL    LIATHISIS    --.-..  774 

V.    FALSE    APPENDICITIS  ---...  782 

VI.    INTESTINAL    TUBERCULOSIS — TUBERCUL.\R    ENTERITIS  -  -  788 

VU.    HYPERTROPHIC   TUBERCULOJIA   OF   THE   C^CUM — DIAGNOSIS   OF  THE 

TUMOURS    OF    THE   RIGHT    ILIAC    FOSSA  -  -  .  -  792 

VIII.    ANO-RECTAL   TUBERCULOSIS  -  -  -  -  -  806 

IX.  SIMPLE    ULCER    OF    THE    DUODENUM — PERFORATION — SUPERACUTE 

PERITONITIS         --.....  808 

X.    CANCER   OF   THE   INTESTINE  .....  813 

XL    INTESTINAL   OCCLUSION  --....  814 

XII.    CANCER   OF   VATER'S    AMPULLA  .....  819 

XIII.  DYSENTERY   ........  821 

XIV.  INTESTINAL   WORMS  ..-..--  828 

VI.    DISEASES   OF   THE   PERITONEUM  -  ....  833 

I.    INTRODUCTION    TO    THE    STUDY    OF    PERITONITIS  -  -  -  833 

n.    ACUTE    AND    SUBACUTE    TUBERCULAR   PERITONITIS    -  -  -  837 

in.    CHRONIC    TUBERCULAR    PERITONITIS  -  .  .  .  839 

IV.    PRIMARY    PNEUMOCOCCAL   PERITONITIS — ASSOCIATION    OF    THE    COLI 

BACILLUS  ---....  846 

V.  PRUIARY   STREPTOCOCCAl.  PERITONITIS            ....  854 
VI.    CANCER   OP   THE   PERITONEUM — CANCEROUS   PERITONITIS      -                 -  860 

VU.    HYDATID    CYSTS    OF   THE   PERITONEUTM  ....  862 

VIII.    ASCITES  ........  864 

IX.    CHYLOUS,    CHYLIFORM,    LACTESCENT  ASCITES  ...  Sfio 

VII.    DISEASES   OF   THE   LIVER  ....--.  870 

X.   ANATO>rY   AND    PHYSIOLOGY    OF   THE   LIVES  -  -  -  870 

n.    CONGESTION   OF   THE   LIVER  .....  874 

ni.    PASSIVE   CONGESTION — CARDIAC   LIVER  ....  875 

rv.    CIRRHOSIS   OF   THE   LIVER   IN   GENERAL  ....  878 

V.    VENOUS    CIRRHOSIS — LAENNEC's    ATROPHIC    CIRRHOSIS — CIRRHOSIS 

BY   GASTRO-INTESTINAL  AUTO-INTOXICATION      -  -  -  881 

VI.    HYPERTROPHIC     ALCOHOLIC     CIRRHOSIS — ^REGENERATION      OF     THE 

LIVER      .-.-..--  896 

VII.    CURABILITY    OF   CIRRHOTIC   ASCITES   AND    CIRRHOSIS  -  -  899 

VIII.    HYPERTROPHIC    CIRRHOSES    .  .....  904 

IX.    PIGMENTARY     UYPERTKOPHIC     CIRRHOSIS — PIGMENTARY     CACHEXIA  904 

X.  HYPERTROPHIC    BILIARY   CIRRHOSIS — HANOT's   DISEASE  -  -  907 
XI.    MIXED   CIRRHOSIS       .... 

XII.    TUBERCULOSIS    OF    THE    LIVER 

XIII.  CANCER   OF   THE   LIVER   AND    BILE-DUCTS       - 

XIV.  SYPHILIS  ..... 
XV.    HYDATID    CY.STS   OF   THE    LIVER 

XVI.   ALVEOLAR  HYDATID    CYST   OF   THE   LIVER     - 

XVII.    FATTY    AND    AMYLOID    DEGENERATION    OF    THK    LIVEK  -  -  949 

XViri.    ABSCESS   OF   THE    LIVER  ..----  9.")! 

XIX.    APPENDICULAR    LIVER  ...-.-  9.").") 


915 

917 
922 
!»29 
934 
948 


xiv  CONTENTS  OF  VOL.  I 

CHAPTER  PAGE 

VII.  DISEASES  OF  THE  LiVEK — Continued : 

XX.    GALL-STONES                   -                 -                 -                 -                 -                 -                 -  .    964 

XXL    PERMANENT  OBLITERATION   OF   THE    COMMON   DUCT — DIAGNOSIS   OF 

THE    CAUSE   OF   THE    OBLITERATION          -                 -                 -                 -  987 

XXII.    ANGIOCHOLITIS — CHOLECYSTITIS          -----  997 

XXIII.    ASSOCIATION    OP   APPENDICITIS   AND    CHOLECYSTITIS                  -                 -  999 

XXIV.    ABERRANT   LOBE    OF   THE   LIVER         -----  1004 

XXV.    ICTERUS — JAUNDICE — CHOL^MIA        -----  1004 

XXVI.    ICTERUS   GRAVIS — ICTERUS   AND    THE    PUERPERAL    STATE       -                 -  1011 

XXVII.    CATARRHAL   ICTERUS — PROLONGED    CATARRHAL   ICTERUS       -                 -  1021 

VIII.    DISEASES    OF   THE   PANCREAS                   .                 -                 -                 -                 i                 -  1028 

I.    GENERAL   SURVEY    OP   THE   DISEASES    OP   THE   PANCREAS       -                 -  1028 

IL    CANCER   OP   THE   PANCREAS  ------  1029 

III.  CYSTS   OF   THE    PANCREAS       --.---  1029 

IV.  IL^MORRHAGE    OF   THE    PANCREAS      -                 ...                 -  1030 
V.    PANCREATITIS               ---...-  1031 

VI.    PANCREATIC   CALCULI                 ------  1031 

VII.    RELATION      BETWEEN      PANCREATITIS      AND     GALL  -  STONES  —  PAN- 
CREATICO-BILIARY      SYNDROME  —  CYTOSTEATONECROSIS      AND 

PANCREATICO -PERITONEAL  H-3EM0RRHAGE             -                -                -  1032 


TEXT-BOOK    OF    MEDICINE 

PART   T 

DISEASES  OF  THE  RESPIRATORY  SYSTEM 

CHAPTER  I 
DISEASES  OF  THE  NASAL  FOSSAE 

T.  CORYZA. 

Coryza,  or  nasal  catarrh,  is  the  term  applied  to  inflammation  of  the  pituitary 
mucosa. 

I .  Acute  Coryza. 

Description. — Acute  coryza  shows  itself  by  frontal  headache  and  a 
feeling  of  obstruction  and  of  tickling  in  the  nasal  fossae.  At  first  sneezing 
is  frequently  repeated,  and  brought  on  again  by  the  slightest  impression  of 
cold.  The  nasal  mucosa,  at  first  dry,  soon  secretes  a  clear  and  irritating  liquid, 
causing  erythema  of  the  parts  over  which  it  flows.  The  nose  is  shiny  and 
swollen  ;  the  sen.ses  of  smell  and  of  taste  are  blunted  or  abolished.  The 
patient  constantly  keeps  his  mouth  open,  whilst  his  breathing  is  diflicult  and 
noisy.  Suction  and  deglutition  are  rendered  difficult  by  the  blocking  of  the 
nasal  passages.  These  troubles  are  insignificant  in  the  adult,  but  become 
serious  in  the  infant,  who  cannot  take  the  breast  without  suffocating. 

The  inflammation  spreads  in  various  directions  :  to  the  frontal  sinuses 
(sharp  pains  in  the  head)  ;  to  the  conjunctivae  (injection  of  the  eyes  and 
lachrymation)  ;  to  the  mucous  membrane  of  the  Eustachian  tubes  (auditory 
troubles,  buzzing  noises). 

General  malaise  and  transient  fever  may  also  be  present.  By  the 
second  or  third  day  the  cold  is  ripe  :  the  nasal  .secretion  becomes  thick  and 
greenish,  crusts  form,  the  patient's  nose  is  blocked  up,  his  voice  has  a  nasal 
twang,  and  her[)etic  vesicles  often  appear  round  the  nostrils  or  the  lips. 
Towards  the  end  of  the  first  week  the  coryza  ceases.  When  the  inHammation 
reacht's  the,  laryn.x  and  the  trachea,  it  produc^es  laryngitis  and  tracheitis  ; 
in  vulgar  parlance,  "  the  cold  has  settled  on  the  chest," 

1 


2  TEXT-BOOK  OF  MEDICINE 

^Etiology — Diagnosis. — Cold  and  damp  weather,  the  first  sunshine  of 
spring,  chills  of  every  kind,  but  especially  of  the  feet,  are  the  common  causes 
of  coryza.  Influenza  at  its  onset,  measles  during  the  period  of  invasion,  and 
the  iodides,  produce  a  nasal  catarrh  which  differs  in  nature  from  true 
coryza. 

Some  asthmatics  are  suddenly  seized  with  violent  and  repeated  fits  of 
sneezing.  During  the  fit,  which  lasts  from  a  few  minutes  to  a  quarter  of  an 
hour,  the  eyes  are  injected  and  watery  and  the  nose  runs  freely;  but  after 
this  fit,  which  precedes  or  replaces  the  attack  of  asthma,  everything  returns 
to  normal.  True  coryza  differs  as  much  from  this  manifestation  of  asthma 
as  it  does  from  hay-fever,  or  spasmodic  rliino-bronchitis.  This  malady, 
wliich  in  England  has  been  described  under  the  name  of  hay-fever,  and  in 
which  there  is  a  nervous  element  besides  the  catarrhal  one,  is  often  the  ap- 
panage of  gouty  or  asthmatic  patients,  and  usually  appears  at  the  beginning 
of  summer.  It  presents  two  chief  forms,  which  may  follow  one  another  or 
be  present  together — on  the  one  hand,  nasal  catarrh,  with  abundant  secre- 
tion, uncontrollable  sneezing,  pricking  sensations  in  the  eyes,  injection  of  the 
conjunctivae,  violent  headache  and  insomnia  ;  on  the  other  hand,  dyspnoea, 
resembling  that  of  asthma  and  playing  the  chief  part,  while  the  nasal  catarrh 
may  be  of  secondary  moment.  Hay-fever  will  be  discussed  in  detail  under 
Diseases  of  the  Bronchi, 

We  must  not  confuse  coryza  with  the  nasal  forms  of  diphtheria,  of  blen- 
norrhagia,  and  of  glanders.  When  diphtheria  attacks  the  nasal  mucous 
membrane,  it  produces  an  abmidant  secretion,  wliich  is  sometimes  san- 
guineous. On  examining  the  nasal  fossae,  we  can  usually  discern  the  diph- 
theritic membrane,  and  bacteriological  examination  shows  the  presence  of 
Loffier's  bacillus. 

Glanders  likewise  produces  a  specific  coryza  :  the  nasal  mucous  mem- 
brane is  swollen,  excoriated,  and  ulcerated ;  nasal  respiration  is  impossible, 
and  sanious,  foetid  liquid  flows  from  the  nostrils.  This  discharge,  wliich 
constitutes  a  sign  of  the  liighest  importance  in  animals,  is  much  less  profuse 
in  man,  and  its  presence  would  not  suffice  to  establish  the  diagnosis  if  the 
cutaneous  eruptions  and  the  articular  manifestations  of  glanders  were 
absent. 

Treatment. — Inhalations  of  vapour  of  iodine  and  of  ammonia  have  been 
extolled.  In  infants  at  the  breast  care  must  be  taken  to  cleanse  the  nasal 
fossae  of  the  secretions  which  hamper  the  movements  of  sucking  and  swal- 
lowing. 

Some  rehef  may  be  obtained  from  the  following  j)owder  : 

SaHcylate  of  bismuth      . .         . .  . .         . .  . .     oiv. 

Powdered  camphor  . .  . .  . .  . .  . .     3i.ss. 

Cocaine  hydrochlorate    . .         . .         . .         . ,         . .     gr.  i. 


DISEASES  OF  THE  NASAL  FOSS.E  3 

The  pricking  sensations  and  the  secretions  are  reHeved  by  the  use  of  the 
following  ointment  twice  daily  : 

Menthol  . .  . .  . .  . .  . .  . .  . .     gr.  ii. 

Lanoline  . ,  . .  . .  . .  . .  . .     gr.  xlv. 

VaseUne  (pure)  . .         . .  . .  . .  . .  . .     5ii. 

2.  Chronic  Coryza. 

Description. — This  form  may  follow  attacks  of  acute  coryza,  or  may  be 
chronic  from  the  outset. 

The  sneezing,  the  frontal  headache,  and  the  fever  of  acute  coryza  are 
wanting,  but  there  is  no  lack  of  other  signs.  The  nose  is  stuffed  up,  so  that 
the  patient  can  only  breathe  with  liis  mouth  open,  especially  at  night. 
Respiration  is  embarrassed,  noisy,  and  sometimes  accompanied  by  a  kind 
of  snoring  sound ;  the  voice  is  nasal ;  the  senses  of  taste  and  of  smell  are 
blunted  ;  the  hearing  is  less  acute,  and  buzzing  in  the  ears  is  frec^uent.  The 
nasal  secretion  may  be  scant  or  abundant.  In  clironic  dry  rhinitis,  wliich 
is  most  conunon  in  adults,  secretion  is  almost  absent,  and  patients  complain 
of  a  distressing  feeling  of  dryness.  More  commonly,  especially  in  young 
subjects,  the  nasal  secretion  is  abundant,  and  the  nasal  nmcous  membrane 
is  covered  with  crusts  and  dried  mucus.  Chronic  coryza  has  a  slow  course 
and  an  indefinite  duration  ;  it  is  sometimes  interrupted  by  acute  attacks, 
and  at  other  times  more  or  less  lengtliy  remissions  give  some  respite  to  the 
patient.     We  shall  see  later  the  frequency  of  ozaena  in  chronic  coryza. 

On  rhinoscopic  examination,  the  mucous  membrane  appears  red  and 
hypertrophied,  especially  over  the  anterior  part  of  the  inferior  turbinate 
bone  (hypertropliic  rliinitis).  When  the  coryza  is  of  very  long  duration,  the 
nmcous  membrane  is  indurated  and  fibrous,  wliile  the  glandular  elements 
show  a  tendency  to  disappear. 

Under  the  name  of  posterior  coryza,  Desnos  has  described  a  chronic 
inflammation  of  the  naso-pharyngeal  cavity.  This  variety  is  cliiefly  asso- 
ciated with  glandular  angina  ;  the  local  lesions  can  only  be  discerned  by 
rhinoscopy,  and  its  chief  symptoms  are  snuffling  and  hawking. 

In  lymphatic  cliildren  a  chronic  herpetic  coryza  has  been  described. 
The  orifice  of  the  nostrils  and  the  septum  are  covered  by  crusts  like  those  of 
impetiginous  eczema.  After  the  crusts  fall  off,  they  leave  bare  slight  ulcers, 
which  become  covered  with  new  crusts,  and  the  duration  of  the  illness  is 
indefinite. 

TJie  changes  in  the  so-called  scrofulous  coryza  of  infants  arc  character- 
ized by  hypertrophy  of  the  nasal  mucous  membrane  which  shows  fungating 
vegetations,  by  deep  ulcers  wliich  may  attack  the  bones,  by  deformity  and 
flattening  of  the  nose.  This  old  descri[)tion  jnust  be  r(^vis«'(l,  for  niosi  of  these 
lesions  are  due  to  tubercular  disease,  or  to  early  or  late  hereditary  syphilis. 

1—2 


4  TEXT-BOOK  OF  MEDICINE 

Diagnosis. — In  the  following  chapters  we  shall  give  the  diagnosis  ot 
chronic  coryza  from  nasal  syphihs  and  tuberculosis.  It  is  enough  for  me 
to  mention  here  that  chronic  coryza  has  many  symptoms  in  common  with 
adenoid  growths  of  the  naso-pharynx  and  with  mucous  polypi  of  the 
nose.     Rhinoscopic  examination  will  remove  all  doubts. 

Treatment. — The  local  treatment  of  chronic  coryza  consists  in  cleaning 
the  mucosa  by  means  of  appropriate  douches  ;  cauterization,  powders,  and 
snuffs  are  then  employed.  Lavage  may  be  carried  out  by  a  siphon  douche, 
the  nozzle  of  wliich  fits  the  nostril  tightly  ;  the  fluid,  introduced  without 
force,  into  one  nostril,  flows  back  through  the  opposite  one  without  passing 
into  the  pharynx.  These  douches  consist  of  lukewarm  saline  solutions, 
weak  boric  lotions,  or  solutions  of  chlorate  of  potash.  The  cures  at  Challes 
and  Mont-Dore  are  of  much  service.  As  a  snufE,  one  of  the  following 
preparations  may  be  recommended  : 

1.  Bismuth  subnitrate  )  --  t*" 
Venetian  talc              J            * '          ' '          ' '          ' '       '•->•"• 
Precipitated  chalk      . .          . .          . .          . .          . .  gr.  v. 

2 .  Chlorate  of  potash     . .  . .  . .  . .         . .  gr.  xlv. 

Powdered  sugar  . .  , .  . .  . .  . .  5v. 

Arsenical  preparations,  taken  internally,  are  useful  when  the  rhinitis  is 
associated  with  the  gouty  diathesis. 

II.  NASAL  DIPHTHERIA. 

Description. — Nasal  diphtheria  is  nearly  always  associated  with  diph- 
theria of  the  fauces,  which  it  may  precede  or  follow.  It  begins  somewhat 
like  a  simple  coryza,  with  redness  of  the  nostrils  and  nasal  discharge.  There 
is  but  little  sneezing.  The  nasal  discharge  is  sanious,  muco-purulent,  or 
sanguineous,  and  contains  membranes.  Epistaxis  is  common,  and  usually 
precedes  the  formation  of  membranes.  Repeated  and  profuse  epistaxis 
was  thought  by  Trousseau  to  be  of  evil  omen. 

The  patient's  voice  is  nasal,  and  he  can  only  breathe  with  his  mouth  open. 

The  submaxillary  glands  are  swollen.  On  rhinoscopic  examination,  the 
mucous  membrane  is  swollen  and  coated  with  membrane,  which  is  adherent, 
and  usually  localized  to  the  posterior  half  of  the  nasal  fossae. 

In  some  cases,  especially  in  children  with  measles,  the  diphtheria  may 
reach  the  nasal  duct,  and  spread  to  the  eyelids  and  the  eyes.  This  oculo- 
palpebral  variety  shows  itself  by  lachrymation,  Avith  redness  and  swelling 
of  the  conjunctiva  and  of  the  eyelids.  Sero-purulent  secretion  appears,  the 
eyelids  and  the  ocular  conjunctiva  are  covered  with  false  membrane,  and 
in  some  cases  perforation  of  the  cornea  and  destruction  of  the  eye  result 
when  streptococcal  infection  is  also  present. 


DISEASES  OF  THE  NASAL  FOSS^  5 

Nasal  diphtheria,  described  by  the  term  "  fibrinous  rhinitis,"  may  be 
of  such  duration  as  to  be  chronic. 

The  diagnosis  of  diphtheritic  coryza  is  easy  wlien  the  patient  is  already 
suffering  from  pharyngeal  or  laryngeal  diphtheria  ;  if  coryza  be  the  first 
symptom  hesitation  is  pardonable.  The  diagnosis  is  very  difficult,  especially 
at  the  commencement,  and  I  know  only  one  way  of  settling  the  question 
— viz.,  by  culture  and  bacteriological  examination  of  the  membrane  or  of 
the  nasal  mucus  {vide  Diphtheritic  Angina). 

The  prognosis  is  not  very  grave  if  the  disease  remain  limited  to  the  nasal 
fossae,  and  if  the  diphtheria  bacillus  be  present  alone  without  the  strepto- 
coccus. If  both  organisms  are  present,  the  membranes  usually  present  a 
different  aspect,  being  diffluent  and  gangrenous,  while  the  discharge  is 
profuse,  persistent,  and  accompanied  by  epistaxis.  Such  a  coryza  usually 
points  to  very  severe  diphtheria,  and  is  one  of  the  manifestations  of  Trous- 
seau's malignant  diphtheria.  Loffler's  bacillus  finds  so  favourable  a  soil  in 
the  nasal  fossae  that  its  localization  in  the  nose  appears  to  me  to  have  great 
weight  in  determining  diphtheritic  paralysis. 

We  often  find  virulent  bacilli  in  the  nasal  cavities  several  weeks  after  tlie 
cure  of  diphtheritic  angina. 

Diphtheritic  coryza,  like  all  thja  varieties  of  diphtheria,  should  be  treated 
mth  injections  of  serum.  The  earlier  the  injection,  the  better  the  chance 
of  success  ;  hence  the  importance  of  making  a  correct  chagnosis  from  the 
very  first. 

III.  NASAL  SYPHILIS— SYPHILITIC  RHINITIS. 

In  this  chapter  I  shall  review  (1)  the  primary  lesion,  the  chancre;  (2) 
secondary  troubles  ;  and  (.'3)  tertiary  troubles. 

1.  Nasal  Chancre. 

Description. — The  study  of  nasal  chancres  comprises  chancre  of  the 
skin  of  the  nose  and  chancre  of  the  nasal  fossa\  Every  sy{)hilitic  chancre 
is  composed  of  a  mass  of  embryonif  cells,  and  i'onns  a  small  tumour  (primary 
syphiloma),  developed  at  the  expense  of  the  skin  and  of  the  subcutaneous 
tissue.  The  appearance  of  the  chancre  differs,  however,  on  the  skin  and  on 
the  mucous  membrane.  On  the  skin  it  is  covered  by  a  crust,  due  to  tiie 
j)resence  of  the  horny  layer,  which  does  not  exist  in  the  nuico.sa  ;  the  lesions 
of  the  mucous  epithelium,  soaked  with  fibrino-purulent  licpiid,  end,  not  in  the 
formation  of  a  crust,  but  of  a  false  membrane,  which  is  flaccid,  greyish,  and 
diphtheroid. 

1.  Let  us  first  consider  chancre  of  the  skin.  It  is  situated  «tn  the 
bridge   of   the   nose,  on   tin*   nostrils,  on   the    ti[)  of   the   nose,  or  on   the 


6  TEXT-BOOK  OF  MEDICINE 

nasolabial  fold.  On  the  bridge  the  chancre  is  flat ;  elsewhere  it  is  bulky, 
prominent,  and  spread  out,  forming  a  hypertrophic  papule  (Fournier).  It 
runs  the  same  course  as  all  cutaneous  chancres  :  at  first  it  is  a  crack,  or  a 
reddish  erosive  papule,  then  it  grows  larger,  becomes  prominent  and  en- 
crusted, but  always  remains  painless. 

This  encrusted  or  pustulo-crustaceous  chancre  has  the  appearance  of 
ordinary  ecthyma.  If  the  crust  be  raised,  after  having  been  first  softened, 
the  chancre  appears  with  all  its  characteristics — viz.,  flat  or  slightly  convex 
surface,  erosive,  but  not  ulcerated,  smooth,  reddish,  often  bleeding  and 
covered  with  papillae.  Sometimes  a  scanty  purulent  secretion  may  be 
noticed.  The  edges  of  the  chancre  are  flat,  not  perpendicular ;  strictly 
speaking,  there  is  no  edge,  because  there  is  no  ulceration.  Its  base  is 
indurated  and  parchment-like.  Adenopathy  is  constant  and  may  be  uni- 
lateral or  bilateral ;  the  condition  is  somewhat  indolent,  and  is  confined  to 
the  glands  at  the  angle  of  the  jaw,  while  one  gland  is  often  much  larger  than 
the  'others. 

After  about  two  months  the  chancre  heals  without  cicatrization ;  the 
induration  and  the  adenopathy,  however,  persist  for  a  long  while. 

The  nasal  chancre  must  not  be  confounded  with  a  furuncle.  From  the 
first  the  part  on  which  a  boil  is  about  to  develop  is  swollen,  painful,  red,  and 
shiny  ;  later  it  becomes  purulent — characters  which  are  quite  different  from 
those  presented  by  a  chancre.  Chancre  will  not  be  mistaken  for  epithelioma, 
as  the  latter  is  a  painful  tumour,  infinitely  slower  in  its  development, 
ulceration  is  delayed,  the  base  is  not  indurated,  and  enlarged  glands  do 
not  appear  till  much  later.  Epithelioma  does  not  tend  to  spontaneous 
cicatrization,  as  chancre  does. 

2.  Let  us  now  consider  chancre  of  the  nasal  fossae.  This  chancre 
always  occurs  on  the  anterior  or  posterior  part  of  the  nasal  fossa.  I  merely 
mention  chancre  of  the  posterior  orifice  of  the  nasal  fossa  from  accidental 
inoculation  by  an  infected  Eustachian  catheter. 

Chancre  of  the  vestibule  usually  arises  on  the  cartilaginous  septum.  It 
develops  as  a  greyish  or  reddish  lump,  wliich  may  be  indurated  or  softened, 
and  has  rouglily  the  appearance  of  a  mushroom.  This  chancre,  in  its 
hypertrophic  form,  partly  fills  the  nostril  and  causes  an  ichorous  or  bloody 
discharge.  The  nose  is  red  and  swollen ;  though  it  is  deformed  externally, 
no  deviation  of  the  septum  is  present.  Eadiation  of  pain  to  the  nose  or  the 
face  is  common.  Enlarged  glands  at  the  angle  of  the  jaw  are  always  found. 
The  chancre  lasts  from  six  weeks  to  two  months,  and  then  heals  without 
cicatrization. 

The  diagnosis  between  chancre  and  malignant  tumour  of  the  nasal 
fossa  (sarcoma)  must  be  based  upon  the  following  considerations  :  The 
evolution  of  sarcoma  is  much  slower  than  that  of  chancre,  nasal  haemorrhage 


DISEASES  OF  THE  NASAL  FOSS.E  7 

may  be  frequent  and  profuse,  ulceration  appears  late,  pain  is  acute,  en- 
larged glands  appear  slowly ;  lastly,  sarcoma  deforms  the  nasal  fossaj  and 
causes  deviation  of  the  septum. 

2.  Secondary  Troubles — Syphilitic  Coryza. 

I  shall  describe  first  cutaneous  syphilides,  and  secondly  those  of  the 
mucous  membrane. 

1.  Cutaneous  syphilides  show  here,  as  elsewhere,  different  forms,  and 
may  be  dry,  moist,  or  crusted.  The  dry  syphilides  are  papular,  papulo- 
lenticular,  or  papulo-squamous.  They  are  frequent  on  the  alse  nasi,  where 
they  often  present  the  granular  form  (Fournier). 

The  moist,  erosive  syphilides,  or  mucous  patches,  appear  as  cracks  and 
clefts  in  the  ala  nasi  and  the  naso-labial  fold.  Sypliilides  which  are  crus- 
taceous,  papulo-  or  pustulo-crustaceous  may  invade  the  whole  of  the  nose. 

All  these  syphilides  are  indolent  in  character  and  do  not  itch.  They 
are  rarely  confined  to  the  nose  alone,  and  are  generally  found  on  the  cheeks, 
the  chin,  or  the  forehead. 

2.  Secondary  syj)hilis  of  the  mucous  membrane  presents  a  different 
aspect,  according  to  whether  it  attack  the  adult  or  the  new-born  infant,  as 
early  hereditary  syphilis. 

In  the  adult  we  find  bright  red  erythema  of  the  mucous  membrane  and 
erosions,  with  muco-purulent  or  muco-sanguineous  secretions,  and  with 
formation  of  crusts,  which  reform  after  they  have  been  rubbed  off.  These 
crusts  may  block  the  nostrils,  impede  respiration,  and  simulate  eczema. 

In  the  newly-born  coryza  is  often  the  first  sign  of  hereditary  syphilis. 
It  appears  a  few  weeks  after  birth.  The  cliild  breathes  with  great  difficulty 
through  the  nostrils,  and  the  movements  of  sucking  are  hampered ;  but 
so  far  there  is  little  distinction  between  syphilitic  and  simple  coryza.  Sero- 
purulent,  and  in  some  cases  bloody,  fluid  exudes  from  the  nose  ;  the  secretion 
becomes  more  and  more  sanious,  without  being  profuse,  irritates  the  alae 
nasi  and  the  upper  lip,  and  produces  ulcers  covered  by  yellowish  or  greenish 
crusts,  which  may  hide  the  upper  lip.  Nasal  syphilis  in  the  new-born,  in 
contradistinction  to  what  is  seen  at  a  later  age,  rarely  results  in  tertiary 
le.sions  and  deformities  (Trousseau).  Specific  coryza,  however,  may  become 
chronic,  with  tliickening  of  the  nmcous  membrane,  ulceration  and  swelling 
of  the  adenoid  tissue.  Perichondritis  of  the  septum,  destruction  of  the 
vomer,  and  obliteration  of  the  lachrymal  duct,  have  also  been  seen  (Ziem). 

We  must  recognize  sypliilitic  coryza  of  the  new-born  in  order  to  treat  it 
without  delay,  and  to  avoid  the  possible  contamination  of  the  nurse  from  the 
child.  Coryza  rarely  exists  as  the  only  manifestation  of  syphilis,  and  is 
usually  accompanied  or  followed  by  other  troubles  which  are  an  aid  to 
diagnosis.     We  must,  therefore,  examine  the  child's  body  for  skin  cruption.s, 


8  TEXT-BOOK  OF  MEDICINE 

roseola,  erythema  of  an  ashy  tint  on  the  neck,  Imnds,  or  feet,  and  patches 
which  are  scalloped,  do  not  itch,  and  are  often  scaly.  We  may  sometimes 
find  mucous  patches  round  the  anus  or  the  navel,  behind  the  ears,  upon 
the  scrotum  or  the  labia  majora,  and  Trousseau  used  to  lay  stress  upon 
unhealthy  fissures  and  ulcers  of  the  folds  of  the  skm.  From  this  time 
many  children  with  hereditary  syphilis  show  changes  in  appearance  :  their 
bodies  take  on  a  brownish  colour,  the  eyebrows  fall  out,  and  are  replaced 
by  the  yellowish,  scaly  plaques  of  psoriasis.  These  marks  of  hereditary 
syphilis  will  aid  in  the  diagnosis  of  syphilitic  coryza. 

3.  Tertiary  Troubles  of  Nasal  Syphilis. 

The  tertiary  lesions  of  nasal  syphilis  which  may  result  from  the  acquired 
or  hereditary  disease  are  in  each  case  identical.  As,  however,  syphilis  may 
invade  the  nose  or  the  nasal  fossae,  it  is  necessary  to  study  each  form. 

1.  Tertiary  Syphilis  of  the  Nose. — The  skin  lesion  here  is  essentially 
the  tubercle,  which  much  resembles  the  chancre  in  structure,  and  is 
composed  of  a  mass  of  embryonic  cells.  The  syphilitic  tubercle  is  a 
cutaneous  gumma,  and  forms  a  small  tumour  of  the  size  of  a  millet-seed, 
a  small  pea,  or  a  cherry-stone.  This  gumma,  which  is,  as  it  were,  set  in  the 
skm,  is  at  first  firm  and  resistant,  and  projects  above  the  surface  of  the 
skin.  The  syphilitic  tubercle  is  rarely  solitary,  and  variable  numbers  are 
seen  in  the  same  region  ;  they  may  be  grouped  in  a  mass,  form  segments 
of  a  circle,  or  sometimes  fuse  together  and  produce'  a  true  gummatous 
infiltration,  "  a  kind  of  plaque  of  hyperplastic  integuments,  studded  or 
bordered  by  tubercular  nodules." 

These  dermatoses  are  common  upon  the  face,  but  the  nose  is  the  "  victim 
by  choice  "  (Fournier).  They  are  sometimes  confined  to  one  part  of  the 
nose  ;  at  other  times  they  invade  the  whole  nose  and  spread  to  the  face. 
The  lesion,  as  we  have  said,  appears  as  a  tubercle  (nodular  syphiloma)  or 
an  infiltration  (dilTuse  sypliiloma).  For  several  months  the  disease  is  in- 
sidious in  its  development ;  pain,  fever,  enlargement  of  glands — in  short,  all 
signs — are  absent.  The  nose,  however,  loses  its  normal  aspect,  becoming 
deformed  and  increased  in  size,  while  the  affected  skin  is  studded  by  dull 
red  projections,  and  slight  desquamation  of  the  epidermis  occurs.  At  a 
more  advanced  stage  the  dermatosis  may  present  different  aspects  :  in  rare 
cases  the  tubercles,  especially  those  which  are  isolated,  spread,  become 
indurated  or  almost  horny,  and  end  in  atrophy.  As  a  rule,  however,  both 
the  nodular  and  the  diffuse  syphiloma,  when  untreated,  end  in  softening, 
ulceration,  suppuration,  and  formation  of  crusts.  These  syphilides  are 
known  as  tuberculo  -  ulcerating  and  tuberculo-crustaceous,  or  as  the 
gummatous  ulcer  which  is  serpiginous  and  perforating. 

Tliis  phase,  in  which  the  gummatous  tissue  softens    and  ulcerates,  is 


DISEASES  OF  THE  NASAL  FOSS.E  9 

relatively  rapid,  and  contrasts  with  the  slowness  of  the  preceding  phase. 
At  this  period  the  nose  is  deformed,  enlarged,  budding  out  at  one  spot, 
ulcerated  at  another,  sometimes  gullied  by  purulent  ulcers,  and  covered  in 
places  by  brownish  or  greenish  crusts,  which  are  thick,  stratified,  and 
adherent.  In  spite  of  these  lesions,  we  usually  notice  no  functional  trouble 
no  fever,  and  little  or  no  pain. 

When  the  lesions  are  deep,  and  especially  when  they  have  not  beep 
treated  in  time,  tertiary  syphilis  leaves  indelible  marks  :  the  alae  nasi  are 
scalloped  and  destroyed  ;  the  nose  is  deformed,  flattened,  thinned,  and 
furrowed  with  hard,  wliite,  and  honeycombed  scars. 

2.  Tertiary  Syphilis  of  the  Nasal  Fossae.— The  lesions  usually  com- 
mence in  the  mucosa,  and  then  invade  the  perichondrium,  the  cartilages. 
the  periosteum,  and  the  bone.  The  cartilage  and  the  bone  may  be  attacked 
from  the  outset.  Sometimes  the  disease  produces  only  superficial  ulcers, 
which  are  not  serious  and  readily  recover,  but  at  other  times  it  destroys 
by  invasion  and  perforation.  It  attacks  the  bony  and  the  cartilaginous 
framework  of  the  nose,  lays  bare  the  cartilages  and  the  bones,  gives  risf 
to  sequestra,  and  mutilates  the  organ,  causing  irremediable  destruction. 

These  lesions  must  be  studied  separately,  for  they  present  different 
symptoms  according  to  the  regioij.  affected. 

(a)  Hypertrophic  Syphilitic  Rhinitis. — The  picture  is  one  of  chronic 
coryza  :  nasal  respiration  is  incomplete  or  impossible,  the  patient  wipes 
away  thick  mucus  with  crusts,  and  acute  attacks  sometimes  supervene. 
On  examination  of  the  nasal  fossa^,  we  find  hypertrophy  of  the  mucosa  ;  but 
this  hypertrophy,  which  may  be  polypoid,  must  not  be  confounded  with 
adenoid  vegetations.  The  rhinitis  is  not  always  general,  and  may  confine 
itself  to  one  fossa,  or  to  the  inferior  turbinate  bone  which  fills  the  meatus. 
Ozaena  often  accompanies  this  syphilitic  rliinitis. 

(6)  Perforatiofi  of  the  Septum. — The  nasal  fossae  are  separated  by  a  bony 
and  cartilaginous  partition  ;  the  bony  part  is  formed,  above  by  the  per- 
pendicular plate  of  the  etlimoid,  below  by  the  vomer,  while  the  cartilaginous 
l)art  is  formed  by  the  triangular  cartilage,  which  fills  up  the  gap  left  by  the 
bony  plates.  The  cartilage  is  usually  first  affected  by  syphilis  :  the  lesion 
Itegins  in  the  mucosa,  reaches  the  perichondrium,  which  if  lays  bare,  sets  up 
necrosis  of  the  subjacent  cartilage,  and  then  causes  a  round  or  oval  perfora- 
tion of  variable  size.  In  some  cases  the  lesion  extends  to  the  vomer  <tr  the 
ethmoid,  whence  .se<|uestra  and  more  or  less  extensive  losses  of  substance 
result.  This  process  goes  on  insidiously,  without  pain  and  under  cover  of 
the  deceptive  symptoms  of  chronic  coryza. 

Syphilitic  perforations  of  the  se{)tum  must  be  diagnosed  from  tho.se 
due  to  other  causes.  We  see  a  .simple  perforating  ulcer,  which  begin.s 
simultaneoasly  on  both  sides  of  the  septum  at  a  symmetrical  spot.      It 


10  TEXT-BOOK  OF  MEDICINE 

always  respects  the  bony  septum,  frequently  causes  epistaxis,  and  appears 
to  be  associated  with  the  presence  of  staphylococci  or  streptococci.  The 
tubercular  ulcer — and  I  speak  now  of  primary  tuberculosis  exclusively — ■ 
affects  the  nasal  septum,  and  hardly  ever  its  bony  part.  The  malady 
appears  as  a  fungating,  mushroom-like  growth,  which  causes  perforation 
of  the  septum.  The  edges  of  this  ulcer  are  prominent,  sanious,  and  obstruct 
both  nostrils.  Bacteriological  examination  may  reveal  the  presence  of 
bacilli.     Perforation  of  the  septum  may  also  result  from  typhoid  fever. 

(c)  Destruction  of  the  Suhseptum. — The  subseptum  of  the  nose  is  formed 
by  the  cartilage  of  the  septum,  against  which  the  horseshoe-like  branches  of 
the  cartilages  of  the  alse  nasi  rest.  When  the  subseptum  is  destroyed  by  a 
syphilitic  lesion,  the  two  nostrils  have  one  triangular  gaping  opening,  and, 
as  the  point  of  the  nose  is  no  longer  supported,  it  bends  back,  and  assumes 
the  curved  appearance  of  a  parrot's  beak  (Fournier). 

(d)  Destruction  of  the  True  Bones  of  the  Nose. — The  root  is  formed  by  the 
true  bones  of  the  nose.  When  the  bony  framework  is  attacked  by  syphilitic 
necrosis  and  disappears,  the  soft  parts  sink  in — the  nose  looks  as  though  the 
bridge  had  been  crushed  in  by  the  blow  of  a  hammer — and  the  tip  turns  up. 
"  This  deformity  is  a  certificate  of  syphilis  "  (Fournier). 

(e)  Destruction  of  the  Cartilaginous  Vault. — Below  the  true  bones  which 
form  the  upper  framework  there  is  a  cartilaginous  roof,  which  forms  the 
inferior  framework  of  the  nose.  When  the  cartilage  is  destroyed  by  syphilis, 
the  lower  half  of  the  nose  sinks  in  and  is  drawn  backwards  ;  the  lower 
segment  is  invaginated  into  the  upper  segment.  By  pulling  the  tip  of  the 
nose,  the  normal  shape  can  be  restored  for  a  moment,  but  the  invagination 
at  once  recurs.  Fournier  has  called  it  the  "  opera-glass "  nose.  Two 
remarkable  examples  were  seen  in  my  wards  at  the  Necker  Hospital  and 
at  the  Hotel  Dieu.  This  special  shape  is  said  to  be  due,  according  to  some 
writers,  to  the  absence  of  the  cartilaginous  framework  ;  but,  according  to 
others,  it  is  cliiefly  caused  by  retraction  of  the  cicatricial  tissue. 

(/)  Lachrymal  Tumour. — Nasal  syphilis  may  produce  an  exostosis  of 
the  lachrymal  bone  and  of  the  nasal  process  of  the  superior  maxilla.  Stenosis 
of  the  nasal  canal  with  lachrymal  tumour  results. 

(g)  Perforation  of  the  Palatine  Vault. — The  floor  of  the  nasal  fossae,  like 
the  vault  of  the  palate,  is  formed  by  the  superior  maxillary  bones,  which 
articulate  behind  with  the  palate  bones.  As  the  result  of  ulcerating 
syphilides,  or  periosteal  gummata  of  the  floor  of  the  nasal  fossae,  a  part  of 
the  superior  maxilla  is  laid  bare ;  the  bare  bone  necroses,  a  sequestrum  is 
formed,  and  an  abscess  results  on  the  buccal  aspect,  between  the  bone  and  the 
mucous  membrane.  This  abscess  projects  into  the  mouth  as  a  small  indolent 
tumour.  It  may  open  itself  or  have  to  be  opened.  We  then  find,  with  the 
probe,  that  there  is  a  sequestrum,  which  may  be  movable  or  fixed,  and 


DISEASES  OF  THE  NASAL  FOSS.E  11 

when  the  sequestrum  is  detached,  a  perforation  results.  This  perforation 
generally  appears  in  the  middle  line,  a  little  in  front  of  the  palate  bones. 
Its  shape  may  be  round  or  oval,  and  in  size  it  may  be  as  large  as  a  pin's 
head,  a  lentil,  a  sixpenny- piece,  or  even  larger,  for  it  may  invade  a  part  of 
the  palatine  vault. 

There  are  two  quite  distinct  phases  in  this  process.  During  the  first 
phase,  which  is  very  slow,  the  process  is  purely  nasal ;  the  lesion  shows  itself 
by  chronic  coryza,  with  muco-purulent  secretion,  appearance  of  crusts,  and 
formation  of  sequestra,  which  are  easily  recognized  by  exploration  with  a 
probe.  Ozsena  is  a  very  common  symptom  ;  the  f  oetor  is  sometimes  appalling, 
and  the  stench  improves,  or  ceases,  only  after  elimination  of  the  dead  bone. 

This  nasal  phase,  which  for  a  long  time  is  insidious  and  almost  painless, 
is  followed  by  a  buccal  phase,  in  which  we  see  the  formation  of  the  palatal 
abscess  and  perforation  of  the  arch.  As  soon  as  perforation  occurs,  two  new 
symptoms  appear  :  the  voice  becomes  nasal,  and  solids  or  liquids  taken  by 
the  mouth  pass  back  through  the  nose.* 

It  was  long  believed  that  the  perforation  of  the  palate  in  syphilis  proceeded 
from  the  mouth  to  the  nose.  This  is  an  error.  The  lesion  starts  in  the  nose, 
and  the  perforation  proceeds  towards  the  mouth  (Fournier,  Duplay).  When 
the  perforation  is  small,  specific  treatment  may  succeed  in  closing  it ; 
when  it  is  large,  surgical  intervention  is  necessary. 

(h)  Naso-cranial  Syphilis. — Under  this  heading  I  shall  describe  the 
syphilitic  lesions  wliich,  at  first  limited  to  the  roof  of  the  nasal  fossa?,  later 
attack  the  organs  of  the  cranial  cavity. 

The  vault,  or  upper  wall,  of  the  nasal  fossfe  forms  a  narrow  gutter, 
composed  of  several  bones,  of  which  the  cribriform  plate  of  the  ethmoid  and 
the  sphenoid  play,  in  the  present  question,  the  chief  part.  (Jummatous 
osteoperiostitis  in  this  region  may  readily  extend  to  the  cranial  cavity. 

If  the  lesion  remain  limited  to  the  upper  wall  of  the  nasal  fossnp,  we 
only  find  nasal  symptoms.  This  stage  is  sometimes  painless,  at  others 
accompanied  by  nasal  or  frontal  pain  and  intense  headache.  The  symptoms 
are  those  of  a  chronic  coryza,  with  discharge  and  crusts,  and,  in  addition, 
epistaxis,  ozaena,  and  elimination  of  sequestra.  Ozgena  is,  however,  rarer 
in  this  variety  of  nasal  syphilis  than  in  the  others  which  we  have  already 
studied.  The  use  of  the  probe  is  not  always  free  from  accidents,  and  1  have 
had  tmder  my  care  a  woman  in  whom  it  produced  giddiness,  acute  frontal 
pain,  and  almost  syncope. 

The    lesion    may    long    remain    confined    to    the    roof    of    the    nasal 

fossae,  and  affect  the  sphenoid  and  the  ethmoid,  without  causing  cerebral 

troubles  ;  but  in  other  cases  symptoms  of   meningitis  and  of  encephalitis 

may  supervene  at  any  moment.     Frontal  pain,  which  sometimes  is  very 

*   For  furUtfr  «l(l;iils,  sec  cliaptcr  on  I'orforation  of  tho  Vault  of  tho  I'iklalo, 


12  TEXT-BOOK  OF  MEDICINE 

sharp,  paralyses  of  the  motor  or  sensory  cranial  nerves,  vomiting,  epilepti- 
form convulsions,  apoplexy,  and  fatal  coma,  are  the  complications  which 
may  appear,  slowly  or  with  extraordinary  rapidity,  and  make  up  the  cerebral 
phase  of  syphilitic  naso-cranial  osteitis. 

Autopsies  show  the  cause  of  these  severe  troubles.  Osteitis  and  necrosis 
of  the  sphenoid  and  ethmoid  bones,  phlebitis  of  the  coronary,  cavernous,  or 
petrous  sinuses,  phlebitis  of  the  ophthalmic  vein,  intra-orbital  suppuration, 
purulent  meningitis,  and  encephalitis  of  the  frontal  lobes  are  often  found. 

The  preceding  descriptions  suffice  to  show  the  great  importance  of  nasal 
syphilis. 

Diagnosis. — For  want  of  attention,  syphilitic  rhinitis  is  often  mistaken 
for  a  simple  coryza.  The  patient  thinks  but  little  of  his  "  cold,"  and  treats 
himself.  Noting  its  tenacity,  he  seeks  advice.  If  the  physician  do  not 
recognize  syphilis,  he  rests  content  with  prescribing  nasal  douches,  snuffs, 
and  a  cure  at  Challes  or  elsewhere,  when  he  should  employ  mercury.  As  a 
general  rule,  every  individual  who  for  a  long  while  wipes  thick  mucus  or 
crusts  from  his  nose  should  be  suspected  of  syphilitic  rhinitis,  especially  if 
ozaena  be  present.  Exploration  of  the  nasal  fossae  may  then  show  the  pres- 
ence of  erosions,  ulcerations,  or  more  or  less  extensive  losses  of  substance. 

The  diagnosis  between  tertiary  nasal  syphilis  (hereditary  or  acquired) 
and  tuberculosis  of  the  nose  is  sometimes  most  difficult. 

First,  let  us  consider  the  "  dry  tubercular "  lesions.  We  have  two 
patients,  the  one  suffering  from  lupus  of  the  nose,  the  other  from  tubercular 
syphilis.  On  examination  we  find  at  first  nothing  but  resemblances  :  in 
both  cases  an  eruption  of  tubercles  upon  a  red  infiltrated  base,  in  both  cases 
tubercles  identical  in  size  and  shape  and  grouped  in  like  pattern.  The 
diagnosis  appears  very  difficult  :  the  lupus  tubercle,  however,  is  more 
transparent,  like  barley-sugar,  while  the  syphilitic  one  is  of  a  dark  reddish 
tint,  like  muscular  tissue  ;  the  lupus  tubercle  is  flabby  and  sinks  in,  while 
the  syphilitic  one  is  much  harder  to  the  touch  ;  lastly,  lupus  is  infinitely 
slower  in  its  course  than  syphilis. 

Let  us  now  pass  to  the  diagnosis  of  ulcerating  lesions  of  the  nose.  We 
have  two  patients,  one  suffering  from  syphilitic  ulcers,  the  other  from  those 
of  lupus  ;  in  both  cases  the  ulcers  may  be  covered  with  crusts.  How  can  a 
differential  diagnosis  be  made  ?  Here  again  the  resemblances  appear  at 
first  sight  to  outweigh  the  differences,  but  more  careful  scrutiny  reveals 
points  of  distinction.  The  areola  round  the  syphilitic  ulcer  is  of  a  dull  red, 
dark,  and  pigmented,  while  the  areola  round  the  lupus  ulcer  is  clearer  and 
more  bluish.  The  edges  of  the  syphilitic  ulcer  are  hard,  perpendicular, 
adherent,  and  not  flattened,  while  those  of  the  lupus  ulcer  are  flat,  thin,  soft, 
flabby,  moist,  and  not  perpendicular.  The  floor  of  the  syphilitic  ulcer  is 
hollow,  anfractuous,  and  sloughy,  while  the  floor  of  the  other  is  abnost  flat. 


DISEASES  OF  THE  NASAL  FOSS.E  13 

In  both  cases  the  ulcer  is  covered  with  crusts,  but  the  crusts  of  syphiHs  are 
more  compact,  harder,  more  stratified,  more  brownish-green  and  hke  oyster- 
shells  than  those  of  lupus.  As  regards  progress,  syphilis  does  in  a  month 
what  lupus  does  in  a  year. 

We  now  come  to  the  diagnosis  between  the  destructive  lesions  of  syphilis 
and  of  lupus.  Syphilis  destroys  the  nose  in  large  pieces,  while  scrofula 
eats  it  away  atom  by  atom.  The  nose  in  lupus  is  symmetrically  destroyed, 
and  cut  off  as  by  a  hatchet  blow,  from  before  backwards,  from  the  lower  level 
of  the  nasal  bones  to  the  upper  lip  ;  the  aspect  is  that  of  a  death's-head. 
Syphilis,  on  the  other  hand,  causes  more  irregular  and  less  symmetrical 
mutilation.  Lupus  may  very  rarely  attack  the  mucous  membrane,  for 
primary  lupus  of  the  septum  exists,  but  acquired  or  hereditary  syphilis 
has  a  special  tendency  to  attack  this  part.  When  lupus  spreads  to 
the  nasal  fossae  it  is  usually  limited  to  the  vestibule,  the  cartilages,  and  the 
floor  of  the  maxilla  ;  in  any  case  it  rarely  attacks  the  nasal  skeleton.  Syphilis, 
on  the  other  hand,  does  not  show  these  restrictions,  and  the  different  bones 
of  the  nasal  fossae  may  fall  under  its  blows.  Flattening  of  the  bridge,  the 
"  opera-glass  "  nose,  and  perforation  of  the  roof  of  the  palate,  are  almost 
always  the  result  of  acquired  or  of  hereditary  syphilis,  and  are  not,  as  a 
rule,  seen  in  tuberculosis. 

The  details  into  which  I  have  entered  regarding  the  differences  between 
syphilitic  and  tubercular  lesions  of  the  nose  prove  that  diagnosis  is  not  always 
easy.  The  difficulty  is  still  greater  when  both  diseases  are  present  together. 
Ricord,  in  his  picturesque  language,  calls  this  "  Le  scrofulatc  de  verole." 
In  some  cases  (even  more  frequent  in  the  larynx  and  in  the  lungs)  syphilis 
and  tubercle  successively  invade  the  same  organ,  and  the  two  infections  are 
juxtajKJsed.  In  other  cases,  however,  we  might  truly  speak  of  a  hybrid 
afTection,  as  in  certain  syphilo-tubercular  affections  of  glands  and  in  certain 
lui)oid  lesions  of  the  skin  and  the  iiasal  nmcosa,  which  are  ecivially  syphilo- 
tubercular.  M.  Leloir  has  ([uoted  cases  which  appear  to  me  conclusive. 
Treatment  alone  can  settle  the  question. 

All  I  have  said  of  tertiary  nasal  syphilis  is  equally  applicable  to  late 
hereditary  sy})hilis,  which  supervenes  at  a  more  or  less  advanced  age. 

The  Jiasal  lesions  of  hereditary  or  acquired  syphilis  show  themselves  by 
troubles  which  are,  on  the  one  hand,  temporary  and  curable  ;  on  the  other, 
irremediable.  These  troubles-  rhinitis,  with  its  crusts  and  ulcers;  ozaona, 
with  its  fearful  stench  ;  destruction  of  the  soft  and  bony  parts  of  the  nose  ; 
perforation  of  the  vault  of  the  palate  ;  nasal  deformities  ;  and  the  terrible 
coiisequences  of  naso-cranial  syphilis— are  the  more  formidable  as  they  are 
usually  latent  in  the  early  stages. 

We  cannot,  then,  use  too  murli  care  in  the  diagnosis  of  nasal  syphilis. 
These  lesions,  especially  in  dealing  with  the  hereditary  disease,  are  too  often 


14  TEXT-BOOK  OF  MEDICINE 

taken  for  those  of  scrofula,  strumous  eczema,  or  lupus.     Failing  clear  proof 
to  the  contrary,  we  must  always  think  of  syphilis  and  act  accordingly. 

Treatment. — The  treatment  of  nasal  syphiHs  does  not  differ  from  that 
of  syphilis  in  general.  Mercury  is  the  essential  agent.  Mercury,  rather 
than  iodide  of  potash,  is  the  drug  for  tertiary  syphilis.  For  many  years  I 
have  almost  entirely  given  up  iodide  of  potash  and  employed  mercury. 
The  most  efficacious  preparation  is  the  aqueous  solution  of  the  biniodide. 
An  intramuscular  injection  of  this  solution  is  given  daily  for  a  fortnight. 
Later  the  dose  may  be  increased.  The  treatment  is  stopped  for  a  fortnight, 
and  then  resumed  again  for  a  like  period,  and  so  on  for  tlu:ee  months.  For 
further  details,  see  Appendix  on  Therapeutics. 

4.  Tuberculosis  of  the  Nasal  Fossae — Lupus  of  the  Nose. 

(1)  Tuberculosis  of  the  Nasal  Foss^. 

Description. — Tuberculosis  of   the  nasal  fossa)  is  not  very  rare ;  it 
relative  frequency  is  shown  by  the  following  table  : 

Tongue 
Pharynx 
Mouth 
Soft  palate 
Tonsils 
Nasal  fossaj 

It  may  be  primary  or  secondary. 

(a)  The  primary,  or  at  least  the  apparently  primary,  form  is  confined 
to  the  nasal  fossa?,  independently  of  any  other  region.  It  nearly  always  takes 
the  form  of  a  muslu-oom-like  or  polypoid  excrescence,  simulating  sarcoma. 
It  begins  in  almost  every  case  on  the  cartilaginous  septum,  as  a  submucous 
infiltration,  and  the  mucosa  may  remain  unaffected  for  a  long  time.  Later 
the  mucosa  ulcerates,  and  the  growth  forms  a  -hernia  of  fungating,  mush- 
room-like tissue,  occupying  both  nostrils,  which  are  partly  obstructed. 

The  process  spreads  by  eccentric  growth  :  at  the  centre  of  the  tumour 
softening  and  destruction  occur ;  in  the  tissue  around  the  tumour  young 
granulations  appear.  When  the  process  ends  in  perforation  of  the  septum, 
the  edges  of  the  perforation  are  formed  by  fungating  and  encrusted  masses 
of  tissue. 

The  course  of  the  lesion  is  slow  and  painless.  The  symptoms  at  first 
are  those  of  chronic  coryza.  Later,  when  the  fungating  mushroom  is  formed, 
the  question  of  diagnosis  from  chancre  and  from  sarcoma  arises.  Chancre 
is  unilateral,  indurated  at  its  base,  accompanied  by  early  enlargement  of 
glands,  and  rapid  in  its  growth,  while  the  tubercular  mass  is  bilateral,  flabby, 
and  very  slow  in  its  growth. 

The  diagnosis  from  sarcoma  is  clinically  very  difficult ;  careful  search 


51 

cases 

21 

22 

8 

4 

5 

DISEASES  OF  THE  NASAL  FOSSAE  15 

must  be  made  for  the  tubercle  bacillus,  which  is  sometimes  only  found  after 
making  many  preparations. 

The  diagnosis  of  nasal  tuberculosis  must  also  be  made  in  the  ulcerated 
stage.  To  avoid  repetition,  I  would  refer  the  reader  to  the  preceding  chapter 
on  Nasal  SyphiUs. 

(6)  Secondary  tuberculosis  of  the  nasal  fossae  is  much  more  frequent  than 
the  primary  form.  It  supervenes  in  the  course  of  pulmonary  or  laryngeal 
phthisis,  and  may  also  accompany  tuberculosis  of  the  mouth  and  pharynx. 
It  rarely  shows  the  polypoid,  fungating  appearances  of  the  primary  form. 
It  usually  gives  rise  to  multiple  ulcers,  which  are  confined  to  the  vestibule 
and  the  anterior  part  of  the  inferior  turbinate  bone.  The  ulcers  vary  in 
size  ;  the  edges  are  usually  jagged,  and  the  floor  is  greyish  and  covered  with 
purulent  secretion  or  crusts.  Bacilli  are  rare  in  the  primary  form,  but 
very  abundant  in  the  ulcers  of  the  secondary  variety.  These  ulcers  are 
generally  but  little  painful,  and  thus  differ  from  bucco- pharyngeal  tuber- 
culosis, which  gives  rise  to  very  severe  pain. 

Tuberculosis  of  the  nasal  fossse  per  se  is  not  of  much  gravity.  In  some 
cases,  however,  it  forms  the  starting- place  of  tubercular  meningitis. 

Treatment  which  is  ineffective  in  the  secondary  forms  may  be  efficacious 
in  the  primary  form.  Extirpation,  cauterization,  scraping,  and  applica- 
tion of  a  concentrated  solution  of  lactic  acid  would  seem  to  be  the 
best  methods. 

(2)  Lupus  of  the  Nose. 

Speaking  generally,  lupus  vulgaris  (Willan's  lupus)  is  an  attenuated 
tuberculosis  of  the  skin  and  the  adjacent  mucosae.  It  may  be  said  that  the 
varieties  of  cutaneous  tuberculosis  have  but  little  vindence,  and  lui)us  is 
remarkable  for  its  slow  course  and  attenuated  virulence.  Lupus  vulgaris, 
nevertheless,  belongs  to  the  tubercular  group.  Lupoid  tissue  contains  very 
few  bacilli,  seeing  that  they  are  only  found  once  in  every  eleven  cases  (Cornil 
and  Leloir),  and  yet  Leloir  has  nearly  always  succeeded  in  producing  tuber- 
culosis in  animals  by  inoculation  of  the  anterior  chamber  of  the  eye  with 
fragments  of  lupus.  Furthermore,  the  local  reactions  of  tuberculin  are 
evident  in  lupus,  just  as  they  are  in  true  tuberculous  lesions  ;  this  is  a  fresh 
proof  of  the  tubercular  nature  of  lupus  vulgaris. 

Lupus  may  invade  the  skin  in  diverse  places,  but  the  nose  is  the  "  seat 
of  election."  Sometimes  the  nose  alone  is  invaded  ;  at  other  times  lu[)us 
extends  to  the  cheeks  or  the  lips. 

Description. — Lupus  vulgaris  of  the  nose  is  characterized  by  the  develop- 
ment of  small  intradermal  nodules.  These  nodules,  or  luj)us  tubercles, 
form  the  primary  element  of  the  disease.  They  vary  in  size  from  a  millet- 
seed  to  a  lentil,  or  larger. 


16  TEXT-BOOK  OF  MEDICINE 

The  tubercle  is  fairly  transparent.  In  colour  it  looks  like  barley-sugar 
or  apple -jelly.  Its  consistency  is  somewhat  soft  and  easily  appreciable  to 
the  touch.  It  runs  a  very  slow  course.  In  certain  cases  it  undergoes 
interstitial  absorption,  and  gives  place  to  white  depressed  scars,  which 
deform  the  nose  ;  but  more  often  it  undergoes  ulceration,  and  produces  loss 
of  substance.  It  is  by  no  means  rare  to  find  cicatrized  tubercles,  ulcers,  and 
tubercles  in  full  growth  in  the  same  area. 

The  tubercles  often  form  a  patch.  In  the  simplest  form  of  nasal  lupus, 
the  patch,  I  think,  occupies  the  ala  nasi ;  it  is  reddish,  round  or  oval,  but 
the  tubercles  are  not  prominent.  This  type  is  known  as  flat  or  macular 
lupus,  in  which  the  ulceration  is  usually  slight  and  superficial. 

In  other  cases  lupus,  instead  of  being  flat,  is  exuberant,  the  tubercles 
being  prominent  and  higlily  coloured.  This  form,  unlike  the  flat  kind, 
has  a  great  tendency  to  ulcerate,  and  is  called  lupus  vegetans,  exuberans, 
or  exedens.  From  its  invading  nature  it  is  sometimes  named  lupus  vorax  ; 
it  attacks  the  nose,  the  cheeks,  the  lips,  and  the  eyelids. 

The  ulcerations  of  lupus  are  indolent  and  of  a  reddish  colour  ;  they  have 
an  irregular  floor,  carpeted  by  flabby  granulations,  bathed  in  fluid  and 
covered  with  more  or  less  thickened  crusts.  The  ulcers  are  irregular,  with 
infiltrated  and  livid  edges.  The  crusts  are  greyish,  sometimes  brownish, 
thickened  and  stratified  ;  when  they  fall  off,  an  ulcer,  which  is  often  studded 
with  tubercles,  is  left  uncovered. 

The  course  of  lupus  is  extremely  slow,  and  the  difeease  lasts  years  or 
decades.  The  ulcers  are  replaced  by  dark  scars,  which  later  become  whitish 
and  are  traversed  by  prominent  bands.  These  ulcers  slowly  determine  the 
destruction  of  the  soft  parts  of  the  nose,  and  the  scars  cause  stenosis  of  the 
nostrils. 

The  diagnosis  between  lupus  and  syphilis  has  been  given  in  the  pre- 
ceding chapter.  The  cure  of  lupus,  either  spontaneously  or  by  treatment,  is 
rarely  permanent,  and  the  lesions  often  reappear  after  several  years  of 
apparent  cure 

Lupus  vulgaris  may  invade  the  nasal  mucosa  primarily,  or  may  be 
secondary  to  lupus  of  the  skin.  Primary  lupas  of  the  septum  and  of  the 
subseptum  is  seen.  Lupus  of  the  nasal  mucosa  has  the  same  slow  and  indo- 
lent course  as  lupus  of  the  skin,  and,  while  it  may  affect  the  cartilages,  it  is 
quite  exceptional  for  it  to  attack  the  bones. 

I  must  now  say  a  few  words  about  lupus  erythematosus,  which  some 
consider  to  be  a  very  mild  cutaneous  tuberculosis,  while  others  deny  its 
tubercular  nature.  It  is  still  called  acneiform  lupus.  In  most  cases  it 
occupies  the  bridge  of  the  nose  and  the  adjacent  part  of  the  cheeks,  having 
somewhat  the  shape  of  a  butterfly.  It  begins  as  a  red  stain,  and  is  covered 
with  scales  ;  it  spreads,  and  finally  becomes  colourless  and  atropliied  with 


DISEASES  OF  THE  NASAL  FOSS.E  17 

the  formation  of  glossy,  whitish,  superficial  scars,  without  ulceration.    Lupus 
erythematosus  may  be  associated  mth  lupus  vulgaris. 

The  treatment  of  nasal  lupus  has  benefited  by  the  employment  of  photo- 
therapy in  dermatological  practice  (Finsen). 

5.  Ozaena. 

Ozaena  is  the  foetid  odour  which  proceeds  from  the  nose  in  some  people. 
It  is,  however,  important  not  to  confuse  ozaena — that  is  to  say,  the  smell 
which  has  its  origin  in  the  nose — with  the  foetid  odour  which  the  breath 
acquires  from  the  affections  of  the  mouth  and  throat.  Carious  teeth, 
alveolar  periostitis,  inflammatory  conditions  of  the  gums,  secretions  which 
accumulate  during  the  night  on  the  buccal  and  lingual  mucous  membranes, 
also  cause  foetor  of  the  breath.  The  caseous  products  which  block  the 
tonsillar  crypts  are  a  cause  of  foetor.  I  would  mention,  too,  the  foul  breath 
which  accompanies  foetid  bronchitis  and  dilatation  of  the  bronchi.  Ozajna 
must  not  be  confounded  with  these  different  conditions. 

etiology. — Though  we  do  not  know  the  exact  cause  of  ozaena,  clinical 
cases  teach  us  that  in  certain  people  ozsena  exists,  although  ulceration, 
deformity,  and  atrophic  rhinitis  are  not  present  in  the  nose.  Wc  might  say 
that  the  nasal  secretion  in  these  people,  just  as  the  vaginal  or  pharyngeal 
secretions  in  others,  and  in  yet  others  the  perspiration  of  the  axilla  or  of 
the  feet  takes  on  a  fa?tor,  the  primary  cause  of  which  is  unknowii. 

In  some  individuals,  chiefly  herpetics,  this  tendency  to  foetor  of  tlie  nasal 
secretions  may  be  absent  in  the  normal  state,  but  is  at  once  awakened  by 
coryza,  and  especially  by  chronic  coryza.  On  the  other  hand,  we  see  patients 
with  ozsena  in  whom  an  acute  coryza  causes  the  foetor  to  disappear — for  a 
time,  at  any  rate.  Certain  persons,  from  infancy  or  from  puberty,  suffer 
from  ozaena  which  may  be  called  "  constitutional  "  ;  it  is  associated  with 
a  sero- purulent  nasal  secretion,  persists  with  alternations  up  to  adult  life, 
and  only  diminishes  at  a  very  advanced  age. 

Ozasna  is  sometimes  associated  with  ulcers  of  the  mucosa,  with  lesions  of 
the  cartilages  and  the  bones  of  the  nose,  and  with  the  nasal  deformities  which 
arise  from  hereditary  or  acquired  syphilis.  This  important  variety  of 
syphilitic  ozaena  has  been  studied  under  Nasal  Syphilis. 

In  certain  individuals  oza;na  may  be  considered  as  a  true  morbid  entity, 
having  its  origin  in  a  congenital  malformation  of  the  nasal  fossae  (atrophic 
rhinitis).  This  variety  would  be  true  oza>na,  other  kinds  being  considered 
symptomatic.  This  malformation  consists  in  a  considerable  enlargement 
of  the  nasal  fossa;,  with  atrophy  of  the  turbinate  bones  (especially  the 
inferior  ones)  and  thickening  of  the  mucosa  (Zaufal).  This  gaping  of  the 
nasal  fossa;  allows  such  a  free  passage  to  tiie  current  of  e.\[)ired  air  that  the 
secretions  arc  imperfectly  swept  away,  the  mucus  becomes  stagnant,  and 

2 


18  TEXT-BOOK  OF  MEDICINE 

crusts  form.  In  this  alkaline  medium  a  special  micro-organism  (a  large 
diplococcus)  has  been  described  by  M.  Loewenberg,  who  considers  it  to  be 
the  specific  cause  of  the  foetor. 

Ozgena  does  not  always  develop  in  the  same  way.  Its  evolution  is  more 
or  less  rapid.  True  oza3na,  which  seems  to  be  due  to  a  congenital  malforma- 
tion of  the  nose,  generally  shows  itself  during  late  infancy,  when  the  nasal 
cavities  are  growing  ;  it  takes  months  and  years  to  develop.  The  foetor 
varies  in  different  subjects,  but  is  especially  marked  when  crusts  and  mucus 
are  expelled,  and  is  so  intense  in  certain  patients  that  a  whole  ward  may 
be  tainted.  As  the  sense  of  smell  is  lost,  the  patient  is  unconscious  of  the 
fcetor,  but  the  disgust  which  he  causes  to  those  around  him  makes  life 
miserable.  The  social  consequences  of  this  affection  are  terrible ;  life  in 
common  with  others  becomes  difficult,  marriage  is  impossible  for  young 
girls,  and  the  tendency  to  suicide  is  not  rare.  The  patient  often  speaks 
with  a  nasal  tone,  which  results  from  the  resonance  of  the  voice  in  the 
abnormally  enlarged  nasal  cavities.  The  nose  is  often  saddle-backed,  the  tip 
is  tilted,  and  the  nostrils  gape. 

The  infection  which  produces  ozsena  may  be  propagated  in  different 
directions,  and  give  rise  to  dacryocystitis,  conjunctivitis,  keratitis,  or 
sinusitis.     M.  Luc  has  described  tracheal  ozaena. 

The  treatment  of  ozsena  consists  in  the  daily  use  of  a  nasal  douche  of 
bichloride  of  mercury  (1  part  of  mercury  in  10,000  of  water).  After  the 
douche  boric  powder  (Loewenberg)  is  carefully  blown' into  the  nasal  fossae 
and  upper  parts  of  the  pharynx.  Aspirations  of  very  hot  saline  solution 
morning  and  evening  for  several  months  give  excellent  results  (Bonnier). 
In  the  case  of  syphilis  mercury  as  described  in  the  preceding  chapter  must 
be  exhibited. 

6.  Epistaxis. 

Description. — Epistaxis  is  hoemorrhage  from  the  nasal  mucosa.  The 
bleeding,  which  is  usually  slight,  consists  in  the  flow  of  bright  blood,  drop  by 
•drop,  from  one  nostril,  rarely  from  both.*  If  the  bleeding  be  abundant,  and 
especially  if  it  occur  while  the  patient  is  lying  down  with  the  head  back,  the 
blood  flows  through  the  posterior  nares,  and  may  then  pass  along  the  pharynx 
and  oesophagus  into  the  stomach,  to  be  rejected  by  vomiting.  A  mistake 
may  thus  occur  if  the  patient  does  not  recognize  the  epistaxis,  and  is  content 
with  saying  that  he  has  vomited  blood ;  hence  the  rule  to  explore  the  nasal 
fossae  carefully  in  doubtful  cases  of  haematemesis.  I  have  several  times  seen 
such  errors  in  diagnosis. 

This  year,  at  the  Hotel-Dieu,  one  of  my  patients  vomited  fluid  blood 

*  Galen  has  noticed  that  the  blood  generally  comes  from  the  right  nostril  in 
diseases  of  the  liver. 


DISEASES  OF  THE  NASAL  FOSSAE  19 

and  clots  ;  the  hsematemesis  resulted  from  nasal  haemorrhage  diverted  into 
the  stomach.  On  depressing  the  tongue  we  saw  the  blood  flowing  down 
the  posterior  wall  of  the  pharynx,  and  examination  of  the  septum  revealed 
the  source  of  the  haemorrhage,  which  was  at  once  arrested. 

The  quantity  of  blood  lost  is  very  variable.  In  some  cases  the  loss 
is  slow,  lasts  from  ten  minutes  to  a  quarter  of  an  hour,  and  the  subject 
does  not  lose  more  than  one  or  two  ounces  of  blood.  In  other  cases  the  flow 
is  rapid  and  profuse,  appears  from  the  nose  and  mouth  at  once,  and  may  last 
several  hours  if  efficacious  treatment  do  not  intervene ;  the  loss  may  then 
amount  to  more  than  a  pint.  Furthermore,  as  the  bleeding  readily  recurs — ■ 
since  any  effort,  such  as  blowing  the  nose  or  sneezing,  is  enough  to  detach 
the  clots — it  follows  that  in  predisposed  subjects  (haemophilia)  the  loss  of 
blood  may  assume  large  proportions.  When  the  epistaxis  is  repeated  and 
abundant,  the  patient  becomes  pale  and  weak,  and  is  liable  to  fits  of  dizziness, 
vertigo,  and  syncope,  as  is  customary  after  any  great  loss  of  blood. 

Nasal  haemorrhage  has  a  most  irregular  course  ;  it  may  appear  daily, 
several  times  in  the  twenty-four  hours,  or  months  and  years  apart.  It 
sometimes  assumes  an  intermittent  form,  or  returns  at  certain  seasons  of  the 
year. 

etiology. — Epistaxis  is  very  common  at  the  age  of  puberty,  but  is 
more  rare  in  old  age.  The  abundance  and  the  distribution  of  the  vessels 
on  the  surface  of  the  mucous  membrane  explain  the  frequency  of  these 
haemorrhages.  Capillary  aneurysips  have  been  met  with.  Epistaxis  may 
be  active  or  passive.  It  is  active  when  it  is  the  result  of  an  afflux  of  blood. 
I  may  quote,  among  other  examples,  the  epistaxis  favoured  by  the  hyper- 
trophy of  the  heart  in  aortic  insufficiency ;  the  supplementary  epistaxis  of 
the  menstrual  periods  and  of  piles  ;  the  haemorrhages  which  supervene  after 
the  suppression  of  a  cutaneous  affection,  such  as  erysipelas  (Sore) ;  and  those 
which  are  the  result  of  sunstroke  and  of  sudden  changes  of  temperature  or 
of  atmospheric  pressure.  Epistaxis  is  frequent  at  the  onset  of  typhoid  fever 
and  of  measles,  and  is  seen  in  the  course  of  articular  rheumatism  (Trousseau) 
and  of  phthisis  (Leudet) ;  it  is  sometimes  the  herald  of  haemoptysis.  Passive 
epistaxis  is  seen  in  blood  stases,  when  the  venous  tension  is  increased  (mitral 
and  tricuspid  lesions),  or  when  the  return  of  blood  from  the  head  is  impeded 
(compression  of  veins  by  tumours  of  the  neck  and  the  mediastinum). 

Epistaxis  in  icterus  simplex  and  icterus  gravis,  in  the  haemorrhagic  forms 
of  the  eruptive  fevers,  in  malarial  infection,  purpura,  and  Icucocytlurmia 
results  from  changes  in  the  blood.  Epistaxis  is  fre(]uent  in  diabetes  and 
in  Bright's  disease  ;  indeed,  diabetes  predisposes  to  great  bleeding.  In 
the  cliapter  on  Bright's  Disease  I  shall  dwell  in  detail  on  the  epista.xis  of 
chronic  nephritis  and  on  severe  epistaxis,  wliicii  is  sometimes  one  of  tlie 
first  symptoms  of  Bright's  disease.     Epidemics  of  epistaxis,  which  could  only 

2—2 


20  TEXT-BOOK  OF  MEDICINE 

have  been  a  larval  fever,  have  been  noted.  The  epistaxis  which  follows  a 
fall  upon  the  head  sometimes  indicates  a  fracture  of  the  base  of  the  skull, 
involving  the  upper  wall  of  the  nasal  fossae. 

I  must  make  special  mention  of  epistaxis  of  local  origin  in  ulcers  of  the 
mucosa,  varices,  angiomata,  polypi,  and  vascular  tumours  of  the  septum. 

Epistaxis  is  rarely  the  result  of  haemorrhage  from  a  wide  area.  Rhino- 
scopy shows  in  most  cases  that  the  rupture  of  the  small  vessels  which  gives 
rise  to  epistaxis  occurs  in  certain  defined  regions — to  wit,  the  antero-inferior 
and  the  central  portion  of  the  septum  and  the  inferior  turbinate  bone,  where 
erectile  tissue  exists. 

Diagnosis — Prognosis. — It  is  necessary  to  trace  the  cause  of  the  bleed- 
ing to  ascertain  if  it  depend  on  some  general  state  or  on  a  purely  local  lesion 
(ulcer,  varix,  erectile  tumour,  angioma  of  the  septum),  to  find  out  whether 
it  be  symptomatic  of  some  affection  of  the  liver,  the  heart,  or  the  kidney, 
or  whether  it  be  supplementary  to  a  suppressed  haemorrhage,  and  to  ask  if  it 
may  not  denote  the  onset  of  enteric  fever,  or  if  it  be  not  the  first  sign  of  a 
hsemorrhagic  form  of  some  eruptive  fever.  The  prognosis  depends  on  the 
quantity  of  blood  lost,  the  strength  of  the  patient,  and  the  cause  of  the 
bleeding.  Each  of  these  factors  must  be  carefully  considered.  Epistaxis 
is  sometimes  a  grave  complication  in  measles  and  in  typhoid  fever. 

Treatment. — To  arrest  epistaxis  the  simplest  measures,  such  as  injection 
of  very  hot  water  (especially  oxygenated  water)  into  the  nasal  fossae  or 
compression  of  the  nose,  sometimes  suffice  ;  but  in  obstinate  cases  we  must 
resort  to  plugging,  which  exerts  direct  pressure  upon  the  seat  of  the  haemor- 
rhage. It  is  first  necessary  to  make  out  the  site  of  the  bleeding  by  direct 
examination.  In  twenty-five  cases  of  epistaxis  Chiarri  has  shown  that  the 
haemorrhage  in  twenty-two  of  them  came  from  the  anterior  part  of  the 
septum.  It  is  the  "  seat  of  election  "  in  epistaxis,  a  seat  easy  to  recognize, 
and  we  have  only  to  look  for  it.  "  Raise  the  ala  nasi,  so  that  the  orifice  of 
the  nostril  is  turned  outwards  as  much  as  possible,  follow  an  oblique  line 
upwards  and  backwards,  and  at  a  distance  of  1  inch  the  zone  of  bleeding 
will  be  found."  We  then  apply  a  plug  of  wool  at  the  point  in  question, 
and  we  can  exert  efficient  pressure  by  keeping  the  plug  in  place  •with,  a  stop- 
clamp  applied  astride  the  bridge  of  the  nose,  or  by  introducing  into  each  nostril 
one  jaw  of  the  clamp  forceps,  previously  wrapped  with  gauze  (Range). 
If  this  plugging  do  not  suffice,  or  if  the  seat  of  the  bleeding  be  higher  up  or 
farther  back,  we  introduce  into  the  nostril,  by  means  of  forceps,  a  series  of 
plugs  of  absorbent  wool  soaked  in  oxygenated  water  :  percliloride  of  iron 
must  not  be  used.  After  plugging,  we  survey  the  posterior  orifice  of  the 
nasal  fossae,  so  as  to  be  certain  that  the  blood  does  not  continue  to  flow  back- 
Avards  into  the  pharynx.  We  can  also  perform  plugging  by  means  of  a 
bladder  of  gold-beater's  skin.     For  this  purpose  fix  the  bladder  on  a  rigid 


DISEASES  OF  THE  NASAL  FOSS.E  21 

urethral  sound  of  small  calibre,  introduce  the  empty  bladder  into  the  nose, 
inject  water  througli  the  sound,  so  as  to  distend  the  bladder  and  plug  the 
sound.  This  apparatus  is  easily  kept  in  place,  and  has  often  yielded  me  the 
best  results. 

If,  in  spite  of  these  means,  the  epistaxis  continue,  posterior  plugging 
must  be  employed.  To  plug  the  posterior  nares  use  Belloc's  sound,  or  a 
flexible  uretliral  bougie.  Introduce  the  sound,  smeared  with  vaseline,  into 
the  inferior  meatus^,  push  it  horizontally  till  it  emerges  behind  the  soft 
palate,  seize  it  with  forceps,  and  draw  it  out  of  the  mouth.  By  means  of  a 
strong  thread  of  sufficient  length,  suspend  from  this  end  of  the  sound  a  plug 
of  wool  smeared  vnih  boric  vaseline,  1  inch  long  and  half  as  broad.  Next 
pull  back  the  sound  introduced  into  the  nose.  The  gauze  plug  may  be  thus 
fixed  in  the  posterior  opening  of  the  nose,  while  the  index-finger,  introduced 
into  the  mouth,  helps  the  passage  of  the  plug  behind  the  soft  palate.  The 
thread  is  fixed  to  the  cheek  by  means  of  diachylon  or  collodion  ;  it  is  kept 
in  place  by  anterior  plugging,  which  is  usually  combined  with  posterior 
plugging. 

The  plug,  however,  soon  becomes  painful  to  the  patient.  The  nose 
swells,  breathing  is  impeded,  and  the  patient  can  rarely  tolerate  the  plugs 
for  more  than  twenty  to  thirty  hours.  To  withdraw  them,  moisten  by 
injecting  tepid  water  into  the  nostrils.  The  anterior  plugs  come  out  easily, 
while  the  posterior  ones  are  detached  by  means  of  the  injection,  and  are 
finally  spat  out  by  the  patient. 

In  some  cases  (erectile  tumour,  angioma)  plugging  is  not  the  best  treat- 
ment, and  the  bleeding  surfaces  must  be  cauterized  with  nitrate  of  silver, 
or  preferably  with  the  galvano-cautery  at  a  dull  red  heat.  By  this  means 
M.  Luc  was  able  at  one  sitting  to  arrest  profuse  epistaxis  which  threatened 
the  life  of  one  of  my  patients  admitted  for  an  angioma. 

Adrenalin  must  enter  into  the  thera[)eutics  of  epistaxis.  The  bleeding 
mucosa  is  touched  with  a  plug  soaked  in  a  solution  of  adrenalin  (I  in  1, ()()()). 
A  plug  of  wool  saturated  with  a  weaker  solution  (say,  1  in  r),()()()  or  I  in 
10,000)  may  also  be  left  in  situ.  The  vaso-constriction  which  results  some- 
times produces  paleness  from  the  decoloration  of  the  mucosa. 

When  the  haemorrhage  has  been  abundant,  give  iced  driidvs,  use  sub- 
cutaneous injections  of  ergotin,  and  administer,  in  tablespoonful  doses,  the 
following  hnemostatic  draught : 

1^   Acid,  sulphuric,  dil.  . .  . .  , ,  ll[  x. 

Tinct.  ferri  perchlor.  . .  . .  . .  ]]\x. 

Tinct.  opii  .  .  . .  . .  . .  ii;  v. 

A(|uam       .  .  . .  .  .  . .  . .  ad  7,ss. 

Employ  injections  of  serum  (see  Appendix  on  Therapeutics). 

If  these  means  fail  to  stop  tlic  blcfMJing,  and  if  the  patient's  life  be  in 


22  TEXT-BOOK  OF  MEDICINE 

danger,  transfusion  of  blood  muvst  be  employed.  It  is  an  operation  which 
has  often  yielded  me  excellent  results. 

Some  years  ago  I  performed  transfusion  upon  two  patients  :  the  one  was 
suffering  from  epistaxis  of  diabetic  origin,  the  other  from  bleeding  due  to 
haemophilia.  The  former  was  an  adult,  the  latter  a  child.  In  both 
cases  the  bleeding  was  exceedingly  serious,  on  account  of  its  amount 
and  its  persistence.     The  bleeding  was  at  once  arrested  by  transfusion. 

Periodic  epistaxis,  even  though  it  is  not  due  to  a  larval  fever,  is  success- 
fully treated  with  sulphate  of  quinine.  Lastly,  it  is  necessary  to  remember 
that  certain  supplementary  or  critical  bleedings  must  be  respected,  especially 
in  old  people,  in  whom  they  are  often  a  safety-valve. 


CHAPTER  II 
DISEASES  OF  THE  LARYNX 

I.  GENERAL  SURVEY  OF  THE  ANATOMY  AND  PHYSIOLOGY 

OF  THE  LARYNX. 

Vocal  and  respiratory  troubles  comprise  nearly  the  whole  of  laryngeal  pathology. 
As  we  cannot  understand  aphonia  and  dysphonia,  with  all  their  shades,  and  cannot 
grasp  the  mechanism  of  spasm  of  the  glottis  and  the  genesis  of  paralyses  of  the  vocal 
cords,  or  diagnose  changes  in  the  recurrent  and  external  laryngeal  nerves,  if  we  have 
not  a  mental  picture  of  the  normal  functions  of  the  laryngeal  apparatus,  I  must  briefly 
indicate  the  principal  points  in  the  physiology  of  the  larynx. 

The  skeleton  of  the  larynx  is  formed  l)y  the  cricoid,  thyroid,  and  arytenoid  cartilages. 
The  cricoid  is  shaped  like  a  ring,  and  is  much  broader  behind  than  in  front. 

The  thyroid  has  been  compared  ta  a  sliield  :  it  protects  the  vocal  cords,  which  are 
inserted  in  the  angle  of  its  posterior  surface. 

The  arytenoids,  which  resemble  a  funnel  in  shape,  play  a  most  important  part. 
They  swing  on  their  base  at  the  crico-arytenoid  articulation,  and  the  opening  or  closing 
of  the  vocal  cords  is  jiroduced  by  their  different  movements. 

Function  of  the  Glottis. — The  glottis  is  the  space  limited  by  the  vocal  cords  (inter- 
ligamentous  glottis)  and  by  the  arytenoid  cartilages  (intercartilaginous  glottis).  The 
inferior  cords  alone  merit  the  name  of  vocal  cords,  for  sound  is  produced  at  their  level ; 
the  superior  vocal  cords  have  usurped  the  term  "  cords,"  which  must  bo  replaced  by  that 
of  "  ventricular  bands." 

All  the  parts  of  the  larynx,  including  its  cartilages  and  joints  (passive  organs),  its 
muscles  and  nerves  (active  organs),  combine  for  one  purpose — i.e.,  for  the  movements  of 
tlio  vocal  cords  and  tlie  different  shapes  of  the  glottis. 

The  glottis  plays  two  chief  parts — the  one,  which  concerns  the  individual's  life,  is 
the  passage  of  air  into  the  respiratory  channels  ;  and  the  other,  which  is  an  attribute 
of  species,  is  the  emission  of  sound,  from  the  simple  cry  to  the  modulations  of  the  human 
voice. 

Respiration,  therefore,  on  the  one  hand,  and  emission  of  sound  on  the  other,  are 
functions  which  show  clearly  the  importance  and  gravity  of  diseases  of  the  larynx. 

Muscles  of  the  Larynx.— The  muscles  of  the  larynx  may  bo  classified  in  several 
groups.  The  posterior  crico-arytenoids  form  the  first  group.  They  are  inserted  into 
the  i)osterior  surface  of  the  cricoid,  and  into  the  external  and  posterior  process  of  the 
arytenoid.  Their  contraction  draws  the  vocal  processes  outwards,  especially  if  inspira- 
tion bo  very  deep. 

The  posterior  crico-arytenoids,  then,  are  the  muscles  of  respiration  ;  their  r61e  is  to 
open  the  vocal  cords,  allow  free  passage  to  the  air,  and  keep  the  glottis  open  durinij 
respir.-vtion.  By  their  contraction  they  oppose  the  natural  tendcnc^y  of  the  lips  of  tJwj 
glottis  to  come  together,  like  two  valves,  during  the  aspiration  of  uir  iiitt>  tlie  liuig,  an 
event  which  at  once  happens  when  they  an^  [)aralyzod. 

2:3 


24  TEXT-BOOX  OF  MEDICINE 

Such  is  the  isolated  action  of  the  posterior  crico -arytenoid  muscles  as  muscles  of 
respiration.  When  they  contract  synchronously  with  the  arytenoideus,  they  form  a 
muscular  band,  which  straightens  the  two  arytenoid  cartilages  upon  the  cricoid.  They 
thus  become  the  antagonists  of  the  thryo -arytenoid  muscles,  and  free  the  arytenoids 
from  the  traction  of  the  cords  which  would  draw  them  forwards. 

They  may  also  be  looked  upon  as  tensors  of  the  vocal  cords.  This  tension  is  effected 
by  their  means,  and  without  them  would  be  impossible.  Furthermore,  by  acting  in 
concert  with  the  adductors,  the  posterior  crico-arytenoids  fix  the  arytenoid  cartilages 
on  the  cricoid,  make  their  movements  firm,  and  thus  allow  the  vocal  cords  at  their 
posterior  insertion  to  follow  the  movements  of  the  cricoid.  They  are,  therefore,  muscles 
of  inspiration,  tension,  and  fixation. 

The  second  group  is  formed  by  the  lateral  crico -arytenoid  muscles,  which  are  the 
constrictors  of  the  interligamentous  glottis  and  the  single  ary-arytenoideus,  which 
constricts  the  intercartilaginous  and,  consecutively,  the  interligamentous  glottis.  These 
muscles,  )jy  drawing  the  vocal  cords  together,  shut  the  glottis,  and  place  it  in  the  desired 
position  for  the  production  of  vocal  efforts. 

For  this  act  the  glottis  is  quite  shut,  while  in  the  production  of  the  voice  the  cords 
do  not.  come  quite  in  contact,  but  leave  a  space  of  variable  shape  and  size  between  one 
another. 

By  bringing  the  vocal  cords  together  the  constrictor  muscles  of  the  glottis  assist 
in  the  production  of  sound — they  jirepare  it.  Sounds  can  only  be  produced  if  the  vocal 
cords  be  sufficiently  approximated  ;  if  they  be  too  open,  the  expired  air  escapes,  and  is 
wasted  without  being  used  in  the  production  of  sound.  This  fact  can  easily  be  verified 
upon  the  larynx  of  a  corpse. 

The  third  group  comprises  the  muscles  of  phonation  ;  these  are  the  thyro -arytenoid 
and  crico -thyroid  muscles. 

The  thyro -arytenoid  muscles  are  composed  of  two  chief  bundles,  the  one  situated 
in  the  thickness  of  the  vocal  cord,  the  other  outside  it.  This  latter  bundle,  which  is 
much  the  larger,  is  flattened  against  the  thyroid  cartilage,  terminates  at  the  outer  edge 
of  the  arytenoid,  and  blends  with  the  muscular  loop,  which  the  arytenoideus  completes 
behind.  The  contraction  of  this  muscular  Ioojd  shuts  the  glottis.  The  thyro-ary- 
tenoid  is,  then,  a  muscle  of  effort ;  it  is  an  adductor,  like  the  lateral  crico-arytenoideus, 
and  it  also  plays  a  part  in  phonation,  by  bringing  together  the  vocal  cords,  which  the 
column  of  expired  air  seeks  to  open.  It  regulates  the  power  of  the  voice  by  its 
opposition  to  the  exjjiratory  muscles  of  the  thorax. 

The  internal  bundle  of  the  thyro-arytenoldeus  (the  muscle  of  the  vocal  cord)  draws 
the  arytenoid  and  the  thyi'oid  cartilages  together.  It  is  not,  therefore,  a  tensor  of  the 
vocal  cord,  neitlier  does  it  stretch  the  cord  at  all  ;  it  shortens  the  vocal  cord  and  loosens, 
instead  of  stretching  it  ;  but,  as  other  muscles — the  distensors  of  the  vocal  cords— begir 
to  contract,  it  can  no  longer  shorten,  and  as  it  cannot  thicken  or  swell,  it  hardens  and 
acquires  a  firmness  and  resistance  which  regulates  the  periodicity  of  the  vibrations. 
The  more  tlie  firmness  is  increased  the  greater  become  the  vibrations  and  the  higher 
the  sound.  This  internal  bundle  is,  then,  the  muscle  of  the  diapason,  as  the  external 
bundle  is  the  muscle  of  the  intensity  of  the  sound.  This  muscle  may  thus  be  looked  upon 
as  a  tensor  of  the  cords,  the  word  "  tension  "  signifying  the  state  of  varying  rigidity 
which  results  both  from  the  passive  distension  of  the  cords  and  from  their  active 
retraction  (Bonnier). 

The  crico-thyroid  muscle  is  the  antagonist  of  the  thyro -arytenoid,  but  it  is  only  so 
by  acting  with  the  muscles  which  straighten  the  arytenoids  upon  the  cricoid.  The 
combined  action  of  these  muscles  does  not,  properly  speaking,  produce  the  tension 
of  the  vocal  cords,  but  only  their  distension.  When  the  elevator  muscles  of  the  larynx 
draw  the  thyroid  cartilage  upwards  and  forwards,  and  with  it  the  anterior  insertion 
of  the  vocal  cords,  the  latter,  in  their  turn,  pull  on  the  arytenoids  and  the  i^ostero- 


DISEASES  OF  THE  LARYNX  25 

cuperior  part  of  the  cricoid.  The  cricoid  cartilage  would  then  swing  forwards,  if 
the  crico-thyroid  muscle,  taking  the  thyroid  for  its  fixed  point,  did  not  straighten  the 
cricoid  by  carrj'ing  the  posterior  insertions  of  the  cords  backwards.  In  that  case  the 
cords  can  be  stretched.  The  crico-thyroid  muscle  is,  then,  one  of  the  distensors  of  the 
cords  ;  its  paralysis,  without  producing  complete  aphonia,  affects  the  voice  and  necessi- 
tates the  assistance  of  the  other  distensor  muscles. 

A  fourth  group  forms  the  extrinsic  musculature  of  the  larjnix.  Some  are  elevators 
of  the  larynx  (mylo-hyoid,  genio-hyoid,  digastric,  stylo-hyoid),  and  their  action  is  con- 
tinued b}'  the  thyro-hyoid  muscle.  The  others  are  depressors  of  the  lar>nax,  towards  the 
sternum  (sterno-hyoid  and  sterno-thyroid)  and  the  shoulder-l)lade  (scapulo-hyoid). 
Lastly,  another  muscle  draws  the  lar\nix  towards  the  vertebral  column  (inferior  con- 
strictor of  the  pharynx)  ;  it  is  a  retractor  and  completes  the  musculature  of  the  apparatus 
of  phonation. 

In  fact,  all  these  intrinsic  and  extrinsic  muscles  are  simultaneously  l)ut  unequally 
in  play  during  phonation.  In  intonation — that  is,  in  the  emission  of  voluntary  sound — 
the  thyroid  prominence  occupies  a  fixed  level  between  the  sternum  and  the  chin.  In 
modulation — that  is,  when  the  intonation  is  varied — the  prominence  rises  for  high 
sounds  and  descends  for  low  ones  ;  as  the  neck  and  the  head  keep  the  same  attitude, 
or  as  the  chin  remains  at  the  same  distance  from  the  sternum,  the  pomum  Adami  always 
occupies  tlie  same  level  for  the  same  intonation. 

When  the  head  is  bent  or  straightened — that  is,  when  the  relations  between  the 
chin  and  sternum  vary — the  levels  occupied  by  the  thyroid  prominence  vary  equally, 
but  a  fixed  height  of  the  tliyroid  prominence  corresponds  for  eacli  sound  to  a  fixed 
attitude  of  the  head.  This  prominence  answers  to  the  anterior  insertion  of  the  vocal 
cords.  The  functicm  whicli  we  have  just  studied  is  due  to  tlie  oombuied  action  of  all 
the  extrinsic  muscles  of  the  larynx. 

Phonation  is  in  harmony  with  the  act  of  expiration.  In  expiration  the  trachea,  the 
cricoid,  and  with  it  the  posterior  insertion  of  the  vocal  cords,  are  raised,  in  proportion 
as  the  air  escapes  and  the  chest  is  emptied.  It  suffices  to  prolong  a  sound  during  the 
whole  period  of  expiration  to  verify  the  ascent  of  the  larynx.  If  the  cricoid  be  raised, 
the  thjToid  must  also  be  raised  to  maintain  the  same  degree  of  tension  of  the  cords, 
and  it  is  only  raised  by  the  action  of  the  elevators,  which  is  modified  by  the  depressgrs 
and  the  retractor.     All  the  musculature,  therefore,  is  in  play. 

Wlien  we  modulate  sounds  (high  sounds)  up  the  scale,  the  cords  are  stretclu-d  and 
the  larynx  is  raised,  while  the  contrary  takes  place  when  our  intonation  becomes  lower. 

The  elevators  of  the  thyroid,  drawing  the  anterior  insertion  of  the  cords  upwards 
and  forwards,  are  then^fore  tensor  muscles,  just  as  the  muscles  which  straiglitcn  tht> 
arytenoids  ujion  the  cricoid,  and  as  the  crico-thyroidcus.  whicli  diaws  the  posterior 
insertion  of  tlie  cords  downwards  and  backwards  (Bomiicr). 

Nerves. — The  muscles  of  the  larynx  are  supplied  by  the  re(rurn'nt  and  the  external 
laryngeal  nerves. 

The  recurrent  nerve,  foriiicd  by  the  spinal  accessory  and  vagus  nerves,  supplies  all 
the  muscles  except  the  crico-thyroidei  ;  tlic  fibres  from  the  vagus  seem  more  esi)ecially 
reserved  for  the  posterior  crico-arytenoid  muscles,  which  open  the  glottis,  while  those 
from  the  spinal  a(;cessory  supply  the  other  muscular  groups. 

The  cricothyroid  muscles,  or  indirect  tensors  of  the  vocal  cords,  are  su|)plicd  Ity  llie 
external  laryngeal  brancdu-s  of  the  superior  laryngeal  nerve,  wlu'rli  lakes  origin  from  Ihe 
gangliform  plexus  of  the  vagus. 

The  extrinsic  musculatun^  is  innervated  by  the  motor  branch  of  tin-  trigeuiiuil.  by 
th<'  facial,  the  glosso- pharyngeal,  and  especially  by  the  hyj)oglo.ssal  nerve. 

Hcmnier  has  recorded  seven  cases  of  hysterical  aj)honia  in  which  the  mu.sdes, 
inn(;rvated  by  the  laryngeal  nerves,  were  working  perfectly.  The  want  of  tension  in 
the  cords  was  due  to  the  inertia  of  the  elevators  supplied  by  the  hypoglossal  nerve. 


26  TEXT-BOOK  OF  MEDICINE 

The  larynx  receives  its  sensory  nerves  from  the  vagus  by  the  superior  laryngeal 
nerve,  which  makes  the  upper  part  of  the  organ  exquisitely  sensitive,  and  by  the  external 
laryngeal  nerve,  which  gives  a  more  obtuse  sensibility  to  the  subglottic  portion. 

Respiration — Voice — Effort. — Respiration  goes  on  freely,  thanks  to  the  contraction 
of  the  posterior  crico-arytenoid  muscles,  which  dilate  the  glottis  and  keep  it  open  during 
respiration.  The  laryngoscope  shows  that  the  glottis  forms  a  triangle,  with  its  base 
backwards,  at  the  arytenoid  cartilages. 

The  production  of  the  voice  is  much  more  complicated.  The  air  in  the  ohest  is 
expelled  with  a  variable  force,  which  is  regulated  by  the  contraction  of  the  expiratory 
muscles  on  the  one  hand,  and  by  the  muscles  of  effort  on  the  other,  and  differs  in 
speaking  or  in  singing. 

When  the  voice  is  to  be  produced,  there  is  first  accommodation  on  the  part  of  the 
glottis — that  is,  the  ary-arjrtenoid,  lateral  crico-arytenoid,  and  external  thyro -arytenoid 
muscles  draw  the  vocal  cords  together  to  the  proper  degree,  so  that  they  may  vibrate 
under  the  pressure  of  the  expired  air.  At  this  moment  the  glottis  presents  the  appear- 
ance of  a  fusiform  cleft,  which  may  attain  as  much  as  2  or  3  milUmetres  in  its  greatest 
diameter. 

The  external  muscles  fix  the  thyroid  at  a  given  level ;  the  crico-thyroideus  carries 
the  cricoid  backwards  and  downwards  ;  the  posterior  crico-arytenoid  muscles,  assisted 
by  the  ary-arytenoideus,  draw  the  arytenoids  backwards  ;  and  the  cords  would  be 
extended,  without  being  really  stretched,  if  the  internal  bundle  of  the  thyro-aryte- 
noideus  did  not  struggle  against  the  passive  distension  of  the  cords  by  their  active 
retraction.  The  latter  thus  acquire  a  physiological  aptitude  for  vibration,  which  may 
be  looked  upon  as  a  tension  peculiar  to  these  organs. 

The  height  of  the  soimd  is,  then,  produced  by  the  tension  of  the  vocal  oords.  In 
the  chest-voice  the  sound  is  produced  by  the  rapid  periodic  variations  of  pressure  of 
the  air  at  the  glottis  :  the  quicker  the  vibrations,  the  higher  the  sound  ;  the  greater  the 
resistance  to  expiration — that  is,  the  greater  the  difference  ,of  pressure — the  more 
intense  the  sound. 

The  sound  is  not  produced  by  the  resonance  proper  of  the  vocal  cords,  but  by  the 
variations  of  tension  which  their  vibrations  give  to  the  column  of  expired  air  at  the 
level  of  the  glottis. 

The  mechanism  of  the  production  of  the  head-voice  is  still  imperfectly  known. 

According  to  some  (Lermoyez),  the  mucosa  of  the  cord  is  said  to  be  the  only  vibra- 
tory part ;  according  to  others  (Bonnier),  the  larynx  is  said  to  act  like  a  whistle  of  variable 
shapes,  the  column  of  air  which  comes  out  of  the  glottis  breaking  against  the  edge  of 
the  ventricular  bands.  The  height  of  the  soimd  may  be  equally  produced  by  the 
pressure  of  the  expired  air  ;  greater  and  greater  pressure  may  thus  raise  the  sound  by 
a  fourth,  and  even  a  fifth,  the  tension  of  the  vocal  cords  remaining  the  same.  Further- 
more, some  authors  admit  that  the  tension  of  the  vocal  cords  may  be  compensated,  in 
a  certain  measure,  by  their  approximation — that  is  to  say,  almost  the  same  effect  is 
obtained  with  the  vocal  cords  when  little  stretched  but  close  together  and  with  the 
cords  more  open  but  very  tense.  Thanks  to  these  different  combinations  of  length, 
tension,  opening,  and  pressure,  the  larynx  gives  the  infinite  shades  and  modulations  of 
the  voice  in  the  acts  of  singing,  lecturing,  and  conversing. 

The  shape  of  the  glottis,  the  vibrations  of  the  cords,  and  the  limits  of  these  vibrations, 
can  be  verified  by  means  of  the  laryngoscope.  During  the  emission  of  a  high  soimd 
the  anterior  part  of  the  vocal  cords  vibrate,  and,  in  proportion  as  the  sound  becomes 
deeper,  we  see  the  glottis  assume  the  ellipsoid  shape,  the  vibrations  being  produced  in 
the  posterior  parts  of  the  vocal  cords,  and  even  in  the  interarytenoid  glottis,  which  not 
only  takes  part  in  resjjiration,  as  was  long  supposed,  but  which  also  contributes  to  the 
production  of  low  notes.  These  few  remarks  on  the  production  of  the  luiman  voice 
will  help  us  to  understand  how  a  simple  ulceration,  the  presence  of  a  false  membrane. 


DISEASES  OF  THE  LARYNX  27 

the  paralysis  of  a  muscle,  the  ankylosis  of  an  articulation,  or  oedema  of  the  arytenoid, 
reacts  at  once  on  such  a  delicate  organ  in  different  ways. 

The  timbre  of  the  voice  varies  in  each  individual,  according  to  conditions  which  were 
unknown  until  the  researches  of  Helmholtz.  I  will  briefly  recapitulate  them.  Every 
sound  is  formed  of  a  fundamental  note,  and  certain  accessory  notes,  called  harmonics, 
which  have  a  fixed  relation  to  the  fundamental  note.  The  harmonics  are  always  higher 
in  the  scale  than  the  fundamental  note,  ^\^len  they  do  not  bear  a  regular  ratio  to  the 
fundamental  note,  the  sound  is  simply  a  noise.  WTien,  on  the  contrary,  they  are  in 
regular  proportion,  a  musical  note  is  produced.  The  timbre  of  the  note,  then,  depends 
upon  the  grouping  and  the  number  of  the  harmonics.  In  the  human  voice  the  funda- 
mental notes  and  the  harmonics  are  produced  at  the  vocal  cords,  but  other  harmonics 
are  also  produced  in  the  pharynx,  the  nose,  and  the  mouth.  Lesions  of  the  mouth,  the 
nose,  and  the  pharynx,  as  well  as  those  of  the  larynx,  are  therefore  able  to  modify  the 
timbre  of  the  voice,  which  becomes  throaty  or  nasal  in  different  cases. 

The  act  of  effort  is  only  possible  when  the  framework  of  the  thorax,  on  which  almost 
all  the  muscles  of  tlie  trunk  and  some  of  the  muscles  of  the  upper  Umbs  are  inserted,  is 
firmly  fixed.  The  thorax  then  becomes  the  fixed  insertion -jjoint  of  the  muscles  which 
are  to  be  brought  into  play  in  the  effort.  This  initial  fixation  of  the  thorax  is 
obtained  by  means  of  a  deep  inspiration,  but  on  condition  that  the  firmly  closed  lips 
of  the  glottis  oppose  the  issue  of  the  previously  inspired  air.  In  paralysis  of  the  constrictor 
muscles  of  the  glottis  the  effort  is  impossible. 

II.  ACUTE  CATARRHAL  LARYNGITIS. 

Description.— Acute  catarrhal  laryngitis  may  occur  as  a  distinct 
illness,  or  be  secondary  to  some  other  ailment.  In  both  cases  it  begins 
with  a  feeling  of  tickling  in  the  larynx,  and,  as  the  sensiblity  of  the  mucosa 
is  increased,  the  inspired  air  appears  too  cold,  and  its  passage  into  the 
respiratory  channels  is  painful.  The  cough,  which  is  at  first  dry  and  slight, 
becomes  more  severe  as  mucus  accumulates  on  tlie  lips  of  the  glottis. 

Phonation  and  respiration  soon  become  difficult ;  the  emission  of  sounds 
is  painful,  the  high  notes  are  lost,  the  voice  is  hoarse,  altered  in  its  low 
timbre,  and  almost  inaudible,  because  the  inflamed  and  paretic  vocal  cords 
are  no  longer  in  their  normal  state  of  tension  and  vibration.  Trifling 
laryngitis  only  provokes  hoarseness  ;  when  it  is  intense,  when  the  paralysis 
of  the  vocal  muscles  is  very  marked,  and  wlien  the  ventricular  bands  arc 
oedematous  and  cover  the  vocal  cords,  aphonia  ])ecomes  complete.  The 
voice,  which  is  deep  and  raucous,  is  sometimes  interrupted  by  sliarp  sounds, 
like  those  of  the  falsetto  ;  this  phenomenon  can  be  explained  by  the  vibratory 
nodes  which  are  formed  on  the  cords,  thickened  and  covered  with  mucus. 

Respiration  is  free  in  the  adult.  In  the  child,  whose  glottis  is  much 
narrower,  dyspncea  is  frequent,  and  often  complicated  by  suffocative  attacks, 
which  result  from  spasm  of  the  glottis.  The  expectoration,  insignificant  at 
first,  is  compo.sed  later  of  thick  greyish  sputum,  wliich  is  less  the  result  of 
the  laryngeal  inflamnjation  than  of  the  bronchitis  and  the  tracheitis  which 
are  so  often  present. 

With  the  laryngoscope  we  sec  that  tlie  mucosa  has  taken  on  ;i  ilark  colour 


28  TEXT-BOOK  OF  MEDICINE 

at  several  spots;  the  epiglottis,  the  aryteno-epiglottic  folds  and  the  ar}i:enoids 
are  red  and  swollen  ;  the  vocal  cords  have  lost  their  pearly,  shining  aspect, 
and  are  covered  with  rosy  striations,  though  they  escape  the  swelling  which 
frequently  attacks  the  ventricular  bands.  The  secretion  from  the  mucous 
glands  is  abundant ;  it  sometimes  has  a  gummy  aspect  and  coats  the  different 
regions.  In  the  benign  form  the  fever  is  insignificant.  The  illness  does  not 
last  more  than  a  week  or  a  fortnight,  and  the  different  symptoms  show  rapid 
improvement,  with  the  exception  of  the  vocal  troubles,  which  are  much 
slower  in  their  disappearance. 

We  also  see  acute  laryngo-traclieitis  a  frigore,  which  is  more  intense  ; 
the  fever  is  sliarp  ;  coughing  and  swallowing  cause  much  pain  ;  the  sputum  is 
sometimes  streaked  with  blood  ;  vocal  troubles  are  very  marked  ;  and  the 
breathing  is  as  much  hampered  as  it  is  at  the  onset  of  oedema  of  the  glottis, 
a  fact  which  is  explained  by  the  swelling  of  the  inflamed  parts.  With  the 
laryngoscope  we  discover,  in  addition  to  the  lesions  previously  described, 
ecchymoses,  which  are  most  marked  on  the  anterior  part  and  the  free  edge 
of  the  vocal  cords,  and  which  testify  to  the  severity  of  the  inflammation. 

etiology — Diagnosis. — Acute  laryngitis  is  provoked  by  the  direct 
contact  of  cold  air  with  the  larynx,  and  by  its  indirect  action  upon  some  other 
part  of  the  body  (cold  to  the  feet).  It  is  set  up  by  irritant  vapours,  accom- 
panies tracheitis,  bronchitis,  or  coryza,  and  is  one  of  the  chief  symptoms  of 
influenza.     In  measles  it  assumes  a  special  type. 

The  severe  form  may  simulate  oedema  of  the  glottis  ;  the  slight  form, 
which  is  much  more  frequent,  must  not  be  confounded  with  nervous 
aphonia.  Every  individual  who  is  seized  with  dysphonia  or  hoarseness, 
following  a  chill,  has  not  perforce  laryngitis  ;  he  may  have  vocal  paralysis 
(nervous  aphonia)  (Krishaber).  In  this  case  the  laryngoscope  reveals  no 
trace  of  phlegmasia,  and  the  vocal  cords  have  kept  their  whiteness,  but  are 
incompletely  stretched,  and  the  paralysis,  which  is  usually  unilateral,  causes 
dysphonia.  These  vocal  troubles  are  due  to  paralysis  of  the  external 
laryngeal  nerve,  which  supplies  the  crico-thyroid  muscle,  by  which  the  vocal 
cords  are  made  tense.* 

Laryngitis,  especially  in  children  (laryngeal  cough  and  hoarseness),  is 
often  the  chief  symptom  of  the  invasion  of  measles  ;  the  presence  of  pharyn- 
geal, ocular,  and  nasal  catarrhs  will  settle  the  diagnosis. 

It  must  not  be  forgotten  that  laryngeal  troubles  of  syphilitic  origin, 
such  as  hoarseness  and  loss  of  voice,  due  to  erythema  and  erosive  sypliilides 

*  This  paralysis  of  the  external  laryngeal  nerve  is  not  more  astonishing  than  that 
of  the  facial  or  radial  nerves  from  the  same  cause.  It  is  also  curious  to  see  that  the 
same  agent — cold — destroys  the  function  of  the  motor  nerves  by  causing  paralysis,  and 
exaggerates  that  of  the  sensory  nerves  by  causing  neuralgia  ("  Aphonic  Nerveuse," 
These  de  Paris,  186.5). 


DISEASES  OF  THE  LARYNX  29 

of  the  larynx,  have  the  closest  resemblance  to  simple  laryngitis.  This  fact 
has  an  important  l^earing  upon  treatment. 

Prognosis — ^Treatment. — Acute  catarrhal  laryngitis,  which  is  not  for- 
midable in  the  adult,  is  more  serious  in  children,  because  it  produces  suffo- 
cative attacks.  It  is  subject  to  relapses,  and  is  a  serious  misfortune  in  people 
whose  larynx  is  a  "  professional  instrument "  (Peter  and  Krishaber),  as  in 
singers,  barristers,  or  public  speakers,  who  are  sometimes  obliged  to  abandon 
their  profession  because  the  voice  is  slow  to  regain  its  norm.al  character,  and 
is  lost  afresh  under  the  influence  of  similar  causes. 

Sweating,  hot  drinks,  soothing  gargles,  powders,  inhalations,  blisters 
placed  on  the  front  of  the  neck,  topical  applications  to  the  larynx, and,  lastly, 
local  blood-letting  when  the  inflammation,  is  acute,  form  the  general  treat- 
ment. 

III.  CHRONIC  LARYNGITIS. 

I  shall  describe  three  varieties  of  chronic  laryngitis — catarrhal,  glandular, 
and  hypertrophic.  I  would,  however,  remark  that  these  varieties  are  not 
always  distinct  clinically  ;  in  fact,  they  are  often  associated. 

Chronic  Catarrhal  Laryngitis.— This  variety  is  hardly  ever  primary ; 
it  usually  succeeds  one  or  several  acute  attacks,  and,  like  every  laryngitis, 
is  kept  up  by  the  efforts  of  singing,  by  excess  of  tobacco,  and  of  drink.  Pain 
is  absent,  cough  is  moderate,  and  hoarseness  is  almost  uniform,  but  rarely 
goes  as  far  as  aphonia.  The  laryngoscope  shows  redness  and  swelling  of 
the  mucosa,  with  varicose  vessels  and  glandular  projections.  The  inflam- 
mation is  sometimes  localized  to  certain  spots,  whicli  are,  in  order  of 
frequency,  the  posterior  surface  of  the  epiglottis,  the  aryteno-epiglottic 
ligaments,  tlie  ventricular  bands,  and  the  vocal  cords. 

Gouty  Laryngitis. — Gouty  persons  often  suffer  a  form  of  chronic 
laryngitis  with  exacerbations,  which  are  accompanied  by  rliinitis,  tracheitis, 
and  bronchitis.  The  bronchitis  is  at  times  limited  to  the  bases  of  the  lungs  ; 
if  it  occupy  the  apices,  the  affection  may  be  considered  of  a  tubercular 
nature.  This  laryngitis  is  chiefly  seen  in  singers  during  the  first  years  of 
study,  and  is  more  frequent  in  summer  than  in  winter.  Most  often  it 
disappears  spontaneously,  when  other  manifestations  of  the  diathesis  appear, 
unless  vocal  strain  has  provoked  definite  iiypertrophy  of  tlie  cords  (Bonnier). 

Glandular  Laryngitis.— Glandular  or  granular  laryngitis  is  generally 
chronic  from  the  outsfit,  and  does  not,  like  the  precetliiig  form,  follow  attacks 
of  acute  laryngitis.  It  is  often  associated  with  granular  pliaryngitis,  which 
oj)ens  the  scene  in  many  cases  ;  the  condition  might,  therefore,  be  termed 
"  graimhir  pliaryiigo-laryngitis.'"  Ilcrp('ti(;  and  artlirilic  subjocls  an*  pre- 
dis[)()sed  to  it,  but  abuse  of  drink  or  lobacco,  and  especially  the  iinninderatc 
use  of  the  voice,  are  its  chief  causes,     'i'lic  inll,inini;ilit)n  is  liimictl,  as  a 


30  TEXT-BOOK  OF  MEDICINE 

rule,  to  the  clusters  of  glands  on  the  posterior  surface  of  the  epiglottis,  in 
front  of  the  arytenoid  cartilages,  where  the  glands  form  a  vertical  ridge, 
and  to  those  on  the  ventricular  bands  and  on  the  vocal  cords,  where  their 
mission  is  to  moisten  the  papillary  region  of  the  vocal  cord,  and  thus  prevent 
loss  of  function.  The  inflammation  attacks  the  glands  of  the  arytenoids, 
of  the  base  of  the  epiglottis,  of  the  vestibule  of  the  larynx,  and  of  the  vocal 
cords.  The  hypertrophy  of  the  glands,  together  with  the  increased 
vascularity  of  the  mucosa,  alters  the  voice  ;  the  singer  can  no  longer  sound 
the  low  notes,  and  soon  loses  the  clear  tone  of  the  high  notes.  The  loss 
of  the  high  notes,  which  is  one  of  the  first  symptoms  of  glandular  laryngitis, 
is  easily  explained. 

In  the  normal  state  the  high  notes  are  produced  as  follows  :  The  anterior 
processes  of  the  arytenoid  cartilages,  by  their  approximation,  bring  the 
vocal  cords  into  exact  contact,  and  the  lips  of  the  glottis  vibrate,  especially 
in  their  anterior  third,  when  a  sound  is  emitted.  The  complete  approximation 
of  the  vocal  cords  can  no  longer  take  place  if  the  interarytenoid  mucosa  be 
swollen  and  thickened.  The  high  sounds,  therefore,  are  defective  or  sup- 
pressed. Later  the  patient  loses  the  low  notes,  and  the  middle  notes  are 
also  affected  if  the  lesion  reach  the  vocal  cords. 

When  the  lesions  are  general,  the  laryngoscope  shows  the  granular 
condition  and  the  vascularity  of  the  ventricular  bands  and  of  the  vocal 
cords,  in  addition  to  the  glandular  hypertrophy  described  above.  Erosions 
are  sometimes  seen  at  different  points  of  the  mucosa. 

Hypertrophic  Laryngitis. — This  form  is  usually  associated  with  the 
preceding  variety.  The  hypertrophy  may  be  general  or  local,  and,  in  the 
latter  event,  involves  the  epiglottis,  the  aryteno- epiglottic  folds,  and  the 
vocal  cords.  Tiirck  has  described  a  variety  of  hypertrophy  attacking  the 
vocal  cord,  chorditis  tuberosa.  The  hypertrophied  parts  are  rigid,  often 
deformed  ;  the  epiglottis  bends  backwards,  and  partly  hides  the  entrance 
of  the  larynx ;  the  aryteno-epiglottic  folds  are  thickened  and  shortened ; 
the  arytenoids  resemble  an  irregularly  shaped  nipple ;  and  the  vocal  cords 
are  much  enlarged. 

Besides  the  various  changes  in  the  voice,  hypertrophic  laryngitis  is  some- 
times accompanied  by  dyspnoea,  due  to  the  swelling  of  the  affected  parts, 
which  may  obliterate  the  orifice  of  the  larynx  and  gradually  lead  to  asphyxia. 

In  clu-onic  laryngitis  both  local  and  general  treatment  are  employed. 
The  direct  application  of  a  10  per  cent.,  or  even  20  per  cent.,  solution  of 
nitrate  of  silver,  insufflations  of  bismuth,  inhalations  of  iodine  and  sulphur 
vapour,  and  preparations  of  arsenic  internally,  are  the  therapeutic  agents 
most  employed.  Good  results  are  obtained  from  the  cures  of  Eaux-Bonnes, 
Cauterets,  and  La  Bourboule.  Krishaber  has  successfully  applied  igni- 
puncture  to  the  granulations  of  the  larynx. 


DISEASES  OF  THE  LARYNX  31 

We  must  also  prove  that  the  nasal  fossae  are  clear,  and  must  restore  nasal 
respiration.  Gouty  laryngitis  often  yields  to  hot  local  appHcations  to  the 
neck  and  to  nasal  douches  of  hot  saline  solutions.  It  is  ameliorated  by  very 
warm  gargles.  The  best  of  these  gargles  can  be  made  with  wine,  adding 
infusion  of  cinnamon,  which  makes  the  gargle  astringent ;  the  gargle  must 
be  used  as  hot  as  the  patient  can  bear  it.  As  a  rule,  all  the  symptoms  yield 
very  rapidly  (Bonnier). 

IV.  SYPHILIS  OF  THE  LARYNX  (SECONDARY  LARYNGOPATHIES 
—TERTIARY  LARYNGOPATHIES). 

The  frequence  and  the  importance  of  syphilitic  lesions  of  the  larynx 
deserve  our  careful  attention.  Lewin  says :  "  Next  to  the  skin  and  the 
throat,  syphihs  most  frequently  attacks  the  larynx."  The  epiglottis,  the 
aryteno-epiglottic  folds,  the  ventricular  bands,  the  vocal  cords,  and  the 
skeleton  of  the  larynx,  may  show  most  diverse  changes  due  to  sypliihs. 
These  changes  may  be  superficial  or  deep.  The  superficial  lesions,  which 
comprise  laryngeal  catarrh,  erythema,  mucous  patches,  erosions  and  ulcers, 
with  or  without  oedema,  are  seen  in  the  secondary  stage. 

The  deep  submucous  infiltrations,  which  comprise  diffuse  or  circum- 
scribed syphilomata,  ulceration,  hypertrophy,  vegetations,  changes  in  the 
cartilages,  formation  and  elimination  of  sequestra,  cicatricial  retractions, 
progressive  laryngo-stenoses,  permanent  deformities,  and  perilaryngeal 
phlegmon,  are  found  in  the  tertiary  period. 

Secondary  Laryngopathies. 

Description. — The  chancre  has  never  been  seen  in  the  larynx.  Tlie 
secondary  lesions — erythema,  catarrh,  erosion,  and  ulceration — with  or 
without  oedema,  first  demand  notice. 

Erythema  appears  a  few  weeks  after  infection,  at  the  same  date  as  the 
mucous  or  cutaneous  syphilides,  and  is  a  very  frequent  trouble.  Many 
people  become  hoarse  within  some  weeks  or  months  after  infection,  and 
ascribe  the  trouble  to  a  chill,  or  speak  of  "  loss  of  voice,"  when  the  mischief 
is  really  sypliilitic.  With  the  laryngoscope  the  erythema  is  characterized 
by  a  rosy,  ash-coloured,  or  reddish  tint  of  the  mucosa,  and  often  coincides 
with  erythema  of  the  throat,  which  of  is  a  vermilion  colour,  especially  on 
the  velum  and  the  anterior  pillars.  Tlie  voice  becomes  hoarse,  and  may  be 
almost  lost.  The  erythema  disappears  in  a  few  months,  but  is  prone  to 
relapse  ;  slaty  coloration  of  the  vocal  cords  sometimes  remains.  In  some 
cases  erythema  is  accompanied  by  secretion,  and  laryngeal  catarrh  is 
found. 

Secondary  syphiiides  of  the  larynx  may  be  erosive  or  ulcerative.      The 


32  TEXT-BOOK  OF  MEDICINE 

erosions  are  superficial  ulcerations,  which  are  opaline,  rounded,  or  oval,  and 
surrounded  by  a  red  border  ;  on  the  vocal  cords  they  are  usually  elongated 
and  situated  on  the  free  edge.  Erosive  syphilides  sometimes  coincide  with 
erythema  and  provoke  vocal  troubles,  but  are  not,  as  a  rule,  accompanied 
by  oedema  or  dyspnoea.  Swallowing  is  painful  when  the  aryteno- epiglottic 
folds  are  involved.  These  erosive  syphilides  form  part  of  the  early  secondary 
troubles,  whilst  the  ulcerative  syphilides  appear  later.  The  latter  (and  I 
do  not  allude  to  the  deep  ulcerations  of  the  tertiary  period)  are  much  broader 
and  more  hollow  than  the  erosive  syphilides,  their  edges  are  sometimes 
prominent  and  of  a  vivid  red,  while  the  surrounding  mucosa  is  oedematous  ; 
they  occupy  the  epiglottis,  the  arytenoid  region,  the  ventricular  bands,  and 
the  vocal  cords. 

It  must  not  be  thought  that  the  superficial  lesions  of  the  larynx  belong 
solely  to  the  first  year  after  infection  ;  catarrh,  erythema,  erosions,  and 
superficial  ulcerations,  with  or  without  oedema,  although  they  be  slight  and 
part  of  the  "  secondary  troubles,"  may  still  appear  many  years  after  the 
primary  infection.  Most  of  these  lesions,  which  may  be  called  "  benign," 
only  cause  vocal  troubles. 

Pain  is  absent,  and  cough,  so  frequent  in  other  forms  of  laryngitis,  is 
often  wanting  in  these  cases.  The  voice  is,  however,  altered  and  rough- 
ened ;  this  is  the  most  constant  symptom.  Hoarseness,  dysphonia,  and 
sometimes  aphonia,  may  supervene  slowly  or  rapidly,  and  may  be  very 
obstinate.  Persons  suffering  from  sypliilis  of  the  larynx  are  certainly 
more  sensitive  to  the  action  of  cold,  and  chills  are  no  doubt  to  blame  for 
first  attacks,  and  also  relapses,  of  these  secondary  troubles.  Tliis  knowledge 
will  prevent  us  considering  a  laryngitis  in  which  syphilis  plays  the  chief  part 
as  a  simple  laryngitis  a  frigore. 

Dyspnoea  is  rare  in  these  cases  ;  nevertheless,  superficial  and  apparently 
benign  lesions  are  sometimes  accompanied  by  oedema  of  the  larynx  and 
respiratory  troubles.  This  fact  is  very  important ;  Krishaber  lays  great 
stress  upon  it.  Although  dyspnoea  may  be  exceptional  in  secondary  laryngo- 
pathies,  the  oppression  may  rapidly  increase,  and  tracheotomy  would  be 
necessary  if  the  dyspnoea  did  not  speedily  yield  to  treatment.  I  have 
.several  times  proved  this  statement,  and  M.  Mauriac,  like  Krishaber,  affirms 
that  "  almost  insignificant  erosions  may  become  a  dangerous  inflammatory 
centre,  around  which  oedema  of  the  glottis  suddenly  develojDs." 

In  dealing  with  a  laryngitis  apparently  due  to  chill,  or  with  an  apparently 
simple  loss  of  voice,  syphilis  must  always  be  thought  of,  and  due  investiga- 
tions made,  to  avoid  an  error  in  diagnosis.  The  discovery  of  the  chancre  and 
its  satellite  glands,  the  presence  of  syphilides  of  the  skin  (roseola),  and  of 
the  mucosa}  (mucous  patches),  headache,  and  alopecia,  will  all  help  to  settle 
the  pathogenic  diagnosis. 


DISEASES  OF  THE  LARYNX  33 

Tertiary  Laryngopathies. 

Description. — ^Tlie  tertiary  lesions  are  much  rarer,  but  much  graver, 
than  the  secondary  ones.  Though  they  do  not  appear,  as  a  rule,  witliin 
two  years  from  the  date  of  infection,  they  may  be  very  early  (during  the 
first  year)  or  very  late  (after  the  twentieth  year).  The  tertiary  laryngo- 
pathies coincide  fairly  often  with  specific  lesions  of  the  trachea  and  the 
lungs  ("  they  are,  as  it  were,  the  root "),  while  the  secondary  laryngopatliies 
are  especially  associated  with  specific  lesions  of  the  velum  palati  and  of  the 
throat.  • 

1.  Ulcerative  Syphiloma— Gummata.— The  gumma  may  be  super- 
ficial or  deep,  and  may  attack  tlie  soft  parts  or  the  skeleton  of  the  larynx. 
In  some  cases  it  forms  a  small  swelling,  and  is  the  gumma,  properly 
speaking  ;  in  others  it  infiltrates  the  tissues,  and  is  the  diffuse  syphiloma 
(syphiloma  en  nappe). 

The  Gumma  is  the  most  typical  lesion  of  tertiary  laryngeal  syphihs. 
It  may  vary  in  size  from  a  pin's  head  to  a  hazel-nut.  Several  isolated  or 
confluent  gummata  in  different  stages  of  growth  may  be  met  with.  As  a 
rule,  the  gumma,  seen  with  the  laryngoscope,  forms  a  rounded  projection, 
which  is  of  sombre  hue  and  surrounded  by  reddish  oedema.  As  softening 
takes  place,  it  becomes  yellowish  at  the  centre,  and  in  a  few  days  an  ulcer 
is  formed,  wliich  shows  little  tendency  to  spontaneous  lieahng.  The  edges 
of  the  ulcer  are  perpendicular,  the  floor  is  greyish,  the  surrounding  tissues  are 
hard  and  elastic.     The  area  on  which  the  ulcer  is  situated  is  oedematous. 

Tlie  gummatous  neoplasm  is  not  always  circumscribed  ;  it  may  infiltrate 
the  mucosa  and  submucous  tissue  in  a  diffuse  manner,  and  is  then  termed 
'■  syphiloma  en  nappe."  This  sypliiloma  is  often  capricious,  like  the 
phagedaenic  lesions,  and  produces  serpiginous  ulcers,  wliich  not  only 
destroy  the  mucosa,  but  also  attack  the  perichondrium,  cartilages,  and 
joints ;  they  may  even  reach  the  extralaryngeal  tissues,  producing  inflam- 
mation of  the  neck  (Mauriac).  This  diffuse  syphiloma  commences  in  the 
submucosa  ;  it  may,  however,  start  in  the  skeleton  of  the  larynx. 

We  see,  lastly,  other  ulcerations  which  do  not  result  from  the  necrobiosis 
of  a  gumma.  In  addition  to  the  gummatous  ulcers  which  I  have  just 
described,  we  may  see  tertiary  ulcers,  which  at  first  look  like  a  simple  con- 
gestion of  the  mucosa  or  superficial  erosions.  We  must  not,  however,  trust 
to  the  "  benign  appearance,"  for  this  lesion,  though  apparently  congestive, 
may  be  the  prelude  of  severe  phagedtena. 

The  gummatous  and  ulcerative  lesions  which  I  have  just  described 
present  the  most  varied  pictures  with  the  laryngoscope.  The;  <^|)i<:l<)ttis, 
which  is  so  fre((uently  attacked  by  syphilis,  is  thickened,  hyperjilastic, 
oedematous,  and  deformed;  it  forms  a  dull  red  tumour,  which  obliterates  the 


34  TEXT-BOOK  OF  MEDICINE 

vestibule  of  the  larynx  to  a  variable  extent.  In  other  cases  the  epiglottis 
is  indented,  loopholed,  or  covered  by  ulcerations  "  from  the  slight  erosion 
of  its  surface  and  of  its  edges  to  the  serpiginous  and  gangrenous  ulcers  which 
reduce  it  to  shreds  "  ;  it  is  sometimes  converted  into  an  irregular  stump. 
Phagedgena  of  the  epiglottis  is  also  frequent. 

The  arytenoid  region  and  the  aryteno-epiglottic  folds  are  deformed, 
cedematous,  and  hypertropliied  by  the  gummatous  tissue ;  they  block  up 
the  vestibule  and  hide  the  vocal  cords.  Vegetations  are  not  rare.  The 
folds  are  the  seat  of  ulcerations  with  greyish  floor  and  dark  perpendicular 
edges. 

The  vocal  cords  undergo  the  most  varied  changes  :  they  are  red,  hyper- 
trophied,  and  ulcerated.  The  ulceration  begins  in  the  free  border,  eats  into 
the  cord,  making  it  look  like  a  saw  ;  the  cord  may  be  reduced  to  shreds,  or 
the  ulcer  may  end  in  vicious  scars  and  adhesions. 

2.  Non-Ulcerating  Syphiloma.  —  The  diffuse  infiltration  does  not 
always  go  on  to  ulceration  ;  it  may  run  a  very  slow  course,  and  may  cause 
in  the  lar}mx  (as  in  the  lips  and  the  prepuce)  fibrous  thickening  which  has 
no  tendency  to  ulcerate.  This  thickening,  which  is  rarely  general,  narrows 
the  cavity  of  the  larynx  ;  it  affects  the  subglottic  part  of  the  organ,  the 
epiglottis,  the  ventricular  bands,  and  may  be  confined  to  one  of  these  parts. 
The  laryngoscope  shows  the  affected  part  to  be  deformed  and  of  a  dull  red  ; 
its  surface  is  granular,  mammillated,  and  sometimes  covered  by  vegetations. 
In  an  old  syphilitic  patient  whom  I  have  just  seen  hypertrophy  of  the  left 
ventricular  band  and  two  vegetations  in  the  arytenoid  region  were  present. 

3.  Vegetations. — The  neoplasm  often  takes  the  form  of  a  vegetation. 
The  vegetations  are  rarely  solitary ;  they  may  be  isolated  or  confluent, 
sessile  or  pedmiculated,  and  may  vary  in  size  from  a  millet-seed  to  a  pea. 
Their  "  seat  of  election  "  is  the  vocal  cords  and  the  ventricular  bands. 
They  develop  on  the  surface,  on  the  edges,  and  at  the  angle  of  the  junction, 
but  rarely  invade  the  epiglottis,  in  distinction  to  ulcerations  which  have 
a  marked  preference  for  it.  These  vegetations,  as  a  rule,  develop  in  mucous 
membrane  which  is  already  diseased,  and  may,  by  reason  of  their  number 
or  of  their  size,  narrow  or  block  the  glottis  and  the  cavity  of  the  larynx. 

4.  Lesions  of  the  Skeleton. — The  syphiloma  may  primarily  attack 
the  cartilages,  or  only  invade  them  after  the  soft  parts.  The  affected 
cartilages  are,  in  order  of  frequency,  the  arytenoids  and  the  cricoid.  The 
thyroid  is  usually  respected.  The  first  result  is  calcification  of  the  cartilage  ; 
the  calcified  tissue  then  necroses,  and  the  separation  of  the  sequestrum  is 
accompanied  by  suppuration,  fistulas,  and  oedema.  The  necrobiotic  process, 
which  begins  on  the  inner  wall  of  the  cartilage,  may  invade  its  whole  thick- 
ness, and,  after  eating  through  it,  set  up  inflammation  in  the  front  of  the 
neck. 


DISEASES  OF  THE  LARYNX  35 

Dislocations  and  ankyloses  of  the  joints  result  from  the  syphilomatous 
process.  In  some  cases  a  fragment  of  cartilage,  or  an  entire  arytenoid, 
may  be  cast  off  through  a  fistula,  be  rejected  by  the  mouth,  or  fall  into  the 
air- passages  and  provoke  asphyxia. 

The  changes  in  the  cartilages  of  Wrisberg  and  of  Santorini  are  perfectly 
visible  \vith  the  laryngoscope.  Crico- arytenoid  ankylosis  is  almost  always 
unilateral,  and  fixes  the  vocal  cord  on  the  affected  side. 

5.  (Edema. — CEdema  of  variable  colour  often  accompanies  tertiary 
laryngopathies.  Laryngeal  oedema  plays  a  considerable  part  in  these 
cases  ;  it  may  be  more  or  less  extensive,  and  invades,  in  order  of  frequency, 
the  epiglottis,  the  ventricular  bands,  the  aryteno-epiglottic  folds,  the  vocal 
cords,  the  parts  below  the  cords,  and  the  trachea.  The  symptoms  present 
are  stridor,  sucking-in,  and  dyspncBa  which  borders  on  asphyxia.  The 
laryngoscope  reveals  the  deformity  and  the  swelling  of  the  cederaatous 
parts  ;  the  epiglottis  "  is  rolled  up  like  a  paper-twist,  and  swollen  so  as  to 
resemble  a  chestnut  or  the  cervix  uteri,"  while  the  arytenoids  form  large 
pads,  which  obliterate  the  supraglottic  region. 

Syphilitic  oedema  of  the  larynx  will  be  studied  in  detail  in  Section  8. 

6.  Tracheo-Laryngeal  Adenopathy.— The  numerous  glands  which  are 
present  in  the  trachea  and  tlie  larynx  are  sometimes  attacked  by  syphilis, 
and  we  therefore  find  the  symptoms  which  accompany  lesions  of  the  recurrent 
nerves  (spasm  of  the  glottis,  or  paralysis  of  the  vocal  cords). 

7.  Cicatrices — Laryngo-Stenosis.— Ulcerous  lesions  of  the  larynx  some- 
times leave  deformities,  adhesions,  and  retractions,  which  affect  both  the 
voice  and  the  breathing.  The  epiglottis  may  be  displaced  or  deformed  by 
the  cicatricial  bands,  wliich  draw  it  towards  the  aryteno-epiglottic  folds 
or  towards  the  lateral  wall  of  the  pharynx  ;  the  result  is  complete  deformity 
of  the  aperture  of  the  larynx.  The  vocal  cords  may  be  converted  into 
fibrous  bands,  which  dislocate  the  vocal  process  ;  the  axis  and  the  calibre  of 
the  laryngeal  cavity  are  altered,  and  gradual  laryngo-stenosis  results.  In 
some  cases  the  stenosis  arises  from  the  welding  of  the  ulcerated  vocal  cords, 
which  then  form  a  kind  of  diaphragm,  and  partially  obhterate  the  glottis. 

8.  Paralysis.  —The  existence  of  syphilitic  paralysis  of  the  laryngeal 
muscles  can  only  be  recognized  with  the  laryngo.scope.  The  paralysis  is 
often  unilateral,  and  chiefly  affects  tlie  left  cord.  Paralysis  of  the  posterior 
crico-arytenoid  muscles  is  characterized  by  immobility  of  the  vocal  cords 
at  the  moment  of  inspiration  ;  the  glottis,  instead  of  being  open  during 
inspiration,  tends  to  close,  and  asphyxia  becomes  imminent.  When  one 
lateral  crico-arytenoid  muscle  is  paralyzed,  the  cord  on  the  corresponding 
side  does  not  approach  the  other  cord  during  phonation.  Syi)l)ilitic  para- 
lysis of  the  arv-arytenoidcus  is  very  rare  ;  the  laryngoscope  shows  that  the 
intercartilaginous   glottis   remains   open   during    the    emission   of   sounds. 


36  TEXT-BOOK  OF  MEDICINE 

Laryngoplegias  are  very  often  isolated.  Their  pathology  is  still  imperfectly 
known  :  they  may  be  due  either  to  lesions  of  the  glands  adjoining  the  re- 
current nerves,  or  to  an  intracranial  lesion,  though  it  is  far  more  likely  that 
these  partial  paralyses  have  a  peripheral  origin.  They  may  be  compared 
with  the  paralysis  of  the  oculo- motor  nerves  and  with  the  various  forms 
of  facial  paralysis  which  are  seen  in  all  stages  of  syphilis. 

Symptoms. — Vocal  troubles  are  often  the  first  to  appear,  and  may  vary 
from  hoarseness  to  complete  and  persistent  aphonia.  Cough  is  rare  and  not 
important.  Respiratory  troubles,  from  shortness  of  breath  to  the  most 
violent  dyspnoea,  are  practically  constant.  Many  patients  suffer  from 
breathlessness,  to  which  they  become  accustomed  by  avoiding  violent 
efforts.  In  some  the  attacks  of  dyspnoea  are  very  severe ;  in  others  the 
dyspnoea  may  improve  for  a  while,  only  to  return  in  a  worse  form ;  lastly, 
in  some  cases,  especially  when  oedema  is  present,  the  dyspnoea  is  so  rapid 
in  its  onset  that  asphyxia  becomes  imminent,  and  intervention  is  imperative. 

Stridor  and  sucking-in  accompany  almost  every  case  of  severe  laryngeal 
dyspnoea. 

This  dj^spnoea  is  due  to  the  stenosis  of  the  larynx  ;  the  narrowing  may 
be  rapid  (acute  laryngo-stenosis)  or  slow  (progressive  laryngo-stenosis). 
(Edema  and  abscesses  are  the  commonest  causes  of  acute  laryngo-stenosis. 

Progressive  laryngo-stenosis  is  due  to  many  causes,  such  as  develop- 
ment of  gummata,  diffuse  hypertrophic  syphiloma,  presence  of  vegetations, 
oedema,  abscesses,  cicatrices,  deformity  of  the  aryteno-epiglottic  region, 
dislocations  of  the  arytenoids,  and  adhesions  of  the  vocal  cords.  This 
enumeration  explains  sufficiently  the  diversity,  the  continuous  or  inter- 
mittent character,  and  the  intensity  of  the  respiratory  troubles. 

I  may  remind  the  reader  that  asphyxia  may  follow  the  fall  of  a  necrosed 
cartilage  into  the  trachea. 

Swallowing  is  very  painful,  or  almost  impossible,  in  some  patients, 
especially  when  the  edges  of  the  epiglottis  and  the  arytenoids  are  inflamed 
and  ulcerated.  Sharp  pains  in  the  ear  may  accompany  the  dysphagia. 
Foetor  of  the  breath  is  not  so  common  as  in  cancer. 

Diagnosis. — There  is  often  difficulty  in  diagnosis,  because  so  many 
lesions  of  the  larynx  (hypertrophic  laryngitis,  syphilitic,  tubercular,  and 
cancerous  disease,  and  oedema  in  Bright's  disease)  may  cause  the  same  vocal 
and  respiratory  troubles.  Another  difficulty  in  diagnosis  results  from  the 
fact  that  such  lesions  as  hypertrophic  infiltrations,  polypoid  excrescences, 
ulcerations,  and  oedema  may  show  an  identical  appearance  with  the  laryngo- 
scope. The  signs  and  symptoms  which  may  help  us  in  diagnosis  demand 
mention. 

1.  Chronic  Hypertrophic  Laryngitis. — General  health  excellent,  no 
loss  of  flesh,  appetite  good,  dys^moea  absent  or  trifling,  obstinate  cough, 


DISEASES  OF  THE  LARYNX  37 

and  dryness  of  the  throat ;  for  a  long  time  past  gradual  change  of  the  voice, 
loss  of  high  sounds,  hoarseness,  and  muffling  of  the  voice. 

With  the  laryngoscope  :  Hypertrophy  and  granulations  on  the  ventricular 
bands  ;  redness  and  granulations  on  the  vocal  cords,  especially  on  their 
free  border  ;  hypertrophy  of  the  glands  of  the  larvnx,  chiefly  in  the  arvtenoid 
region.  Result :  incomplete  approach  of  the  arytenoids ;  insignificant 
erosions  of  the  mucosa ;  pharyngo-laryngeal  catarrh,  jvith  abundant 
secretion. 

Gouty  laryngitis  presents  during  each  acute  attack  marked  erythema 
of  the  larynx,  the  pharynx,  and  the  trachea.  The  periodicity  of  the  crises, 
however,  eliminates  syphilitic  erythema.  The  vocal  cords  have  sometimes 
a  blood-red  appearance. 

2.  Tubercular  Laryngopathy. — Wasting,  loss  of  appetite,  bronchitic 
cough,  haemoptysis,  or  pre\'ious  pleurisy,  pulmonary  lesions  in  course  of 
development.  In  some  exceptional  cases  primary  laryngeal  tuberculosis  ; 
vocal  troubles  of  every  degree  ;  d3^spnoea  absent  or  marked,  according  to 
the  site  and  the  severity  of  the  lesions  ;  pain  and  dysphagia,  which  may  be 
very  acute. 

With  the  laryngoscope :  Unusual  pallor  of  the  palate  and  of  the 
vestibule  of  the  larynx  ;  isolated  -or  combined  lesions  of  the  larynx,  which 
present  the  following  forms  : 

(a)  Tubercular  infiltration,  without  ulceration,  confined  especially 
to  the  interarytenoid  region,  tlie  epiglottic  folds,  and  the  ventricular 
bands  ;  hypertrophy  and  deformity  of  these  parts,  notably  conical  swelling 
of  one  or  both  arytenoids  ;  epiglottis  enormous  ;  great  swelling  of  the  ven- 
tricular bands  ;  vocal  cords  dull  and  rough  ;  epiglottis  asually  healthy ; 
enlarged  glands  ;  laryngeal  catarrh. 

(6)  Tubercular  vegetations,  which  may  be  large,  are  found  in  the  inter- 
arytenoid region.  They  are  dull,  livid,  covered  with  purulent  mucus,  and 
often  implanted  upon  an  ulcerated  base  ;  surrounding  oedema  pale. 

(r)  Tubercular  Ulcerations. — Their  edges  are  jagged  and  Hat ;  they  are 
not  deep,  and  the  surrounding  oedema  is  soft  and  pale.  These  ulcers  in 
time  destroy  the  ventricular  bands,  the  vocal  cords,  and  the  folds  of  the 
epiglottis.  By  curetting  the  ulcers,  li<|uid  which  sometimes  contains  the 
tubercle  bacillus  may  be  obtained. 

(d)  Paralysis,  or  paresis  of  a  vocal  cord,  a  fairly  frequent  sign  at  the 
commencement  of  laryngeal  tuberculosis  (Libermann). 

3.  Syphilitic  Laryngopathies.  Health  excellent ;  no  loss  of  appetite; 
no  wasting  ;  cough  absent  or  IrKling  ;  previous  syphilis;  vocal  tr()ul)I('.s. 
from  simple  hoarseness  to  comj)l('te  and  persistent  aphonia  ;  respiratory 
troubles,  varying  from  shortness  of  breath  to  dyspnoj^i,  with  stridor  and 
sucking-in  ;   pain  on  dculiitition  and  in  the  ears,  according  to  the  lesion. 


38  TEXT-BOOK  OF  MEDICINE 

Examination  with  the  laryngoscope  :  Pallor  of  the  palate,  the  pharynx, 
and  the  larynx,  so  common  in  tuberculosis,  is  not  seen.  The  laryngeal 
lesions,  whether  isolated  or  combined,  are  : 

(a)  Rounded,  prominent  and  reddish  gumma,  situated  on  the  epiglottis, 
the  folds,  or  the  ventricular  bands,  projecting  into  the  larynx  and  causing 
deformity. 

(b)  Diffuse  syphiloma  of  the  hypertrophic  form,  situated  in  different 
regions,  and  often  coinciding  with  excrescences  and  ulcerations. 

(c)  Ulcerations. — Slightly  different  according  as  they  are  consecutive  to 
gumma,  diffuse  syphiloma,  or  tertiary  non-gummatous  ulcerations.  The 
syphilitic  ulcer  has  generally  thick  perpendicular  edges,  whereas  the  edges 
of  the  tuberculous  ulcer  are  jagged  and  flat.  The  syphilitic  ulcer  is  usually 
deeper  and  more  excavated  than  the  tubercular  one  ;  the  oedematous  tissues 
which  surround  the  syphilitic  ulcer  are  usually  red  and  hard  (in  tubercular 
ulceration  they  are  pale  and  soft).  The  syphilitic  ulceration  rapidly  hollows 
out  channels  and  perforates  the  tissues  (tubercular  ulceration  is  slOW  in  its 
progress).  Syphilitic  ulceration  is  found  in  every  part  of  the  larynx,  but 
has  a  marked  predilection  for  the  epiglottis,  and  especially  invades  its 
laryngeal  surface.  Syphilitic  ulcers  are  less  numerous  than  tubercular  ones, 
and  leave  scars  behind  them  ;  tubercular  ulcers  do  not. 

(d)  Vegetations. — They  are  rarer  in  syphilis  than  in  tuberculosis.  In 
syphilis  vegetations  are  chiefly  found  on  the  base  of  the  epiglottis,  on  the 
ventricular  bands  and  the  vocal  cords  (in  tuberculosis  they  are  usually 
found  in  the  interarytenoid  region).  Syphilitic  vegetations  show  a  peculiar 
tendency  to  bud  out ;  they  are  usually  associated  with  ulceration,  tend  to 
disappear  and  give  place  to  a  cicatrix.  Tubercular  vegetations  continue  to 
grow. 

If  tuberculosis  complicate  syphilis,  the  diagnosis  is  exceedingly  difficult. 
This  association  is  not  rare.  It  is  remarkable  that  tuberculosi.s,  if  it  be  asso- 
ciated with  syphilis,  is  less  severe  and  less  rapid  than  when  it  is  present  alone 
in  the  larynx. 

4.  Cancerous  Laryngopathy. — The  diagnosis  is  extremely  difficult, 
becsuse  cancer  of  the  larynx  may  be  almost  latent  for  a  year  or  two  ;  it  does 
not  affect  the  general  health,  the  appetite  remains  good,  the  patient  does  not 
waste  away,  and  the  glands  are  not  yet  infectec'.  Vocal  troubles  alone  are 
present,  but  they  have  no  distinctive  character.  Later,  when  the  cancer  has 
ulcerated,  the  nature  of  the  lesion,  the  ready  bleeding,  the  foetor  of  the 
breath,  the  acute  pains  in  the  throat  and  the  ear,  and  the  bloody  expectora- 
tion, are  signs  in  favour  of  cancer.  But  during  the  first  period — and  this 
period  may  be  lengthy — how  can  a  diagnosis  be  made  ?  In  the  first  place, 
if  the  patient  have  no  syphilitic  nor  tubercular  taint,  the  question  is  somewhat 
simphfied.    Cancer  at  the  outset  is  always  unilateral,  and  the  lesion  is  clearly 


DISEASES  OF  THE  LARYNX  39 

circumscribed  ;  the  "  seat  of  election  "  is  the  ventricular  band  or  the  vocal 
cord.  When  the  cancer  is  polypoid,  it  is  distinguished  from  other  vegeta- 
tions by  the  fact  that  the  ulcer  deepens  in  proportion  as  the  tumour  grows 
(Krishaber).  The  f ungating  mass  of  cancer  resembles  a  cauliflower  ;  it  is 
ulcerated  and  bleeds  easily.  We  find  nothing  similar  in  syphilis  or  tuber- 
culosis. 

5.  Polypi  of  the  Larynx. — The  polypoid  growths  of  syphilis  must  not 
be  confounded  with  the  vegetations  of  tuberculosis  and  with  papillomata. 
Tubercular  vegetations  are  colourless,  covered  ^vith  muco-pus,  implanted 
on  an  ulcerated  surface,  and  surrounded  by  more  or  less  oedematous  mucosa  ; 
they  are  usually  situated  on  the  posterior  part  of  the  cord,  or  on  the  anterior 
process  of  the  arytenoid.  The  papilloma  may  be  as  large  as  a  millet-seed 
or  a  hazel-nut ;  it  may  be  pedunculated  or  sessile  ;  it  is  pearly,  wrinkled,  and 
sometimes  covered  by  whitish  mucus.  Its  "  seat  of  election  "  is  the  anterior 
third  of  the  free  edge  of  the  vocal  cords,  because  this  part  is  rich  in  papillfc 
and  glands.     These  polypi  cause  vocal  and  sometimes  respiratory  troubles. 

G.  (Edema  of  the  Larynx. — Oedema  of  the  larynx,  due  to  many  other 
causes,  may  simulate  that  due  to  syphilis.  Dyspnoea,  stridor,  and  sucking-in 
exist  in  both  cases,  and  therefore  careful  examination  should  always  be 
made  as  to  the  cause,  in  order  to  institute  antisyphilitic  treatment  without 
delay  if  it  be  required. 

Treatment. — The  recognition  of  syphilitic  changes  in  the  larynx  is  most 
important,  because,  except  for  certaui  tertiary  lesions  and  cicatricial 
stenoses,  syphilitic  affections  of  the  larynx  yield  very  readily  to  specific 
treatment.  Local  treatment  is  of  only  secondary  importance ;  specific 
treatment  is  imperative.  Inunctions  or  solutions  of  mercury  and  iodide 
of  potassium  in  large  doses  give  very  good  results.  The  vocal  and  respiratory 
troubles  disappear — sometimes  slowly,  at  other  times  quickly — and  in  many 
instances  specific  treatment  has  averted  troubles  which  seemed  to  demand 
tracheotomy.  We  must  bear  these  facts  clearly  in  mind.  Krishaber  has 
pul)lished  some  absolutely  remarkable  cases. 

For  some  years  I  have  exclusively  employed  oily  or  aqueous  injections 
of  biniodide  of  mercury,  and  I  find  this  preparation  so  superior  that  I  treat 
syphilis  by  means  of  these  injections  alone,  and  hardly  ever  use  iodide  of 
potassium.     This  treatment  will  be  found  in  the  Appendix  on  Therapeutics. 

In  some  cases,  however,  this  treatment  does  not  at  first  succeed.  We 
must  persevere,  and  severe  cases  which  have  resisted  treatment  for  twelve 
days  or  a  fortnight  begin  to  yield,  provided  we  keep  on.  I  have  seen  patients 
in  a  state  of  asphyxia  from  syphilis  of  the  larynx.  They  had  already  taken 
mercury  and  iodides,  but  still  the  lesion  had  made  progress,  because  the 
doses  wcro  neither  sufficiently  increased  nor  continued  for  a  sufficiently 
long  period.     1  have  had  the  satisfaction  of  seeing  these  [Kiticiits  recover. 


40  TEXT-BOOK  OF  MEDICINE 

We  must  not  be  too  ready  to  perform  tracheotomy.  Even  when  asphyxia 
appears  imminent,  death  rarely  occurs  from  syphilis  of  the  larynx,  and,  if 
we  push  the  treatment  which  I  have  just  indicated,  we  shall  generally 
succeed  in  averting  the  danger  without  operation. 

When  tuberculosis  and  sypliilis  are  present  together,  it  seems,  according 
to  the  most  recent  statistics,  that  it  may  be  advantageous  not  to  treat  the 
syphilis.  Tonic  treatment  must  especially  be  employed.  In  addition  to 
the  fact  that  mercury  and  iodides  weaken  a  tubercidar  patient,  tuberculosis 
progresses  in  proportion  as  syphilis  improves  ;  indeed,  it  appears  to  assume 
an  exceptionally  serious  character.  On  the  other  hand,  the  two  affections 
appear  to  neutralize  one  another  to  a  certain  degree — at  least,  for  a  time. 

Hereditary  Syphilis  of  the  Larynx. 

The  larynx  is  no  more  secure  from  the  lesions  of  early  or  late  hereditary 
syphilis  than  other  organs.  "  The  laryngeal  manifestations  of  hereditary 
syphilis  are  much  more  common  in  youth  than  we  usually  think.  Mackenzie 
has  met  with  a  great  number  of  cases,  some  in  the  first  year  (early  hereditary), 
and  others  up  to  twelve  and  fifteen  years  (late  hereditary)."  The  lesions 
attack  the  epiglottis  (perichondritis),  which  is  red,  thick,  ulcerated,  and 
adherent  to  the  neighbouring  parts  (larjnigeal  atresia).  The  arytenoid 
regions  and  ventricular  bands  are  infiltrated  and  covered  with  vegetations 
(Moure).  The  vocal  cords  are  sometimes  normal,  at  other  times  thickened 
and  ulcerated.  Vocal  and  respiratory  troubles  are  the  chief  symptoms. 
The  voice  is  husky  or  inaudible,  and  in  the  child  who  cannot  talk  the  cry 
presents  the  same  changes  (Sevestre).  Respiration  is  embarrassed  from 
simple  breathlessness  to  the  most  severe  dyspnoea. 

I  am  convinced  that  many  infants  with  laryngeal  troubles  which  simu- 
late inflammation  or  oedema  of  the  larynx  are  really  suffering  from  heredi- 
tary syphilis.  I  saw,  with  Dr.  Bonin,  a  young  infant  who  had  been  seized 
with  such  severe  attacks  that  tracheotomy  was  discussed.  The  attack 
yielded  after  some  days,  thanks  to  Van  Swieten's  liquor.  M.  Sevestre  has 
reported  several  cases  of  the  same  kind.  We  cannot  pay  too  much  attention 
to  the  pathogenic  diagnosis  of  laryngeal  affections. 

V.  TUBERCULOSIS  OF  THE  LARYNX— LARYNGEAL 
PHTHISIS. 

Pathological  Anatomy. — Each  organ  or  each  tissue  reacts,  in  its  own 
way,  to  the  invasion  of  the  tubercle  bacillus.  The  large  nasal  tubercle,  which 
might  almost  be  taken  for  a  sarcoma,  and  the  small  tubercular  granulations 
scattered  over  the  intestine  or  the  meninges  look  quite  different,  and  yet  the 
same  micro-organism  is  the  cause  in  both  cases.     The  larynx,  too,  has  its 


DISEASES  OF  THE  LARYNX  41 

own  peculiar  kind  of  tuberculosis,  and  we  find  three  varieties  of  lesion,  either 
alone  or  in  combination  :  infiltration,  ulceration,  and  vegetations,  are 
the  usual  lesions  in  tuberculosis  of  tlie  larynx. 

In  acute  cases,  and  especially  in  acute  pharyngo-laryngeal  tul)ercu- 
losis,  the  miliary  granulations  are  scattered  over  the  surface  of  the  larvnx ; 
but  in  chronic  cases,  which  are  much  more  frequent,  the  granulations  are, 
so  to  say,  hidden  in  the  base  or  aroimd  the  ulcerations.  The  chief  feature 
in  tuberculosis  of  the  larynx  is  infiltration  ;  ulcerations  and  vegetations  may 
be  present  or  absent. 

Tuberculous  infiltration  may  attack  all  the  layers  of  the  lar^mx.  It 
invades  the  glands,  and  develops  at  the  expense  of  the  connective  tissue 
and  of  the  epithelial  cells  ;  it  surrounds  the  vessels  like  a  muff ;  the  tunica 
adventitia  is  involved,  and  the  lumen  of  the  vessel  is  obliterated.  In  the 
muscles  it  produces  an  interstitial  myositis.  Lastly,  it  becomes  diffused 
throughout  the  different  tissues,  and  provokes  hypertrophic  indurations, 
which,  though  bordering  on  fibrosis,  only  look  like  (edema  (Doleris). 

In  the  cadaver  the  tuberculous  infiltration  appears  as  a  greyisli  or 
yellowisli  swelling,  with  uniform  or  uneven  surface  ;  it  is  firm  to  the  touch, 
and  fairly  hard  on  cutting.  For  a  long  time  tliis  swelling  was  mistaken  for 
oedema  (Gougenheim). 

The  interarytenoid  region,  the  arytenoids — which  stand  out  like  sugar- 
loaves — the  ventricular  bands,  the  aryteno-epiglottic  folds,  and  the  epi- 
glottis, take  part,  separately  or  simultaneously,  in  the  swelling,  wliich  may  be 
considcra]>le.  The  vocal  cords  are  more  rarely  swollen  ;  they  are  reddish, 
streaked  with  vessels,  and  sometimes  resemble  cushions  in  appearance. 

In  some  regions  of  the  larynx,  as  in  the  vocal  cords,  the  process  is  charac- 
terized by  a  fibrous  or  fibro-caseous  condition,  which  closely  resembles  lupus. 

Laryngeal  tuberculosis  is  often  ulcerative.  The  ulcers  begin  in  the 
superficial  layer  of  the  mucosa,  often  in  a  caseous  gland.  Small  caseous  foci 
are  seen  on  the  interarytenoid  mucous  membrane,  the  epiglottis,  the  folds, 
and  the  vocal  cords.  The  lesion  develops  in  the  corium  of  the  mucosa. 
First,  congestion  of  the  part,  and,  later,  nniltiplication  of  the  connective  cells, 
are  seen.  This  infiltration,  which  is  primarily  submucous,  and  especially 
active  in  the  glandular  acini,  extends  and  undergoes  caseous  degeneration, 
followed  by  ulceration. 

These  ulcers  often  become  more  extensive  by  the  coalescence  of 
secondary  ulcers.  The  edges  are  jagged  and  infiltrated  with  tubercles  ;  the 
floor  is  covered  with  large  polypoid  vegetations,  especially  in  ulcers  of  the 
interarytenoid  region. 

The  arytenoid  region  is  generally  first  affected ;  the  ulceration 
may  deepen  and  attack  ihe  crico-arytenoid  articulation  and  the  perichon- 
drium.    The  arytenoid  and  cricoid  cartihiges  are  frequently  attacked,  while 


42  TEXT-BOOK  OF  MEDICINE 

the  thyroid  cartilage  usually  remains  free.  In  some  cases  the  lesion  starts 
in  the  perichondrium  or  in  the  joint,  and  forms  a  "  tumor  albus  "  con- 
taining bacilli.  The  invasion  of  the  cartilage  is  preceded  by  calcareous 
infiltration  and  ossification,  and  is  followed  by  necrosis,  expulsion  of  the 
sequestrum,  suppuration,  fistula,  and  oedema.  The  sequestrum  is  reddish, 
dry,  and  situated  at  the  bottom  of  a  foul-smelling  anfractuous  cavity.  The 
elimination  of  sequestra  provokes  migratory  abcesses,  and  the  pus  finds  its 
way  into  the  larynx  or  the  pharynx,  or  outwards  through  the  skin.  (Edema 
of  the  larynx,  subcutaneous  emphysema,  and  laryngeal  fistulae  result  from 
this  process. 

Tubercular  ulcerations  also  attack  the  aryteno-epiglottic  folds,  and  may 
destroy  the  ventricular  bands,  obliterating  Morgagni's  ventricles.  The 
epiglottis  is  more  rarely  ulcerated.  When  it  is  attacked,  the  base  and  the 
laryngeal  surface  suffer,  whereas  syphilis  usually  affects  the  lingual  surface. 
The  vocal  cords  are  often  ulcerated,  toothed  like  a  saw,  or  completely 
destroyed. 

The  vegetations  in  laryngeal  tuberculosis  may  show  two  forms.  In  the 
first  form  the  vegetation  develops  in  an  ulcer,  and  forms  a  bud,  which  is 
limited  to  the  ulcerating  surface  and  has  a  papillomatous  appearance. 
These  papillomata,  wliich  are  chiefly  found  at  the  arytenoid  region  and  the 
posterior  part  of  the  vocal  cords,  may  grow  to  a  large  size.  Sometimes  they 
look  like  cauliflowers,  partially  obstruct  the  orifice  of  the  glottis,  and,  as  they 
are  lacking  in  firmness,  are  easily  detached.  If  they  should  fall  into  the 
respiratory  passages,  they  may  give  rise  to  the  gravest  accidents. 

In  the  second  form  the  vegetation  does  not  begin  in  an  ulcer,  but  develops 
on  its  own  account,  and  is  chiefly  met  with  in  primary  tuberculosis  of  the 
larynx  (Mandl). 

In  tubercular  laryngitis  the  peritracheal  and  bronchial  glands  are  often 
attacked  by  inflammation,  and  cause  lesions  of  the  recurrent  nerves. 

Symptoms. — Tuberculous  infiltration  may  exist  at  certain  points  in 
the  larynx  without  causing  any  symptoms.  As  a  rule,  the  lesion  is  slow 
in  its  progress.  At  first  it  invades  the  arytenoid  region,  the  ventricular 
bands,  and  the  vocal  cords,  and  for  some  time  the  only  symptom  is  hoarse- 
ness and  muffling  of  the  voice  ;  neither  respiratory  troubles  nor  pain  are 
present  at  this  stage. 

In  some  cases,  however,  even  from  the  first  the  patient  experiences  a 
tickling  in  the  larynx,  which  is  very  disagreeable,  and  causes  incessant  jerky 
cough.  The  sufferer  firmly  believes  that  a  particle  of  food  has  been  arrested 
in  the  larynx. 

In  some  cases  the  voice  remains  almost  normal,  but  the  breathing  is 
rather  short  and  quick,  and  inspiration  is  more  noisy  than  in  the  normal 
state,  because  the  inspired  air  meets  with  resistance  at  the  swollen  glottis. 


DISEASES  OF  THE  LARYNX  43 

If  tlie  lar}Tix  be  examined  at  this  stage,  which  may  be  of  indefinite 
duration,  we  are  struck  by  the  unusual  pallor  of  the  velum  palati,  the 
pharynx,  and  the  vestibule  of  the  larjmx.  We  find  swelling  of  the  inter- 
arytenoid  tissues,  which  are  specially  affected  by  tubercular  lesions ;  the 
cartilages  of  Santorini,  the  aryteno-epiglottic  folds,  the  ventricular  bands, 
and  the  epiglottis  are  all  swollen.  In  some  cases  the  vocal  cords  are  greyish, 
or  rosy  and  enlarged. 

At  a  more  advanced  stage  these  lesions  are  more  marked  ;  the  infiltration 
causes  the  arytenoids  to  stand  out  like  sugar-loaves,  and  the  interarytenoid 
space  is  covered  with  vegetations,  while  the  ventricular  bands  are  enormous 
and  cover  the  subjacent  vocal  cords,  which  are  no  longer  visible.  The 
aryteno-epiglottic  ligaments,  which  are  fixed  and  swollen,  narrow  the 
aperture  of  the  larynx  ;  the  vocal  cords  are  streaked  with  red,  especially  on 
their  posterior  third,  have  a  skin-like  appearance,  and  show  erosions  and 
indentations,  while  one  cord  is  paretic  and  does  not  approximate  well. 
Finally,  the  larynx  as  a  whole  is  irregular,  funnel-shaped,  and  covered  with 
thick  mucus.  At  this  time  the  vocal  troubles  are  very  marked,  yet  aphonia 
may  not  be  complete  and  dyspnoea  may  not  be  severe. 

The  disease  may  remain  for  an  indefinite  period  in  the  stage  of  tubercular 
infiltration  without  ending  in  ulceration  ;  if  ulceration  ensue,  dyspnoea  and 
acute  pain  supervene.  The  voice  is  almost  completely  lost ;  sometimes 
the  aphonia  is  complete,  and  it  cannot  well  be  otherwise,  since  the  vocal  cords 
are  hypertrophied,  ulcerated,  covered  by  the  enlarged  ventricular  bands,  and 
fixed  by  the  ankylosis  of  the  arytenoids. 

The  cough  depends  rather  upon  the  changes  in  the  lung  than  upon  the 
lesions  of  the  larynx  ;  it  is  stifled  and  belching  (Trousseau  and  Belloc),  so 
that  the  patient,  when  coughing,  appears  to  be  making  attempts  at  belching.* 
Acute  perichondritis  is  revealed  by  sharp  pains,  with  respiratory  embarrass- 
ment. If  an  abscess  forms,  the  dyspnoea  becomes  excessive,  and  the  abscess, 
which  is  situated  in  the  arytenoid,  opens  into  the  pharynx  or  the  larynx. 

Ulcers  on  the  base  of  the  epiglottis  and  on  the  aryteno-epiglottic  folds 
are  often  associated  with  similar  lesions  of  the  base  of  the  tongue  and  of  the 
pharynx  ;  they  render  swallowing  extremely  painful.  This  dysphagia  is 
so  painful  that  in  some  cases  the  patient  feels  as  though  "  a  live  coal  had 
been  swallowed."  Not  only  is  the  pain  made  worse  by  the  least  attempt 
at  swallowing,  but  in  .some  cases  the  patient  experiences  constant  hvpor- 
sosthe.sia  of  the  back  of  the  throat.  The  saliva,  which  is  abundant,  cannot  be 
swallowed,  and  drips  from  the  mouth  ;  the  patient,  deprived  of  rest,  sleep, 

*  Thi.s  phonnmcnon  is  easily  oxplaincd.  In  iho.  j)liy.'*i')l()gi<'al  condition  tin'  smidcn 
opening  of  the  vocal  cords  by  a  jerky  (-xpirat ion  gives  llie  coiigii  its  pciculiar  tunc  ;  but 
in  la^\^l<:(■al  |)litliisis,  as  tlio  wido-opon  glottis  no  longer  offers  any  resistance,  tlio  oxpinxl 
air  is  belched  out. 


44  TEXT-BOOK  OF  MEDICINE 

and  nourishment,  becomes  marasmic  and  disheartened  if  relief  be  not  forth- 
coming. 

Aural  pain,  which  may  be  very  intense  in  all  laryngopathies,  is  sometimes 
present. 

Dyspnoea,  which  is  so  often  seen  in  advanced  tuberculosis  of  the  larynx, 
is  due  to  infiltration,  swelling  of  the  tissues,  oedema  of  the  larynx,  polypoid 
vegetations,  and  to  perichondritis,  with  its  resultant  abscesses.  Every 
variety  occurs  :  it  may  be  slow  or  sudden  in  its  appearance,  and  is  sometimes 
accompanied  by  attacks  of  suffocation  and  spasms  of  the  glottis.  The 
breathing,  which  is  harsh  or  noisy,  sometimes  takes  a  strident  character. 
Laryngoscopic  examination  is  often  difficult  by  reason  of  the  abnormal 
positions  of  the  epiglottis,  the  swelling,  the  oedema,  and  the  muco-purulent 
secretion  which  covers  the  larynx. 

The  course  and  duration  of  the  malady  are  very  variable.  In  some 
cases  the  march  of  events  is  rapid,  and  life  is  threatened  by  an  abscess 
following  acute  perichondritis,  by  oedema  of  the  glottis,  or  by  pulmonary 
phthisis,  which  complicates  the  laryngeal  mischief  and  hastens  events.  The 
patient  becomes  marasmic,  the  wasting  is  extreme,  and  hectic  fever  closes 
the  scene. 

Catarrhal  Form. — I  have  just  described  the  most  common  form  of 
laryngeal  tuoerculosis,  which  runs  a  slow  course  ;  in  some  cases,  however, 
the  disease  begins  abruptly,  like  simple  catarrhal  laryngitis,  with  cough, 
sudden  hoarseness,  and  aphonia,  which  may  be  complete  and  last  for  several 
days.  Laryngoscopy  reveals  nothing  but  redness,  swelling  of  the  mucosa, 
and  more  or  less  abundant  secretion.  If  the  patient  already  have  tubercular 
lesions  in  the  lungs,  though  he  have  only  slight  signs,  the  laryngitis  is  open 
to  discussion.  Some  writers  say  that  it  is  tubercular,  other  writers  call  it 
"  laryngitis  in  tubercular  subjects."  I  do  not  say  that  tubercular  patients 
cannot  have  catarrhal  laryngitis,  but  I  think  that  most  cases  of  so-called 
catarrhal  laryngitis  in  phthisical  subjects  are  tubercular.  They  are  more 
persistent  than  cases  of  simple  catarrh,  they  are  subject  to  relapses,  they  leave 
infiltration  of  the  mucosa  behind  them,  and  though  they  are  sometimes 
completely  cured,  yet  they  may  end  in  infiltration  and  ulceration.  This 
laryngitis,  therefore,  in  a  patient  with  haemoptysis,  pleurisy,  or  tubercular 
lesions  in  the  lungs,  is  really  tubercular,  even  though  it  be  apparently  benign 
and  catarrhal.  Though  it  may  be  cured,  and  may  rarely  end  in  the  other 
forms  of  laryngeal  phthisis,  I  consider  it  as  a  manifestation  of  tuberculosis, 
just  as  are  those  cases  of  pleurisy  or  of  haemoptysis  which  sometimes  super- 
vene during  excellent  health.  They  are,  nevertheless,  the  first  sign  of 
tubercular  mischief  that  will  be  fully  developed  some  months  or  years  later. 

So-called  catarrhal  laryngitis  presents  in  some  cases  frankly  tubercular 
lesions,  which  prove  that  bacillary  infection  may  occur,  not  only  in  the 


DISEASES  OF  THE  LARYNX  45 

depth  of  the  tissues,  but  also  in  the  superficial  layers.  Heintze,  quoted  by 
Hering,  saw  a  trifling  infiltration  of  the  ventricular  band,  and  found  bacilli 
in  it,  between  the  epithelium,  in  the  glands,  and  in  the  cylindrical  epithelial 
cells  of  the  glands.  The  bacillus,  says  M.  Hering,  may  be  introduced  by 
the  glands,  and  thus  provoke  an  infection  of  superficial  origin. 

Diagnosis. — Let  us  first  establish  the  diagnosis  at  the  start  of  the 
malady.  The  symptoms  of  laryngeal  tuberculosis  in  its  first  period — 
namely,  cough,  hoarseness,  and  dysphonia — are  common  to  every  chronic 
laryngitis.  These  symptoms,  therefore,  cannot  give  sufficient  data  either 
Lor  or  against  tuberculosis. 

Laryngeal  tuberculosis  may  begin  with  paralysis  of  a  vocal  cord,  the 
appearance  of  a  papillomatous  vegetation,  or  an  attack  of  catarrh.  An 
affirmative  diagnosis,  therefore,  is  difficult  at  the  outset.  Certain  signs, 
however,  are  of  very  great  importance.  One  of  these  signs  is  the  unusual 
pallor  of  the  velum  palati  and  of  the  epiglottis.  This  pallor  is  sometimes  as 
marked  as  in  most  characteristic  anaamia  ;  the  mucosa  of  the  palate  and  the 
parts  of  the  larynx  which  are  usually  pink  take  on  a  dull,  greyish,  and 
sometimes  opaque  tint  in  tuberculosis.  This  pallor  is  not  seen  in  non- 
tubercular  laryngitis,  and  is  therefore  a  valuable  sign. 

Another  sign  in  laryngeal  tube^rculosis  is  the  initial  localization  of  the 
lesions.  The  interarytenoid  and  the  arytenoid  regions  are  the  seat  of 
election  in  tubercular  lesions  ;  swelling,  granulations,  and  vascularization 
of  the  above  regions,  together  with  the  anjemic  appearance  just  described, 
are  strongly  in  favour  of  tuberculosis. 

At  a  more  advanced  stage  we  must  distinguish  phthisis  from  syphilis 
and  from  cancer  of  the  larynx.  This  question  is  fully  discussed  under 
Syphilis  of  the  Larynx.  Syphilis  rarely  attacks  the  vocal  cords  ;  it  seizes 
the  parts  which  adjoin  the  pharynx — i.e.,  the  epiglottis  and  the  posterior 
surface  of  the  arytenoids.  Furthermore,  syphilitic  idceration  is  usually 
limited  to  one  point,  and  does  not  invade  the  rest  of  the  larynx.  In  tuber- 
culosis the  ulcerations  are  multiple,  and  accompanied  by  more  or  less  inteuso 
laryngitis.  Tubercular  ulcerations  are  frecpioiitly  covered  by  p()ly[)()id 
growths,  which  are  much  rarer  in  syphilis.  Syphilitic  ulcerations  are  quickly 
imjiroved  by  treatment,  whilst  remedies  have  practically  no  effect  on 
tubercular  ulcerations.  SyphiUs,  like  phthisis,  may  attack  the  cartilages, 
but  in  eighteen  cases  out  of  twenty  necrosis  of  the  larynx  is  of  tubercular 
origin.  By  scraping  the  ulcer  we  can  remove  some  particles  of  secretion  and 
fitid  the  tubercle  bacillus. 

Cancer  of  the  larynx,  and  especially  epithelioma,  presents  the  peculi- 
arity of  being  almost  indolent,  and  of  having  a  very  much  slower  course 
in  the  larynx  than  in  other  organs  ;  indeed,  a  patient  with  cancer  of  the 
larynx  may  live  for  two  or  three  years  after  tracheotomy  (Krishaber).    \'ocal 


46  TEXT-BOOK  OF  MEDICINE 

troubles  are  for  a  long  while  the  only  symptom,  and  when  other  local  and 
general  symptoms  supervene,  such  as  haemorrhage,  foetor  of  the  breath, 
dysphagia,  pain,  dyspnoea,  etc.,  the  laryngoscope  generally  reveals  the 
cancerous  vegetations. 

etiology. — According  to  Heintze,  the  larynx  of  adults  who  are  suffering 
from  pulmonary  tuberculosis  is  aiTected  in  50  per  cent,  of  the  cases.  In 
some  cases  the  laryngeal  trouble  is  primary,  and  appears  as  the  first  mani- 
festation of  tubercular  infection.  As  a  rule,  laryngeal  tuberculosis  is 
secondary  to  pulmonary  disease,  and  the  infection  of  the  larynx  takes  place 
either  by  the  deep  path  of  the  vessels  and  lymphatics  or  by  the  superficial 
path  along  the  surface  of  the  mucosa,  or  through  the  excretory  ducts  of  the 
glands.  Louis  supposed  that  the  constant  passage  of  infected  sputum  from 
the  lungs  infected  the  larynx.  As  for  the  other  causes,  they  closely  follow 
the  aitiology  of  pulmonary  phthisis.  Males  appear  more  predisposed  than 
females,  and  the  malady  occurs  in  the  former  between  twenty- five  and 
forty  years  of  age. 

In  the  child  laryngeal  tuberculosis  deserves  special  mention  :  the  younger 
the  child  the  rarer  the  disease.  Parrot  found  tubercular  laryngitis  in  only 
3  per  cent,  of  autopsies  on  infants  under  two  years.  In  the  infant  pul- 
monary tuberculosis  is  usually  of  the  miliary  form ;  the  child  does  not 
expectorate,  and  its  larynx  is  not  bathed  in  pus  swarming  with  bacilli ; 
this  factor,  no  doubt,  helps  to  explain  the  rarity  of  tubercular  laryngitis  in 
children. 

In  my  experiments  with  Krishaber  we  studied  the  results  of  inoculation 
and  contagion  in  the  ape.*  We  were  struck  by  the  fact  that  animals  which 
had  been  inoculated  and  had  died  from  tuberculosis  showed  no  tubercular 
changes  in  the  larynx. 

Treatment. — Laryngeal  tuberculosis  is  not  incurable.  It  sometimes 
remains  stationary,  and  several  cases  (Hering)  prove  that  the  tubercular 
ulcers  may  be  cured.  Every  effort  must  be  made  to  relieve  the  dysphagia 
and  the  hypersesthesia  of  the  back  of  the  throat,  which  cause  such  torture 
to  the  patient. 

For  tliis  purpose  hypodermic  injections  of  morphia  should  be  given 
morning  and  evening.  At  meals  the  painful  parts  should  be  touched  with 
a  brush  or  a  sponge,  mounted  on  a  curved  handle  and  soaked  in  the 
following  solution  : 

Cocaine  hydrochlorate     . .         . .        1  part. 
Water  50  parts. 

With  a  little  practice,  the  patient  himself  can  paint  the  painful  parts  with 

the  solution,  but  he  must  avoid  swallowing  it.     Inhalations  and  sprays  of 

*  Dieulafoy  and  Krishaber,  Arch,  de  Physioloyie,  March,  1881,  No.  3. 


DISEASES  OF  THE  LARYNX  47 

water  containing  a  little  sulphur  (AUevard)  may  render  some  service. 
Painting  the  ulcers  with  a  10  per  cent,  or  20  per  cent,  solution  of  lactic  acid, 
and  later  with  the  pure  acid,  sometimes  yields  good  results.  Ruault  employs 
phenol  and  sulphur  in  castor  oil. 

The  cough  may  be  reUeved  by  careful  intratracheal  injections  of  menthol 
in  oily  solution,  but  this  method  demands  much  judgment.  The  gargles 
of  very  hot  and  astringent  wine  which  Bonnier  employs  for  gouty  laryngitis 
are  also  of  service,  by  soothing  the  cough  and  the  pharyngo-laryngeal 
irritation. 

Bonnier  prefers  insufflations  which  the  patient  can  use  without  the 
physician's  aid,  such  as  iodol,  1  part ;  sodium  benzoate,  6  parts ;  tolu, 
'J  parts ;  taimin,  1  part ;  gum  arable,  3  parts ;  cinnamon,  020  part,  to 
sprays  of  menthol  or  eucalyptus. 

Curetting  the  ulcers  and  cauterization  has  rendered  good  service  in 
experienced  hands. 

The  "  altitude  cure  "  is  not  contra-indicated  in  cases  of  tubercular 
laryngitis.  I  have  seen  the  larynx,  as  well  as  the  lung,  improve  by  the  cure 
at  Davos-Platz. 

VI.  LARYNGEAL  DIPHTHERIA- CROUP.* 

Definition.  —  Croup,  or  pseudo-membranous  laryngitis,  is  charac- 
terized by  tlie  presence  of  membranes  in  the  larynx  and  trachea.  These 
membranes  may  exceptionally  be  due  to  a  non- diphtheritic  lesion,  the 
diphtheria  bacillus  taking  no  part  in  the  process.  CUnical  medicine  had 
created  a  simple  croup,  said  to  be  neither  contagious  nor  infectious,  and, 
indeed,  clinical  medicine  was  right.  Bacteriology  has  shown  that  false 
membranes  in  the  larynx  and  pharynx  may  be  produced  by  microbes  which 
have  nothing  in  common  with  the  diphtheria  bacillus.  A  small  diplococcus 
may  give  birth  to  membranes  in  the  larynx  or  the  pharynx,  although  it  has 
none  of  the  toxic  properties  of  the  diphtheria  bacillas.  We  shall  return  to 
this  point  later. 

We  fuid,  then,  diphtheritic  croup,  Avhich  is  the  rule,  and  non-diphtheritic 
croup,  which  is  the  exception. 

History.t — In  1765  Home,  a  Scotch  physician,  published  an  interesting 
monograph  on  croup.  He  was  the  first  to  indicate  clearly  the  characteristics 
of  tliis  malady,  and  to  separate  it  from  certain  affections  of  the  pharynx 
with  which  it  had  been  previously  confounded  ;  but  he  was  doubly  wrong  in 
mistaking  the  identical  nature  of  diphtheritic  angina  and  of  croup,  which 
other  observers  had  previously  established,  and  in  giving  a  single  description 
for  two  distinct  maladies — i.e.,  false  croup  and  true  croup.     Bretonneau, 

*  To  avoid  rcpelitions,  seo  articK'S  on  Diphtheria  and  Diplitlieritio  Angina. 
t  To  complcto  tho  history,  refer  to  the  cliaptor  on  Diplithoria. 


48  TEXT-BOOK  OF  MEDICINE 

in  his  memorable  work  on  diphtheritis,  re-established  the  identity  which 
Home  had  failed  to  recognize.  He  applied  the  term  "  laryngite  stridu- 
leuse  "  to  a  malady  which  simulates  croup,  but  which  has  nothing  in  common 
with  it.  We  know  how  brilliantly  Trousseau  completed  the  teachings  of 
his  master,  Bretonneau,  on  diphtheria  and  croup,  and  with  what  success  he 
made  the  operation  of  tracheotomy  popular. 

The  bacteriological  researches  of  recent  years  have  given  valuable 
precision  to  the  diagnosis  and  the  prognosis  of  croup,  while  serotherapy 
has  completely  modified  the  treatment. 

Division — etiology. — Croup  is  primary  when  the  diphtheria  which 
engenders  it  attacks  the  patient  while  in  good  health.  It  is  secondary  when 
the  diphtheria  supervenes  as  a  complication  in  the  course  of  some  other 
malady,  such  as  measles,  scarlatina,  whooping-cough,  or  typhoid  fever. 

Croup  usually  follows  diphtheria  of  the  pharynx,  and  statistics  prove 
that  the  larynx  is  chiefly  invaded  from  the  second  to  the  fifth  day  of  the 
angina.  Croup  sometimes  follows  diphtheritic  COryza — that  is  to  say, 
the  diphtheria  begins  in  the  nose  and  spreads  to  the  larynx.  Cases  of  croup 
secondary  to  diphtheria  of  the  bronchi  have  been  seen,  and  have  been 
called  "  ascending  "  croup.  Diphtheria  may  also  invade  the  larynx  before 
other  parts,  and  the  di-sease  is  then  called  primary.  This  form,  however,  is 
very  rare,  and,  in  order  to  vouch  for  this  fact,  we  must  be  certain  that  the 
throat  and  the  nasal  fossae  are  normal. 

In  some  cases  croup  appears  though  false  membranes  in  the  throat  are 
absent,  and  yet  cultures  made  from  the  mucus  on  the  tonsils  may  show 
the  diphtheria  bacillus.  We  see,  therefore,  how  rare  primary  croup 
must  be. 

The  chief  causes  of  croup  are  epidemicity  and  contagion.  Contagion 
is  only  too  well  proved  by  the  numerous  examples  of  physicians  who  have 
contracted  the  disease  from  their  patients.  In  certain  parts — Paris,  for 
example — croup  is  endemic  Epidemic  croup  sometimes  rages  Avith 
terrible  severity,  as  witness  the  epidemics  which  ravaged  Europe  in  the 
sixteenth  and  seventeenth  centuries — the  enfermedal  del  garrotillo  in 
Spain,  the  morbus  strangulatorius  in  Italy.  Croup  spares  no  age,  though 
it  chiefly  attacks  infants  between  the  age  of  two  and  seven  years. 

Symptoms.  —The  present  description  refers  to  diphtheritic  croup  in 
children.  Whether  croup  at  once  invade  the  larynx,  or  whether  it  be 
preceded  by  diphtheritic  tonsillitis  or  coryza,  the  growth  of  membrane  in 
the  larynx  and  the  trachea  is  immediately  announced  by  vocal  and  respira- 
tory trouble.  The  false  membrane  may  be  said  to  sum  up  almost  the 
whole  history  of  croup,  for  its  presence  on  the  vocal  cords  and  in  the  larynx 
alters  the  normal  sounds,  narrows  the  glottis,  and  hinders  or  prevents  the 
entry  of  air  into  the  lungs. 


r 


DISEASES  OF  THE  LARYNX  49 

The  pathological  role  of  the  false  membrane,  however,  is  essentially 
a  mechanical  one.  In  some  cases  this  mechanical  role  is  of  secondary 
importance,  and  the  gravity  of  the  illness  does  not  arise  from  the  obstruction 
of  the  larynx,  but  comes  from  the  preceding  angina,  from  the  poisoning  of 
the  economy  by  the  diphtheritic  toxine,  from  the  concomitant  bronchitis 
and  broncho-pneumonia,  from  the  addition  of  secondary  infections,  from 
the  association  of  the  streptococcus  with  the  diphtheria  bacillus,  etc. 

Cough  is  the  earhest  sign  of  croup.  Slight  and  trifling  at  first,  it  returns 
in  very  short  fits  ;  during  the  next  few  days  it  acquires  a  dull  and  muffled 
quality,  and  becomes  as  inaudible  as  the  voice.  As  the  disease  progresses 
the  cough  becomes  less  frequent,  and  the  fits  only  recur  every  quarter  or 
half  hour,  and  even  at  longer  intervals  (Trousseau).  The  voice  is  at  first 
hoarse,  but  after  some  days  it  becomes  inaudible,  and  the  aphonia  is  com- 
plete.  Vox  nihil  significat,  said  .\jet3eus. 

In  the  child  the  respiratory  troubles  are  early  and  marked,  because  the 
larynx  is  narrower  than  in  the  adult.  The  dyspnoea,  which  is  at  first  slight, 
begins  at  night,  and  is  ushered  in  by  shght  whistling  on  inspiration  ;  it 
increases  as  the  aperture  of  the  glottis  becomes  narrowed  by  the  false 
membrane,  which  forms  chiefly  on  the  aryteno-epiglottic  ligaments  and  the 
vocal  cords,  and  as  the  air  meets. an  obstacle,  the  inspiration  is  changed 
into  a  shrill  and  prolonged  whistling.  At  the  same  time  depression  of 
the  epigastric  hollow  and  of  the  suprasternal  fossse  occurs.  This  "  sucking- 
in  "  is  due  to  the  tendency  each  inspiration  has  to  produce  a  vacuum  in 
the  chest,  and  to  the  compensatory  ascent  of  the  diaphragm. 

As  the  dyspnoea  grows  worse,  the  breathing  becomes  sawing,  like  the 
noise  which  a  saw  makes  when  it  cuts  stone  (Trousseau).  Every  two  or 
three  hours  at  first,  then  every  hour,  and  at  yet  more  frequent  intervals, 
we  ob-serve  terrible  attacks  of  suffocation  ;  they  result  from  spasms  of  the 
glottis,  and  resemble  those  seen  in  cEdematous  or  spasmodic  laryngitis. 
This  struggle  may  last  several  days,  and,  if  the  illness  do  not  take  a  favourable 
turn,  asphyxia  ends  the  scene.  "  The  bloated  and  cyanosed  face,  the  hollow 
and  shining  eyes,  express  the  most  painful  anxiety,  and  at  length  the  death 
struggle  begins,  without  there  being  from  this  time  forward  any  attacks 
of  suffocation,  such  as  tho.se  which  have  already  occurred  might  lead  one 
to  expect  "  (Trousseau). 

Auscultation  of  the  chest,  when  there  is  no  pulmonary  complication, 
reveals  nothing  but  the  echo  of  the  laryngeal  whistling.  The  respiratory 
rhythm  is  altered,  and  expiration  becomes  longer  than  inspiration,  from 
the  difliculty  which  the  expiratory  mascles  experience  in  driving  the  air 
through  the  narrowed  glottis. 

The  expectoration  is  often  characteristic,  and  about  the  third  or  the 
fourth  day  tiie  patient  coughs  up  shreds  of  membrane — Hat  if  they  come  from 

4 


50  TEXT-BOOK  OF  MEDICINE 

the  larynx,  tubular  and  branching  if  the  bronchi  be  invaded.  False 
membranes  are  coughed  up  in  half  the  cases. 

The  fever  in  croup  is  not,  as  a  rule,  high,  and  the  temperature  varies 
between  101°  and  103°  F.  Albuminuria  is  frequent  (See,  Barbosa),  and  is 
due  to  nephritis,  caused  by  the  diphtheritic  toxines. 

Multiple  eruptions  have  often  been  noted  in  croup,  as  in  diphtheritic 
angina  (See) ;  they  show  different  forms  and  simulate  the  exanthems  of 
measles  and  of  scarlet  fever. 

In  adults  the  symptoms  of  croup  present  some  differences,  becau.se  of 
the  shape  and  size  of  the  larynx.  The  modifications  of  the  cough  and 
voice  are  the  same,  but  dyspnoea  and  asphyxia  supervene  slowly,  and  are 
not,  as  a  rule,  accompanied  by  stridor  and  attacks  of  suffocation. 

Course — Duration — Prognosis. — The  course  of  croup  may  be  divided 
into  two  periods — the  first  of  dyspnoea,  the  second  of  asphyxia — while  the 
two  together  may  last  from  three  days  to  a  fortnight ;  but  many  exceptions, 
especially  during  an  epidemic,  are  seen  in  the  course  and  the  succession  of 
symptoms,  and  the  disease  may  be  fatal  on  the  third  or  even  on  the  second 
day.  Trousseau's  lectures  on  diphtheria  and  croup  will  suffice  to  warn  us 
against  the  surprises  of  tliis  disease,  and  to  show  us  how  suddenly  death  may 
appear.  These  fulminant  forms  are  chiefly  seen  in  adults,  and  are  due 
rather  to  the  virulence  of  the  infection  than  to  the  lesions  in  the  larynx. 
A  terrible  attack  of  suffocation  may  occur,  and  be  followed  by  continuous 
dyspnoea,  or  dyspnoea  may  come  on  without  attacks  of  suffocation,  and  the 
patient  succumb  to  the  infection  (malignant  diphtheria). 

Abortive  croup  has  been  described.  I  have  seen  such  an  example  in  a 
little  boy  who,  some  days  before,  had  been  attacked  by  nasal  diphtheria. 
In  abortive  croup  the  false  membrane  remains  limited  to  the  vestibule  of 
the  larynx,  or,  at  least,  the  cords  are  scarcely  affected.  The  vocal  troubles 
are  absent  or  insignificant,  and  the  respiratory  symptoms  are  not  severe. 

The  progress  of  croup  varies  a  httle,  according  to  the  virulence  of  the 
infectious  element.  In  general  terms,  when  we  see  a  relative  calm  between 
the  attacks  of  suffocation,  it  means  that  the  child  is  not  yet  threatened  by 
the  infectious  element.  If  the  little  patient,  however,  be  infected  by  the 
disease  (malignant  diphtheria),  the  truce  is  not  complete  :  no  lull  is  seen 
between  the  attacks,  or  after  the  expulsion  of  false  membranes  ;  permanent 
dyspnoea,  prostration,  thready  pulse,  and  marked  albuminuria  bear  witness 
to  the  virulence  of  the  infection  and  the  gravity  of  the  prognosis. 

Cases  of  prolonged  croup  must  be  recognized.  M.  Cadet  de  Gassicourt 
has  cited  cases  of  croup  which  lasted  fifteen,  twenty,  or  twenty-five  days, 
and  recovered  ;  there  was  no  asphyxial  stage,  and  tracheotomy  was  not  per- 
formed. 

During  the  course  of  the  disease  remissions  are  sometimes  seen :  the 


DISEASES  OF  THE  LAKYNX  51 

voice  regains  its  tone  and  the  breathing  its  freedom  ;  but  this  improvement, 
which  is  due  to  expulsion  of  membrane,  is  too  often  transient,  and  must  not 
be  mistaken  for  recovery.  Croup  is  an  extremely  serious  malady,  which 
formerly,  even  with  surgical  intervention,  often  ended  in  death.  Injections 
of  serum  have  recently  improved  the  prognosis  to  a  striking  extent. 

Complications.— Diphtheria  of  the  bronchi  may  precede  or  follow  the 
laryngeal  disease.  In  every  case  it  increases  the  danger,  because  it  adds  a 
fresh  obstacle  to  that  already  present  in  the  larynx.  The  patient  brings  up 
membranes,  which  may  be  tubular,  rolled  up,  or  like  coagulated  mucus. 

Broncho-pneumonia  is  a  still  worse  complication,  which  appears  at  all 
periods,  both  before  and  after  tracheotomy,  but,  as  a  rule,  from  the  third 
to  the  sixth  day  of  the  disease.  It  is  sometimes  accompanied  by  gangrene 
of  the  lung.  Its  onset  is  followed  by  a  rise  of  temperature  and  violent 
dyspnoea,  so  that  in  a  child  the  respirations  may  exceed  sixty  (Millard). 
Diphtheritic  broncho- pneumonia  is  nearly  always  lobular,  and  not  pseudo- 
lobar.  Anatomically  it  is  characterized  by  a  large  amount  of  fibrin  and 
by  hajmorrhages  into  the  pulmonary  lobules.  Klebs'  bacilli,  and  many 
other  microbes — streptococci,  pneumococci,  and  staphylococci — are  found 
in  the  alveoli.  In  this  variety,  as  in  other  kinds  of  broncho-pneumonia, 
these  secondary  infections  play  a  most  important  part  in  the  production  of 
broncho- pulmonary  lesions. 

Pleurisy  is  sometimes  a  complication,  but  is  of  moderate  importance. 

Diphtheritic  coryza,  considered  by  Trousseau  as  of  evil  augury,  is  often 
present  in  the  malignant  form  of  diphtheria. 

In  children  tuberculosis  is  often  associated  with  diphtheria  of  the 
respiratory  tract.  "  The  gravity  of  tuberculosis  is  such,"  says  Variot, 
"  that  in  fifty-four  deaths  which  occurred  in  January  and  February  at  the 
Bretonneau  Annexe,  we  found  tubercular  lesions  in  the  thoracic  organ? 
sixteen  times." 

After  croup,  as  after  all  the  local  manifestations  of  diphtheria,  we  some- 
times see  paralysis  ;  but,  as  croup  is  rarely  the  only  manifestation  of  diph- 
theria, these  paralyses  are  chiefly  due  to  the  concomitant  angina.  Lastly, 
the  eruptive  fevers  may  appear  in  the  course  of  croup,  and  give  rise  to 
serious  complications. 

Diagnosis. — In  cases  where  the  diagnosis  is  difficult  the  laryngoscope 
must  be  employed,  especially  in  adults.  This  method  has  often  confirmed 
a  doubtful  diagnosis  by  revealing  the  presence  of  membranes  in  the  larynx. 

Acute  laryngitis,  oedema  of  the  larynx,  and  spasmodic  laryngitis  are  the 
diseases  which  most  resemble  croup.  In  simple  acute  laryngitis  the  vocal 
and  respiratory  symptoms  are  not  so  severe,  and  do  not  gradually  get  worse, 
as  they  do  in  croup.  In  oedema  of  the  glottis,  which  is  very  often  but  a 
part  of  some  other  disease,  the  antecedents  at  once  enlighten  us.     In  any 

4—2 


r,2  TEXT-BOOK  OF  MEDICINE 

case,  the  respiratory  symptoms  are  worse  than  the  vocal ;  expiration  is  easier, 
less  prolonged  than  in  croup,  and  sometimes  accompanied  by  a  hruit  de 
drapeau.  The  supraglottic  oedema,  which  causes  the  dyspnoea,  may  also  be 
visible. 

The  diagnosis  between  croup  and  laryngitis  due  to  hereditary  syphilis 
demands  special  notice.  The  symptoms  may  simulate  those  of  croap  so 
closely  that  errors  have  been  made.  In  my  lectures  at  the  Faculte  I 
reported  the  case  of  a  young  child  who  was  about  to  undergo  tracheotomy 
for  asphyxia  set  down  to  croup.  Van  Swieten's  solution  was  given  as  soon 
as  hereditary  syphilis  was  diagnosed,  and  we  succeeded  in  curing  the  child 
in  a  few  days.  M.  Sevestre  has  reported  several  analogous  cases.  The 
possibility  of  laryngeal  syphilis  must  always  be  considered  in  a  young  child 
who,  in  the  absence  of  previous  diphtheritic  angina  and  of  glandular  en- 
largement, presents  symptoms  analogous  to  those  of  croup. 

The  diagnosis  between  croup  and  false  croup  is  somewhat  difficult. 
The  two  diseases  have  a  different  onset.  The  invasion  of  croup  is  more 
insidious,  and  the  respiratory  symptoms  gradually  become  intense.  The 
invasion  of  false  croup  is  more  sudden.  A  cliild  who  has  gone  to  bed  in  good 
health  wakes  suddenly,  in  the  middle  of  the  night,  suffering  from  dyspnoea 
that  reaches  its  height  at  once,  and,  this  attack  over,  the  patient  appears 
next  day  to  be  in  good  health.  In  croup  the  cough  and  the  voice  are  mufHed  ; 
the  presence  of  membrane  on  the  vocal  cords  explains  the  aphonia.  In 
false  croup  the  voice  and  the  cough  are  harsh  and  noisy,  and  resemble  the 
barking  of  a  dog.  They  are  not  muffled,  as  in  croup,  at  any  rate,  between 
the  attacks.    During  the  attack  of  false  croup,  however,  they  may  be  muffled. 

Besides  the  signs  peculiar  to  each  disease  which  I  have  just  enumerated, 
careful  inquiry  should  be  made  into  the  antecedents  of  the  patient :  informa- 
tion should  be  sought  as  to  whether  diphtheritic  angina  have  been  recently 
present,  and  we  must  try  to  discover  if  some  signs  of  it,  such  as  enlargement 
of  the  submaxillary  glands,  do  not  remain  !  we  must  not  forget  that  croup 
is  the  only  malady  of  the  larynx  which  may  be  accompanied  by  the  rejection 
of  false  membranes. 

Bacteriological  Diagnosis. — The  clinical  diagnosis  of  croup  is  in  many 
cases  insufficient,  and  must  be  completed  by  the  bacteriological  examination 
of  the  membranes.  Full  details  are  given  under  Diphtheritic  Angina,  for 
diphtheritic  angina  and  laryngitis  are  closely  associated.  I  recapitulate  here 
the  points  referring  to  croup.  As  I  have  already  said,  the  diphtheria  bacillus 
is  not  the  only  microbe  capable  of  producing  false  membranes.  Just  as 
there  are  pseudo-diphtheritic  anginoe,  so  there  is  a  pseudo-diphtheritic 
croup.  This  form  of  croup  is  neither  contagious  nor  infectious  ;  it  is  not 
accompanied  by  toxic  symptoms,  and  is  not  marked  by  malignancy  ;  it  is 
due  to  a  small  diplococcus  (Brisou's  coccus). 


DISEASES  OF  THE  LARYNX  53 

Martin  records  seven  cases  of  croup  due  to  this  diplococcus,  with  mem- 
braneous angina  of  the  same  nature,  and  twelve  cases  of  croup  due  to  the 
same  coccus,  without  previous  angina.  Non-diphtheritic  croup,  due  to 
the  diplococcus  in  question,  is  infinitely  less  serious  than  diphtheritic  croup. 
It  is  not  toxic  ;  recovery  usually  takes  place  without  secondary  infections 
and  without  tracheotomy.  In  these  attenuated  forms  it  may  simulate 
stridulous  laryngitis ;  indeed,  I  am  of  opinion  that  certam  cases  of  false 
croup  are  nothing  else  than  a  mild  laryngitis,  due  to  the  diplococcus. 

In  other  cases  the  bacteriological  examination  of  the  membrane  in  croup 
reveals  both  the  diphtheria  bacillus  and  the  small  coccus.  This  association 
of  the  diplococcus  and  the  bacillus  is  not  usually  grave,  and  M.  Martin's 
monograph  shows  that  these  cases  recover  without  secondary  infections. 

On  the  other  hand,  when  examination  reveals  the  association  of  the 
diphtheria  bacillus  wdth  the  staphylococcus  or  the  streptococcus,  the  prog- 
no.sis  is  bad.  The  same  remark  applies  in  the  case  of  diphtheritic  angina. 
The  presence  of  the  streptococcus  in  croup,  as  in  angina,  should  make  us 
fear  grave  results.  In  such  a  case  the  symptoms  comprise  marked  glandular 
enlargement  ("the  proconsul's  neck,"  Saint  Germain),  nasal  discharge, 
diarrhoea,  and  albuminuria,  which  lead  us  to  fear  the  death  of  the  child  as 
much  from  the  general  poisoning  as  from  the  croup. 

These  few  data,  with  which  every  physician  must  to-day  be  familiar, 
sufficiently  indicate,  in  my  opinion,  the  importance  of  bacteriology  in 
the  present  question.  If  we  cannot  make  a  direct  examination  of  the 
membranes  from  the  larynx,  the  membranes  and  the  mucus  in  the  throat 
must  be  examined,  and,  even  in  the  absence  of  membrane  in  the  throat,  the 
culture  from  a  piece  of  mucus  removed  from  the  tonsil  or  from  the  pharynx 
may  often  allow  accurate  diagnosis  and  prognosis  to  be  made. 

Secondary  Croup, — This  variety  supervenes  in  the  course  of  some 
other  disease,  such  as  measles,  scarlatina,  whooping-cough,  or  typhoid 
fever.  The  details  will  be  found  under  these  different  diseases.  In  general 
terms,  the  secondary  forms  are  less  characteristic  in  their  ways  than  primary 
croup  and  moro  readily  take  on  an  infectious  character. 

Croup  in  Measles.— Diphtheria  has  a  liking  for  measles.  Orouj)  in 
measles  is  sometimes  primary,  and  may  appear  about  the  same  time  as 
the  rash.  The  disease  is  often  mild,  and  the  laryngeal  symptoms  are  slight : 
yet  the  prognosis  is  extremely  grave,  because  of  the  broncho-pneumonia 
which  accompanies  it,  and  of  the  double  infection  of  meades  and  diphtheria. 
The  membranes  in  the  larynx  are  softer  and  more  diffluent,  and  the  lesions 
are  more  of  the  ulcerative  type. 

Croup  in  Scarlatina. — Croup  is  much  rarer  in  scarlatina  than  in  measles  ; 
it  rarely  occuirs  alone,  and  more  often  coincides  with  diphtheria  of  the 
pharynx  and  the  nasal  fossae. 


54  TEXT-BOOK  OF  MEDICINE 

Croup  in  Whooping-Cough. — Secondary  croup  in  whooping-cough 
comes  next  to  that  of  measles  in  frequency. 

Croup  in  Typhoid  Fever. — Croup  is  excessively  rare  in  the  course  of 

typhoid  fever. 

Pathological  Anatomy. — In  croup  the  catarrhal  inflammation  of  the 
mucosa,  the  congestion  and  the  oedema  of  the  submucosa,  are  of  secondary 
moment ;  the  false  membrane  is  the  chief  lesion.  It  covers  the  different 
parts  of  the  larynx,  and  especially  the  aryteno-epiglottic  ligaments  and  the 
vocal  cords,  either  as  a  continuous  membrane  or  in  isolated  patches.  In 
colour  it  is  a  yellowish-white,  sometimes  tinted  with  minute  haemorrhages. 
In  some  cases  it  is  very  thin,  but  in  other  cases  its  thickness  may  be  as  much 
as  2  millimetres,  owing  to  the  stratified  layers  which  grow  on  its  deep 
surface.  The  younger  these  layers  are  the  greater  their  resistance,  while 
the  older  layers,  which  are  pushed  towards  the  surface,  have  become 
friable.  The  false  membranes  are  composed,  not  only  of  fibrin,  but  also  of 
pus  corpuscles  and  epithelial  cells  from  the  mucosa,  which  undergo  a  colloid 
infiltration,  taken  by  Wagner  for  an  albuminoid  substance.  These  epi- 
thelial cells,  converted  into  refractile  blocks,  are  deformed  and  branched  like 
a  stag's  horn  (Wagner).  Each  stratum  of  the  false  membrane  develops  at 
the  expense  of  the  corresponding  epithelial  layer,  and  becomes  more  super- 
ficial as  a  fresh  subjacent  layer  is  produced.  "  It  has  been  debated  whether 
the  false  membrane  is  above  or  below  the  epithelium ;  from  what  has  been 
stated  above,  we  see  that  it  is  formed  exactly  in  the  superficial  layer  of  the 
epithelium,  and  partly  at  its  expense.  Its  structure,  too,  seems  to  differ 
according  to  its  age  ;  at  the  outset  the  epithelial  network  appears  to  be 
prominent,  but  a  little  later  the  fibrinous  and  purulent  elements  are  in 
excess  "  (Leloir). 

The  mucosa  beneath  the  false  membrane  is  usually  intact,  and  rarely 
ulcerated.  The  diphtheria  bacilh,  the  poison  which  they  elaborate,  and 
their  association  with  other  bacteria,  are  described  in  detail  under  Diph- 
theritic Angina. 

The  diphtheria  bacillus  undoubtedly  gives  rise  to  the  membranes,  and  to 
the  poison  which  provokes  intoxication  and  paralysis. 

Treatment. — I  cannot  here  enter  into  all  the  details  of  serotherapy,  and 
the  reader  is  requested  to  consult  the  chapter  on  Diphtheritic  Angina 
for  further  details.  I  shall  here  describe  the  application  of  serotherapy  to 
croup. 

The  results  of  treatment  largely  depend  upon  the  previous  performance 
of  tracheotomy.  The  results  are  likewise  very  different,  if  the  croup  be  due 
to  the  diphtheria  bacillus  alone,  or  if  it  be  due  to  the  bacillus  associated  with 
the  staphylococcus  or  the  streptococcus. 

Let  us  consider  these  results. 


DISEASES  OF  THE  LAEYNX  55 

1.  A  child  who  is  suffering  from  croup  has  not  yet  been  tracheoto- 
mized.  The  cough  is  raucous,  the  voice  is  inaudible,  the  breathing  difficult, 
and  the  sucking-in  well  marked.  Severe  attacks  of  suffocation  occur  at  brief 
intervals.  At  first  sight  tracheotomy  seems  unavoidable,  but  an  injection 
of  20  centimetres  of  serum  is  given.  Twelve  hours  later  a  second  injection 
is  given,  and  in  the  great  majority  of  cases  the  injections  of  serum  arrest 
the  formation  of  fresh  membranes,  favour  the  r-.pid  disappearance  of  those 
already  formed,  and  recovery  is  rapid.  "  In  169  cliildreu  admitted  for 
diphtheritic  angina,  fifty-six  showed  lar}Tigeal  trouble,  and  in  twenty-five 
tracheotomy  appeared  unavoidable.  Under  the  influence  of  injections  of 
serum  every  twelve  hours,  the  sucking-in  decreased,  and  afterwards  only 
returned  in  fits.  The  child  brought  up  the  false  membrane,  and  after 
two  or  three  days  the  breathing  was  natural,  to  the  great  astonishment 
of  the  house-physicians  and  attendants  in  the  diphtheria  pavilion,  who, 
from  their  large  acquaintance  with  children  suffering  from  croup,  quite 
thought  the  operation  could  not  be  avoided  "  (Roux  and  Martin). 

2.  In  children  suffering  from  croup  who  have  undergone  tracheotomy 
the  success  of  serotherapy  diminishes,  according  to  the  nature  of  the  asso- 
ciated microbes.     These  associations  are  the  same  in  croup  as  in  angina, 

(a)  The  association  of  diphtheria  with  Brisou's  small  COCCUS  is  favour- 
able both  in  croup  and  in  angina.  In  the  statistics  of  Roux  and  Martin, 
the  mortality  was  only  one  in  ten  cases,  and  this  was  due  to  broncho- 
pneumonia following  tracheotomy.  The  quantity  of  serum  injected  amounted 
to  50  c.c.  in  divided  doses. 

(6)  The  association  of  diphtheria  with  the  staphylococcus  is  to  be 
feared.  It  is  not  deadly  in  the  case  of  angina,  but  is  very  fatal  in  cases  of 
croup  after  tracheotomy,  because  it  gives  rise  to  pulmonary  comphcations, 
such  as  broncho-pneumonia,  which  often  follow  the  operation,  and  against 
which  injections  of  serum  are  often  impotent.  In  eleven  cases  Roux  and 
Martin  recorded  seven  deaths,  a  mortality  of  63  per  cent.  The  mean  quantity 
of  serum  employed  in  divided  doses  amounted  to  60  c.c.  In  these  patients 
the  membranes  are  pultaceoiLS  and  very  extensive ;  the  temperature  was 
always  above  103°  F.,  and  the  breathing  was  much  quickened. 

(c)  The  association  of  the  diplitheria  bacillus  with  the  streptoCOCCUS  is 
most  formidable,  both  in  croup  and  in  angina.  In  spite  of  serotherapy,  the 
mortality  in  cases  of  croup  which  have  been  operated  upon  has  b(^en 
63  per  cent.,  according  to  Roux  and  Martin.  Broncho-pneumonia  and 
pseudo- membraneous  bronchitis  are  responsible  for  most  of  the  deaths. 

Since  many  cases  of  secondary  infection  can  be  set  down  to  tracheotomy, 
this  operation  must  in  future  be  replaced,  when  possible,  by  intubation. 

Intubation  of  the  larynx  was  extolled  by  Bouchut,  but  his  instrument 
rendered  the  results  of  intervention  .so  hazardous  that  physicians  followed 


56  TEXT-BOOK  OF  MEDICINE 

Trousseau's  advice,  and  abandoned  intubation,  tracheotomy  being  infinitely 
superior.  Great  progress,  however,  has  been  made  in  the  apparatus  for 
intubation.  The  method  has  been  so  perfected,  thanks  to  Collin's  instru- 
ments and  to  Bayeux's  technique,  that  hesitation  is  no  longer  possible.  In 
the  very  great  majority  of  cases  intubation  will  replace  tracheotomy. 

The  -writings  of  Variot  and  Bayeux  and  of  Martin  give  us  the  most  com- 
plete information  on  this  subject.  As  Bayeux  says  :  "  We  run  the  risks  of 
grave  results — nay,  even  of  the  death  of  children — by  delay.  We  risk 
nothing  by  intubation  when  carried  out  betimes." 


VII.  STRIDULOUS  LARYNGITIS— FALSE  CROUP. 

JEtiology.  —  Stridulous    laryngitis     (Bretonneau),     or     false    croup 

(Guersant),  is  simply  an  acute  catarrhal  laryngitis  of  infancy,  which  derives 
its  spasmodic  character  from  the  tender  age  of  its  victims.  In  small  children 
the  intercartilaginous  glottis  is  rudimentary,  and  the  aperture  of  the  glottis 
is  short  and  narrow.  Changes  in  the  larynx  are,  therefore,  readily  accom- 
panied by  dyspnoea,  wliich  in  children  takes  the  form  of  fits.  This  laryn- 
gitis is  most  frequent  from  two  to  six  years,  is  often  seen  during  the  invasion 
of  measles,  and  may  be  the  forerunner  of  broncho-pneumonia. 

Description. — Trousseau  has  given  so  complete  an  account  of  this 
malady  that  I  cannot  do  better  than  quote  it  in  extenso  ."  "  A  child  between 
the  age  of  two  and  five  years  is  seized  in  the  middle  of  the  night— about 
eleven,  twelve,  or  one  o'clock — with  an  attack  of  dyspnoea.  He  wakes  out 
of  his  sleep  in  a  very  uneasy  and  feverish  state.  His  cough  is  harsh  and 
very  frequent,  but  strong  and  noisy  ;  his  breatliing  is  jerky,  panting,  and 
accompanied  by  inspiratory  stridor.  His  voice,  which  is  modified  in  its 
timbre,  is  inaudible  during  the  fits,  but  rough  and  hoarse  in  the  intervals. 
There  is,  however,  one  capital  fact — it  is  never  extinguished,  as  in  true 
croup." 

Oppression  and  anxiety  are  sometimes  excessive ;  the  face  is  congested, 
and  the  eyes  express  profound  terror.  This  alarming  crisis  may  last  from 
half  an  hour  to  about  three  hours,  but  the  attack  then  ends.  The  child 
becomes  quiet,  sleep  returns,  and  the  pulse-rate  falls.  The  skin  is  slightly 
moist.  Then  the  patient  wakes  up.  The  cough  is  still  croupy,  though 
looser.  During  the  day  it  is  still  more  catarrhal,  the  breatliing  is  less  whist- 
ling, and  the  voice  has  almost  regained  its  natural  tone.  As  a  rule,  the 
attacks  recur  several  nights  in  succession,  but  they  always  decrease  in 
violence,  while  the  days  are  good,  the  patient  having  but  little  fever  or 
malaise,  and  suffering  from  a  loose  and  less  croupy  cough.  On  questioning 
the  parents  we  learn  that  the  child  went  to  bed  quite  well  and  fell  into  a 
peaceful  sleep.     Sometimes,  on  the  contrary,  we  are  informed  that  he  had 


DISEASES  OF  THE  LARYNX  57 

been  out  of  sorts  for  some  days,  that  he  had  taken  cold,  but  had  retained  his 
u^ual  spirits.  Lastly,  if  the  throat  be  examined,  the  most  careful  examina- 
tion shows  that  false  membranes  and  glandular  enlargement  are  absent. 
This  sudden  onset,  with  symptoms  wliich  are  more  alarming  in  appearance 
than  those  at  the  commencement  of  croup,  is  in  most  cases  characteristic 
of  false  croup.     This  malady  results  in  cure,  fatal  cases  being  very  rare. 

Diagnosis — Treatment. — The  diagnosis  of  stridulous  laryngitis  is  given 
under  Croup.  It  is  always  necessary  to  think  of  hereditary  syphilis  of  the 
larjTix,  wliich  simulates  both  croup  and  false  croup. 

If  the  reader  ^vill  refer  to  Croup,  he  will  see,  under  Bacteriological 
Diagnosis,  that  in  some  children  the  laryngeal  troubles  are  due  to  the  presence 
of  a  small  diplococcus,  and  may  resemble  both  true  and  false  croup.  I 
think  that,  even  in  a  condition  which  has  every  appearance  of  false  croup, 
we  should  not  neglect  bacteriological  examination  of  the  mucus  or  of  the 
pharyngo-larpigeal  secretions.  A  case  which  is  taken  for  a  false  croup 
may  be  really  laryngitis,  or  pharyngo -laryngitis,  due  to  the  diplococcus ; 
membranes  may  be  present  or  absent.  False  croup  recovers  without  active 
treatment.  It  is  sufficient  to  apply  blisters,  or  a  sponge  soaked  in  very  hot 
water,  to  the  child's  neck  (Graves).  A  moist  atmosphere  from  a  steam- 
kettle  should  be  maintained  around  the  patient's  bed  and  emollient  drinks 
given.  Tracheotomy  is  only  required  in  exceptional  cases.  False  croup, 
however,  has  proved  fatal. 

VIII.  (EDEMA  OF  THE  LARYNX— (EDEMA  IN  BRIGHT'S 

DISEASE. 

Syphilitic  (Edema. 

Definition.  —  The  terms  "(Edematous  laryngitis,"  '"  oedematous 
laryngeal  angina  "  (Trousseau),  "  laryngeal  infiltration  "  (Jaccoud),  and 
"oedema  of  the  glottis,"  have  been  used  to  describe  infiltrations  of  the 
larynx,  which  differ  shglitly  in  nature,  but  present  almost  identical  symptoms. 
Bayle,  who  first  described  oedematous  laryngitis  (1808),  considered  it,  with 
good  reason,  to  be  dropsy  of  the  larynx,  analogous  to  dropsy  of  tlie  celhilar 
tissue.  Bouillaud  and  Cruveilhier,  on  the  contrary,  endeavoured  to  show 
that  it  had  nothing  to  do  with  dropsy,  but  was  really  an  inflammatory 
lesion,  causing  the  formation  of  purulent  fluid.  Both  opinions  are  true. 
In  some  cases  it  is  a  question  of  oedema  in  the  true  sense  of  the  word,  the 
inflltration  being  purely  serous  (nephritis,  scarlatina,  oedema  from  cold), 
but  at  other  times  the  infiltration  is  sero-purulent  (ulcerative  laryngitis, 
laryngeal  infections,  erysipelas  of  the  pharynx,  tumours  of  the  pliaryux  and 
of  tlie  tongue,  laryngo-typhus,  etc.). 

In  this  chapter,  however,  I  shall  not  consider  purulent  infiltrations  of 


58  TEXT-BOOK  OF  MEDICINE 

the  larynx,  or,  at  least,  only  in  an  incidental  way.  I  have  only  in  view 
oedema  properly  so-called — that  is,  infiltration  of  the  larynx  comparable  to 
oedema  of  the  cellular  tissue.  I  have,  therefore,  headed  this  chapter 
"  (Edema  of  the  Larynx."  I  shall  first  give  a  general  survey  of  the  question 
and  then  discuss  oedema  as  seen  in  Bright's  disease  and  in  syphilis. 

Site  of  the  (Edema. — The  laryngeal  mucosa  is  not  everywhere  ad- 
herent to  the  subjacent  fibro-elastic  tissue.  The  adhesion  is  lax  at  the 
glosso-  and  aryteno-epiglottic  folds  ;  in  the  arytenoid  region  it  is  quite  slight, 
and  it  is  not  close  on  the  vocal  cords.  Certain  of  these  parts  are  rich  in 
cellular  tisssue,  and  therefore  oedema  readily  forms  there. 

According  to  its  site,  the  infiltration  may  be  supraglottic,  glottic,  or 
subglottic.  The  term  "  CBdema  of  the  glottis  "  is  therefore  improper, 
and  comprises  but  a  small  part  of  the  question,  because,  in  most  cases, 
oedema  affects  parts  other  than  the  glottis.  Supraglottic  infiltration  is  the 
most  frequent,  because  of  the  situation  of  the  lesions  which  produce  oedema, 
and  especially  because  the  submucous  connective  tissue  is  abundant  in  this 
region.  The  aryteno-epiglottic  and  glosso-epiglottic  folds,  the  epiglottis, 
the  ventricles  of  Morgagni,  the  interarytenoid  tissue,  and  the  pharynx 
itself,  participate  in  the  trouble,  and  the  cushions  of  oedema  can  be  felt  by 
the  finger.  The  oedema  is  said  to  be  glottic  when  it  occupies  the  vocal 
cords.  When  the  infiltration  is  subglottic,  the  laryngoscope  reveals  a 
reddish  swelling  on  the  side  of  the  trachea. 

Pathological  Anatomy.  —  The  mucosa  which  covers  the  oedematous 
parts  is  sometimes  pale  and  anaemic,  at  other  times  red  and  injected.  The 
vestibule  is  much  infiltrated ;  the  aryteno-epiglottic  folds,  which,  from 
the  abundance  and  laxity  of  their  connective  tissue,  present  the  chief 
lesion,  are  oedematous,  and  may  be  enormously  swollen.*  The  epiglottis 
has  lost  its  shape,  and  may  be  three  times  as  thick  as  normal.  These 
lesions  readily  explain  the  almost  complete  obliteration  of  the  orifice  of  the 
larynx.  The  oedematous  parts,  on  incision,  are  found  to  be  infiltrated  with 
serous  fluid ;  oedema  sums  up  the  whole  lesion.  When  the  infiltration  of 
the  larynx  is  secondary  to  deep  ulcerations — perichondritis,  necrosis  of 
cartilages,  or  sequestra — we  find,  in  addition  to  the  serous  or  sero-purulent 
infiltration,  the  lesions  described  under  Syphilis,  Tuberculosis,  and  Cancer 
of  the  Larynx. 

etiology — Pathogenesis.  —  (Edema  of  the  larynx  may  be  primary, 
accidental,  or  secondary.  Primary  oedema  exists  as  a  distinct  disease,  and 
may  be  produced  by  a  chill.     Trousseau  reports  a  remarkable  case  :    "  A 

*  Sestier,  by  injecting  water  into  the  carotids  of  a  cadaver,  has  produced  artificial 
oedema  of  the  larynx,  studied  its  distribution  and  compared  the  size  of  each  of  the 
affected  parts.  Experimental  research,  in  connection  with  pathology,  shows  that  the 
aryteno-epiglottic  folds  are  chiefly  affected. 


DISEASES  OF  THE  LARYNX  59 

drunken  man,  who  slept  in  the  street  one  cold  night,  was  seized  by  acute 
oedema  of  the  larynx."  The  condition  here  was  "  true  oedema  "  ;  the 
swelling  of  the  laryngeal  mucosa  is  comparable  to  that  of  the  nasal  mucosa  in 
coryza.  I  think,  however,  that  laryngeal  oedema  a  frigqre  is  very  rare,  and, 
on  closer  inspection,  some  other  factor,  such  as  Bright's  disease  or  syphilis, 
is  often  found. 

Accidental  oedema  follows  wounds  and  burns.  Sestier  has  collected 
sixty-nine  cases.  Oedema  secondary  to  some  lesion  of  the  lar5mx,  or  of  a 
neighbouring  part,  is  quite  common.  "  Every  inflammatory  process," 
says  Trousseau,  "  determines  in  its  neighbourhood  oedema  which  varies 
in  direct  ratio  with  the  amount  of  loose  connective  tissue.  In  the  eyelids, 
for  example,  and  on  the  prepuce,  where  the  connective  tissue  is  abundant 
and  loose,  a  pustule  of  variola,  or  a  patch  of  erysipelas,  may  cause  enormous 
swelling.  This  oedema,  which  Virchow  called  collateral,  and  which  is  some- 
times sero- purulent,  finds  a  most  favourable  soil  in  the  abundant  lax  cellular 
tissue  of  the  supraglottic  region. 

Laryngeal  tuberculosis  may  cause  oedema  of  the  larynx.  The  condi- 
tion in  some  cases  is  a  false  oedema,  and  is  really  a  tubercular  infiltration 
which  invades  the  folds,  the  ventricular  bands,  and  the  epiglottis  ;  these 
parts  are  hypertrophied  and  indurated  by  infiltration  of  tubercular  tissue, 
and  the  condition  is  certainly  not  oedema.  Nevertheless,  true  oedema 
may  appear  in  the  course  of  laryngeal  tuberculosis ;  it  is  provoked  by 
ulceration,  and  especially  by  tubercular  perichondritis  and  by  lesions  of  the 
cartilages.  The  oedema  in  tuberculosis  of  the  larynx  chiefly  occupies  the 
arytenoid  region  ;  it  is  asually  soft  and  pale,  because  of  the  ana^niia  of  the 
mucous  membrane. 

Cancer  of  the  larynx  causes  oedema,  which  nearly  always  begins  on  one 
of  the  ventricular  bands.  It  remains  unilateral,  reaches  the  arytenoid  and 
the  corresponding  aryteno-epiglottic  fold  ;  it  rarely  attacks  the  epiglottis, 
docs  not  spread  far,  and  develops  side  by  side  with  the  cancer. 

LaryngO-typhus  may  determine  severe  oedema.  In  the  decline  of  typhoid 
fever  infiltration,  due  to  the  necrosis  of  the  cartilages,  appears;  its  onset 
may  be  slow  or  rapid.  Scarlatina,  especially  during  defervescence,  may  set 
up  oedema  of  the  larynx.  Trousseau  has  reported  several  examples.  Acute 
or  chronic  nephritis  (including  saturnine  nephritis)  may  bring  on  oedema  of 
the  larynx.  (Edema  of  the  edge  of  the  vocal  cords  is  extremely  frequent 
in  young  girls  who  are  learning  to  sing. 


60  TEXT-BOOK  OF  MEDICINE 


CEdema  of  the  Larynx  in  Bright's  Disease. 

The  following  example  will  give  an  exact  idea  of  this  condition  :*  A  man  was  ad- 
mitted into  my  wards  with  symptoms  of  asphyxia.  His  chief  complaint  was  noisy, 
laboured  breathing,  with  stridor  audible  from  one  end  of  the  ward  to  the  other.  Ex- 
piration little  affected  ;  each  inspiration  required  much  effort.  The  inspired  air  finally 
entered  the  limgs,  but  caused  a  sa-nnng  noise.  Inspection  showed  considerable  sucking- 
in,  with  depression  of  the  suprasternal  and  epigastric  hollows  ;  the  diaphragm  was 
apparently  ch'awn  upwards.  The  voice  was  tUghtly  hoarse,  a  proof  that  the  vocal 
cords  were  but  httle  affected. 

The  man  stated  that  he  had  been  sick  for  the  past  month.  The  dyspnoea  was  not 
the  first  symptom,  and  the  illness  began  with  dysphagia,  which  gradually  became  so 
severe  that  the  passage  of  food  and  drink  was  almost  impossible.  Ten  or  twelve  days 
later  the  patient  experienced  a  feeling  of  strangulation,  which  he  compared  to  a  foreign 
body  blocking  the  entrance  of  the  air-passages.  The  dyspnoBa  was  at  first  uniform, 
but  later  interrupted  by  paroxysms.  These  symptoms  finally  made  life  almost  unbear- 
able. He  was  worn  out,  and  could  not  take  food.  Breathing  required  the  greatest 
efl'ort ;  each  inspiration  was  a  struggle  for  life,  and  the  prognosis  was  most  alarming. 


Fig.  1. — CEdema  of  the  Larynx. 

e,  Epiglottis — very  cedematous,  irregular,  and  red.  It  forms  an  enormous  eyebrow 
above  the  vestibule  of  the  larynx,  and  is  continuous  with  the  aryteno-epiglottic  folds, 
which  are  very  cedematous. 

a,  Arytenoid  region — also  swollen,  deformed  and  retracted  towards  the  oesophagus. 

h.  Ventricular  bands,  which  are  very  cedematous,  and  mask  the  vocal  cords  for  the 
greater  part  of  their  extent.     The  anterior  extremity  of  the  vocal  cords  is  visible. 

The  obstruction  was  evidently  in  the  larynx,  but  we  had  to  ascertain  its  nature. 
M.  Bonnier  examined  with  the  mirror.  On  opening  the  mouth,  we  at  once 
noted  a  reddish  oedema  of  the  uvula,  of  the  pillars,  and  of  the  velum  palati.  The 
uvula  was  bulky  and  tremulous,  the  pillars  were  cedematous,  and  the  isthmus  of  the 
gullet  was  narrowed.  Red  oedema  was  visible  at  the  base  of  the  tongue  and  in  the 
vestibule  of  the  larynx.  The  epiglottis  was  bulky  and  much  deformed,  the  aryteno- 
epiglottic  folds  were  enormous,  and  the  cedematous  ventricular  bands  blocked  the 
orifice  of  the  glottis.  The  anterior  part  of  the  vocal  cords  could  be  seen  momentarily, 
and  their  free  edge  was  slightly  cedematous.  The  illustration  above  represents  the 
condition. 

It  is  now  easy  to  follow  the  march  of  events.  The  dysphagia  was  caused  by  the 
oedema  of  the  palate,  the  pharynx,  and  the  epiglottis.  The  dyspnoea  was  due  to 
oedema  of  the  vestibule  and  of  the  ventricular  bands  ;  these  parts,  by  opposing  the 

*  "  (Edeme  Brightique  du  Larynx "  {Climque  Mtdicale  de  VHotel-Dieu,  1897, 
Sme  Le9on,  p.  49). 


DISEASES  OF  THE  LARYNX  61 

passage  of  the  inspired  air,  made  tlie  breatliing  difficult  and  stertorous.  Spa-sms  of 
the  glottis,  which  are  almost  inseparable  from  such  lesions,  caused  the  fits  of  suffoca- 
tion. 

The  diagnosis  of  oedema  of  the  larpix  was  therefore  established.  The  patient  had 
neither  tumour,  laryngeal  polj-pus,  cicatricial  stenosis,  nor  paralysis  of  the  posterior 
cricoarytenoid  muscles,  which  may  all  cause  suffocation,  stertor,  and  sucking-in,  but 
was  suffering  from  progressive  oedema,  which  had  started  in  the  velum  pahiti  and  the 
isthmus  of  the  fauces,  and  had  reached  the  larynx. 

The  diagnosis,  however,  was  not  complete,  for  larjTigeal  oedema,  whether  it  be 
wliite  or  red,  and  local  or  diffuse,  may  be  due  to  many  causes.  Cancer,  tuberculosis, 
and,  above  all,  sypliilis,  may  give  rise  to  oedema  of  the  larynx,  while  the  existing  lesion 
may  be  almost  liidden.  The  oedema  in  this  case  was  due  to  none  of  these  causes  ;  it 
was  not  the  result  of  cold,  but  of  Bright's  disease. 

The  case  was  one  of  Bright's  disease.  It  was  riot  a  case  in  which  oedema  was  severe 
and  uriemic  symptoms  marked  ;  it  was  one  of  those  cases  of  latent  Bright's  disease.  In 
this  patient  we  found  all  the  minor  troubles  of  "  Brightism  " — i.e.,  frequent  micturition, 
cfamp  in  the  calves,  dead  fingers,  cryiesthesia,  and  itching.  The  arterial  tension  was 
exaggerated,  the  urine  contained  albumin,  and  the  depuration  was  incomplete,  as 
examination  of  the  toxicity  of  the  urine  showed  lowering  of  the  toxic  coefficient.     We 


Fig    2. — Laryngeal  (Edema. 

c.  Epiglottis — still  cedematous,  but  regaining  its  normal  shape  somewhat. 
a.  Arytenoid  regions  still  remain  edematous  and  deformed. 

h.  Ventricular  bands.  The  swelling  has  diminished,  the  glottis  is  more  patent,  the 
vocal  cords  can  be  better  seen,  but  their  free  edge  is  still  irregular  and  swollen. 

had,  then,  to  deal  with  redcma  of  the  larynx,  due  to  Blight's  disease,  and  producing 
increasing  asphyxia,  which  might  well  end  fatally. 

His  condition  was  so  grave  that  I  discussed  the  question  of  tracheotomy,  or,  belter 
still,  of  intubation.  I  was  prepared,  therefore,  for  any  eventuality,  but  I  began  by 
applying  several  leeches  to  the  front  of  the  neck.  The  result  was  not  long  delayed. 
On  the  next  day  the  improvement  was  manifest :  the  oedema  of  the  palate  had 
diminished,  the  dysphagia  was  less,  the  stertor  was  not  so  noisy,  the  breathing  was 
easier,  and  the  oed'ma  of  ihv  larynx  was  on  the  road  to  recover,  as  may  be  seen  from 
Fig.  2. 

.Milk  diet  was  ordered  from  th(^  first,  and  two  days  later  the  improvement  was 
still  more  marked.  The  annexed  illustration  (Fig.  .3)  gives  a  good  idea  of  the  im- 
provement which  rapidly  followed  in  the  o-dematous  parts.  Six  days  later  the 
patient  was  cured. 

(Edema  may  HujMirvene  in  the  course  of  acute  or  of  chronic  nepliritis. 
When  nephritis  is  very  acute  (as  in  scarlatinal  and  early  syphilitic  nephritis), 
ft  produces  oedema,  which  tends  to  become  general,  and  the  anasarca  is  often 


62  TEXT-BOOK  OF  MEDICINE 

considerable.  The  serous  cavities — notably  the  pleurae — contain  effusions, 
and  serous  exudate  may  be  present  in  the  brain,  the  lungs,  or  o'ther  organs. 
(Edema  of  the  larynx  is  then  associated  with  these  various  exudations. 

In  chronic  nephritis,  on  the  contrary,  the  oedema  has  much  less  tendency 
to  become  diffuse  ;  it  is  more  isolated  and  more  localized  to  one  region, 
such  as  the  face,  the  lower  limbs,  or  a  single  organ,  and  we  see  patients 
suffering  from  slowly  progressive  nephritis  in  whom  pleural  effusion  or  acute 
oedema  of  the  lung  supervenes,  while  oedema  of  the  extremities  is  absent  or 
slight.  The  same  remark  applies  to  oedema  of  the  larynx  in  chronic 
nephritis.  GEdema  of  the  larynx  may  occur  in  the  course  of  insidious 
Bright' s  disease,  while  other  parts  of  the  body  are  free.  This  patient  had 
never  shown  oedema  in  any  other  part  before  oedema  of  the  palate  and  of 
the  larynx  appeared.  In  a  patient  of  Fauvel's  no  trace  of  oedema  had  been 
seen,  and  the  oedema  of  the  eyelids  only  appeared  after  that  of  the  larynx. 


Fig.  3. — Laryngeal  (Edema. 

e,  The  epiglottis  has  lost  all  trace  of  ojdema. 

a,  The  arytenoid  region  has  regained  its  normal  aspect. 

h.  The  ventricular  bands  still  hide  the  glottis  to  a  slight  extent,  but  they  meet 
only  during  effort  and  phonation.  The  vocal  cords  are  a  little  irregular  along  their 
free  border,  and  the  anterior  half  alone  is  visible  during  inspiration,  but  the  air  enters 
the  larynx  freely. 

In  Jones's  patient  slight  oedema  of  the  lower  limbs  was  present,  when 
oedema  of  the  larynx  supervened.  A  patient  of  Fraenkel's  had  never  had 
any  oedema,  so  that  in  his  case  the  oedema  of  the  larynx  was  considered 
to  be  the  first  sign  of  nephritis.  Hanot's  patient  had  never  shown  the  least 
trace  of  oedema,  when  oedema  of  the  palate  and  of  the  larynx  appeared. 

We  see,  therefore,  that  in  the  course  of  slowly  progressive  and  more  or 
less  insidious  chronic  neplu-itis  oedema  of  the  larynx-  (like  that  of  the  lung) 
may  appear  suddenly,  without  being  preceded  by  peripheral  oedema. 
Accordingly,  several  authors  (Fauvel,  Fraenkel)  have  stated  that  oedema  of 
the  larynx  may  appear  unexpectedly  as  the  first  sign  of  Bright's  disease. 
I  do  not  hold  this  view.  I  admit  that  oedema  of  the  larynx  may  appear 
as  the  first  manifestation  of  oedema  in  a  "  Bright "  case,  but  I  cannot 
accept  the  statement  that  it  may  be  the  first  symptom  of  Bright's  disease. 


DISEASES  OF  THE  LARYNX  G3 

In  fact,  at  the  present  day  we  no  longer  look  upon  Briglit's  disease  as  our 
ancestors  did,  and  we  do  not  wait  for  the  appearance  of  oedema  to  make 
our  diagnosis.  We  hunt  out  "  Brightism,"  wliich  may  not  be  evident  at 
first  sight.  We  know  that  there  is  a  mild  form  of  uraemia  which  is  insidious 
in  its  course,  but  yet  perfectly  recognizable.  The  study  of  the  minor  troubles 
of  "  Brightism,"  the  estimation  of  the  arterial  tension,  and  the  examination 
of  the  toxicity  of  the  urine,  reveal  latent  Bright's  disease.  We  are  thus 
able  to  affirm  that,  although  an  attack  of  epileptiform  fits,  of  coma,  of  super- 
acute  oedema  of  the  lung,  or  of  oedema  of  the  larynx,  may  appear  to  be  the 
first  symptom  of  nephritis,  it  is  in  reality  only  the  first  apparent,  and  not 
the  first  real,  symptom,  and  the  nephritis  has  been  already  shown  by  signs 
which  would  not  have  passed  unnoticed  had  trouble  been  taken  to  look  for 
them.* 

I  must  insist  on  the  fact  that  oedema  of  the  larynx  in  Bright's  disease  is 
almost  always  preceded  by  oedema  of  the  velum  palati.  It  might  truly  be 
said  that  oedema  commences  in  the  throat  and  tlie  uvula,  and  afterwards 
spreads  downwards  to  the  base  of  the  tongue,  the  epiglottis,  and  the  larynx. 
As  a  result,  troubles  in  swallowing  very  often  open  the  scene.  At  first  the 
patient  seems  to  have  only  a  painful  angina,  but  respiratory  troubles  soon 
appear.  The  oedema  spreads  downwards,  causing  a  succession  of  com- 
plications which  I  have  found  in  most  of  my  cases.  In  a  patient  at  the 
Hotel-Dieu  dysphagia  and  cedema  of  the  throat  preceded  oedema  of  the 
larynx  and  dyspnoea  by  ten  or  twelve  days.  In  a  patient  at  the  Necker 
Hospital  oedema  of  the  throat  and  dysphagia  occurred  twenty-four  hours 
before  attacks  of  suffocation.  In  the  cases  reported  by  Abate  and  Jones 
cedema  of  the  larynx  and  oedema  of  the  palate,  with  dysphagia  and  suffoca- 
tion, appeared  almost  simultaneously.  In  M.  Fauvel's  patient  the  cedema 
of  the  palate  preceded  that  of  the  larynx,  and  deglutition  was  impaired 
before  respiration.  In  M.  Hanot's  patient  the  succession  and  tlie  delimita- 
tion of  tlie  oedema  was  even  more  marked.  In  the  first  phase  the  cedema 
remained  localized  to  the  isthmus  of  the  fauces  and  to  the  uvula,  as  an 
(edematous  angina,  causing  acute  dysphagia,  which  was  cured  by  milk  diet. 
Two  months  later,  however,  oedema  of  the  palate  reappeared,  and  also 
oedema  of  the  larynx,  causing  acute  attacks  of  suffocation.  Hanot,  in  his 
notes  on  this  case,  has  been  careful  to  add  :  "  Albuminuric  oedema,  limited 
to  the  uvula,  may  be  the  starting-point  of  oedema  of  the  glottis." 

In  a  patient  with  painful  angina  the  throat  must  be  carefully  examined, 
and  if  red  or  white  (jedema  of  the  uvula,  of  the  pillars,  or  of  the  velum  palati 
be  present,  nephritis  must  be  suspected,  the  urine  examined,  the  patient 
carefully  questioned,  search  made  for  symptoms  of   "  Brightism,"  and  the 

*  Diciiliifoy  :  "  l^lude  sur  Ic  Brightismc,"  Bulletin  dc  r Academic  dc  Medecinc,  sdanco 
dcs  G  et  2U  Juin,  1893. 


64  TEXT-BOOK  OF  MEDICINE 

diagnosis  of  oedema  of  the  throat  due  to  Bright' s  disease  be  made.  TJiis 
oedema  then  becomes  an  important  element  in  diagnosis,  prognosis,  and 
treatment.  It  is  an  element  in  diagnosis,  because  it  helps  us  to  trace 
Bright' s  disease  which  at  first  might  not  be  suspected  ;  it  is  an  element  in 
prognosis,  for  it  leads  us  to  foresee  the  probable  extension  of  the  oedema  to 
the  larynx  ;  it  is  an  element  in  treatment,  for  it  invites  prompt  action  in 
order  to  check  the  disease  and  to  avoid  oedema  of  the  larynx. 

CEdema  of  the  larynx  is  one  of  the  most  formidable  complications  of 
Bright's  disease.  In  some  cases,  it  is  true,  it  may  remain  limited,  and  for 
several  days  and  weeks  betray  itself  only  by  a  trifling  stridor  during  inspira- 
tion ;  or,  again,  it  may  invade  the  larynx  but  slowly,  so  that  complications 
may  be  averted.  In  other  cases,  however,  the  oedema  may  already  be 
most  acute,  and  the  patient  may  rapidly  succumb  before  help  can  be  given. 
The  situation  is  aggravated  by  the  fact  that  oedema  in  Bright's  disease  does 
not  always  remain  confined  to  the  larynx,  but  invades  the  pleura  and  the 
lung.  A  patient  of  mine  in  the  Charite  had  very  extensive  oedema  of  the 
lung,  and  succumbed  some  hours  after  tracheotomy — not  so  much  from  the 
laryngeal  lesions  as  from  the  pulmonary  oedema.  Hanot's  patient,  who 
had  both  csdema  of  the  larynx  and  of  the  lung,  with  2  pints  of  fluid  in  the 
pleural  cavity,  died  some  hours  after  tracheotomy — not  so  much  from  the 
lesions  in  the  larynx  as  Irom  the  pleuro-pulmonary  mischief.  It  is  often 
difficult,  I  grant,  to  gauge  correctly  the  state  of  the  lung  in  a  case  of  oedema 
of  the  -larynx,  because  the  extreme  dyspnoea,  and  the  echo  of  the  "  sawing 
sound  "in  the  larynx  do  not  always  allow  perfect  auscultation  of  the  lung. 

What  treatment  should  we  employ  in  this  condition  of  oedema  ?  If 
death  appear  imminent,  tracheotomy  may  give  some  chance  of  recovery. 
So  many  failures  have  been  noted  that  I  would  rather  advise  intubation, 
which  has  been  tried  and  proved.  Scarification  of  the  oedematous  swelhngs 
does  good.  Bleeding  is  an  excellent  means  of  treatment.  A  dozen  leeches 
are  applied  to  the  front  of  the  neck,  so  as  to  produce  copious  bleeding.  Hot 
compresses,  warm  gargles,  and  sprays  are  sometimes  of  use. 

If  asphyxia  be  imminent,  we  can  facilitate  the  entrance  of  air  into  the 
larynx  by  firm  traction  on  the  tongue.  Do  not  forget  that  oedema  of  tlie 
lung  or  urajmia  may  also  be  present.  Tracheotomy  was  unsuccessful  in 
the  three  cases  which  I  have  reported,  because  two  patients  succumbed  to 
pulmonary  oedema,  and  the  third  to  ursemic  convulsions.  If  pulmonary 
oedema  or  ujsemia  be  present,  both  general  and  local  bleeding  are  necessary. 

The  nephritis  must  also  be  treated,  and  absolute  milk  diet  is  therefore 
prescribed.  In  place  of  milk  by  the  mouth,  we  may  give  injections  of 
lactose  (150  grammes  of  water  and  20  grammes  of  lactose).  No  chlorides 
should  be  taken,  and  injections  of  serum  must  not  be  given. 


DISEASES  OF  THE  LARYNX  65 


Syphilitic  (Edema  of  the  Larynx. 

(Edema  is  fairly  rare  in  the  course  of  secondary  lesions  of  the  larynx. 
Although  they  are  superficial,  and  apparently  benign,  they  are  sometimes 
accompanied  by  oedema  of  the  larynx  and  respiratory  troubles.  This  fact 
is  most  important,  and  has  been  emphasized  by  Krishaber.  Although 
dyspnoea  may  be  exceptional  in  secondary  lesions  of  the  larynx  (or,  at 
least,  it  is  very  shght),  yet  in  some  cases  the  distress  becomes  suddenly 
acute,  and  tracheotomy  would  become  necessary  if  the  condition  did  not 
yield  rapidly  to  appropriate  treatment.  I  have  often  verified  this  fact,  and 
Mauriac,  like  Krishaber,  affirms  that  "  quite  trifling  erosions  may  become 
a  dangerous  centre  of  congestion,  around  which  oedema  of  the  glottis  rapidly 
develops." 

(Edema  of  different  colours,  with  pallor  or  redness  of  the  mucosa,  often 
accompanies  tertiary  lesions.  A  red  tint  is  sometimes  the  sign  of  sero- 
purulent  infiltration.  Laryngeal  oedema  plays  a  considerable  part  in  the 
history  of  tertiary  lesions,  and  is  one  of  the  commonest  causes  of  dyspnoea 
and  of  threatening  asphyxia.  It  may  be  more  or  less  extensive,  and  may 
invade  the  aryteno-epiglottic  folds,  the  epiglottis,  the  ventricular  bands, 
the  vocal  cords,  the  space  below  the  cords,  and  the  trachea.  The  laryngo- 
scope shows  the  deformity  and  the  swelling  of  the  parts  invaded.  The 
epiglottis  is  twisted  up  and  swollen  fike  a  chestnut  or  the  cervix  uteri. 
The  arytenoids  form  large  cusliions,  which  obliterate  the  superglottic 
region. 

All  tertiary  lesions,  etc.,  may  at  any  moment  cause  oedema  of  the  larynx, 
which  may  be  Hmited,  and  not  serious,  or  quite  general.  In  the  latter 
event,  it  may  be  slow  or  rapid  in  its  progress,  Krishaber  and  Mauriac  have 
studied  syphiUtic  oedema  of  the  larynx,  and  have  shown  that  its  intensity 
is  not  always  in  proportion  to  the  severity  of  the  exciting  lesion.  As  a 
matter  of  fact,  we  meet  with  shallow  lesions  which,  though  scarcely  appreci- 
able with  the  laryngoscope,  may  yet  cause  alarming  oedema  of  the  larynx. 
I  have  several  times  verified  the  correctness  of  these  assertions. 

Iji  my  ward  at  the  Necker  Hospital,  I  had  two  patients  with  Laryngeal  oedema. 
One  of  them  had  stridor  and  sucking-in,  and  was  almost  in  a  state  of  asphyxia.  The 
danger  was  averted  by  energetic  specific  treatment.  The  other  patient  also  had  stridor, 
sucking-in,  and  feeling  of  strangulation,  and  with  orthopncca,  which  left  no  doubt  as 
to  a  laryngeal  lesion.  It  wa.s  of  several  weeks'  duration,  and  had  previously  caused 
only  vocal  trouble.  Bonnier  found  oedema  of  the  larynx.  The  oedema  had,  in  the 
case  of  one  vocal  cord,  the  polypoid  appearance  which  can  be  seen  in  the  subjoined 
figures.  No  suspicion  of  syphilis  existed  until  I  discovered  on  the  right  wrist  a  pustulo- 
crustaceous  syphilide,  which  gave  me  the  key  to  the  case.  I  ordered  active  specific 
treatment,  and  in  three  weeks,  as  the  Figs.  4,  5,  6,  and  7  indicate,  the  oedema  of  the 
larynx  disappeared,  and  with  it  all  the  troubles. 

5 


66  TEXT-BOOK  OF  MEDICINE 

Syphilis  may  produce  oedema  of  the  larynx  in  yet  another  way-— not  by 
lesions  limited  to  the  larynx,  but  by  setting  up  early  nephritis,  which  is 
rapidly  followed  by  peripheral  oedema,  anasarca,  effusion  into  the  serous 
membranes,  and  oedema  of  the  lung  and  of  the  larynx. 

This  sketch  of  the  importance  of  syphilitic  oedema  of  the  larynx  proves 
how  carefully  syphilis  must  be  looked  for,  in  order  to  give  injections  of 
biniodide  of  mercury  without  delay. 


Fig.  4. — CEdema  of  the  Lakynx. 

December  21. — Day  of  patient's  admission.  Appearance  of  the  glottis  during  forced 
inspiration. 

e.  Swollen  and  turgescent  epiglottis. 

a,  (Edematous  arytenoid  region. 

h.  Ventricular  bands,  which  are  markedly  cedematous.  A  small  portion  of  the 
vocal  cords  can  be  seen  in  front. 


Fig.  5. — (Edema  of  the  Larynx. 

January  12.— e,  Epiglottis,  still  swollen,  but  less  flabby. 
a.  Arytenoid  region,  which  is  less  prominent. 

h,  The  ventricular  bands  have  diminished  in  size,  allowing  the  vocal  cords  and  an 
cedematous  polypoid  mass  to  be  seen. 

General  Description. — I  have  given  the  special  characters  of  certain 
varieties  of  oedema  of  the  larynx,  and  will  therefore  recapitulate  the  general 
description.  I  would  call  attention  to  the  fact  that  the  march  of  events  is 
sudden  or  slow,  according  to  the  cause.  The  palato -laryngeal  infiltration, 
which  is  secondary  to  nephritis,  sypliilis,  scarlatina,  or  a  cliill,  may  rapidly 
become  general,  and  asphyxia  soon  appears,  while  the  progress  is  much 
slower  when  the  oedema  is  secondary  to  certain  lesions  of  the  larynx.     In 


DISEASES  OF  THE  LARYNX  67 

the  case  of  generalized  cedema,  respiration  is  rapidly  compromised.  The 
patient  has  the  sensation  of  a  foreign  body  wliich  is  strangling  liim,  and 
makes  desperate  efforts  to  get  rid  of  it.  During  the  com'se  of  the  increasing 
dyspnoea  attacks  of  suffocation  supervene,  "  in  which,"  says  Trousseau, 
"  the  patient,  with  livid  face,  open  mouth,  gaping  nostrils,  eyes  starting 
from  the  sockets,  and  skin  running  with  sweat,"  grasps  any  support  for  his 
inspiratory  muscles.  These  attacks  last  from  ten  to  fifteen  minutes,  and 
are  repeated  in  fatal  cases  at  shorter  intervals  till  death  occurs.     They  are 


Fig.  6. — (Edema  of  the  Larynx. 

January  16. — e,  Epiglottis  normal. 

a.  Arytenoid  region  normal. 

b.  Ventricular  bands,  which  are  still  cedematous,  though  they  allow  the  whole  of 
the  glottis  to  be  seen.  The  polypoid  swelling  is  implanted  on  the  right  vocal  cord ;  it 
is  notably  smaller. 


Fig.  7. — CEdema  of  the  Larynx. 

January  18. — The  larynx  has  resumed  its  normal  appearance,  with  the  exception 
of  the  right  vocal  cord,  on  which  a  remnant  of  the  polypoid  excrescence  is  seen.  It 
may  well  have  originated  in  a  syphilitic  papule. 

the  result  of  spasm  of  the  glottis,  and  are  only  seen  in  60  per  cent,  of  cases. 
Inspiration,  wliich  is  noisy  and  accompanied  ])y  Stridor,  is  usually  nuicli 
more  painful  than  expiration,  because  the  aryteno-e[)iglottic  cusliions  at  the 
moment  of  inspiration  are  said  to  act  as  a  valve  wliich  blocks  the  upper 
orifice  of  the  larynx.  These  cushions,  pushed  back  like  floating  bodies 
by  expiration,  produce  a  characteristic  hruil  dc  drapeau  (Sestier)  in  some 
cases. 

5—2 


68  TEXT-BOOK  OF  MEDICINE 

DyspncBa  is  not  so  rapid  and  so  severe  in  many  cases.  In  persons  with 
syphilitic,  tubercular,  or  cancerous  lesions  of  the  larynx,  oedema  supervenes 
as  a  complication,  and  increases  gradually  and  slowly  before  compromising 
life.  In  some  cases,  however,  dyspnoea  due  to  oedema  may  be  rapid  and 
terrible. 

The  voice  and  the  cough  are  not  greatly  altered,  as  in  croup,  but  still 
may  be  raucous  or  muffled  if  the  vocal  cords  are  involved,  or  if  the  oedematous 
parts  come  in  contact. 

Deglutition  is  painful,  because  of  the  swelling  of  the  laryngeal  folds 
and  epiglottis,  and  also  because  of  the  palato-pharyngeal  oedema.  The 
oedema  of  the  pharynx  and  of  the  vestibule  may  be  recognized  both  by 
sight  and  touch. 

OEdema,  when  consecutive  to  syphilitic,  tubercular,  or  cancerous  lesions, 
usually  remains  limited  to  the  larynx,  but  oedema  due  to  nephritis  is  often 
palato-pharyngo-laryngeal :  the  uvula  looks  like  a  lump  of  jelly,  the  mucosa 
of  the  throat  is  oedematous,  and  dysphagia  precedes  dyspnoea. 

Laryngoscopy  is  sometimes  dangerous,  for  it  may  produce  a  severe  fit 
of  choking. 

The  symptoms  which  I  have' just  enumerated  readily  explain  the  gravity 
of  oedema  of  the  larynx.  Death  often  occurs  unless  we  employ  active  inter- 
vention. QSdema  of  the  larynx  in  nephritis  is  very  dangerous.  In  ten 
cases  of  oedema  appearing  at  the  OUtset  of  nephritis,  five  died,  two  before  and 
three  after  tracheotomy  ;  and  in  ten  cases  of  oedenia  supervening  in  the 
course  of  nepliritis,  nine  died,  four  before  and  five  after  tracheotomy  (Amero). 

Diagnosis. — Foreign  bodies  and  polypi  in  the  larynx,  spasms  of  the 
glottis  caused  by  aneurysm  of  the  aortic  arch,  croup  and  stridulous  laryn- 
gitis, abscess  of  the  pharynx,  paralysis  of  the  posterior  crico- arytenoid 
muscles,  and  tumours  of  the  mediastinum,  may  simulate  oedema  of  the 
larynx,  for  all  these  conditions  give  rise  to  stridor  and  sucking-in.  They 
have,  however,  the  distinctive  signs  which  I  shall  now  enumerate.  Polypi 
are  easily  recognized  with  the  laryngoscope.  The  same  remark  appHes  to 
paralysis  of  the  posterior  crico-arytenoid  muscles.  Aneurysm  of  the  aortic 
arch  shows  dullness,  blowing  murmurs,  and  expansile  pulsation  if  the  tumour 
is  large.  With  the  laryngoscope,  lesions  of  the  larynx  are  absent,  or 
limited  to  the  paralysis  of  a  vocal  cord,  from  the  compression  of  the  recurrent 
nerve  by  the  tumour.  In  croup  we  may  note  the  presence  or  the  remains 
of  the  diphtheritic  angina  which  nearly  always  precedes  it,  the  false  mem- 
branes wliich  are  so  often  coughed  up,  the  early  and  gradual  alteration  of 
the  voice,  the  slow  and  difficult  expiration,  and  often  the  glandular  enlarge- 
ment in  the  neck.  Stridulous  laryngitis  chooses  early  life,  and  appears 
suddenly.  The  dyspnoea  at  once  reaches  its  limit,  and  after  the  suffocative 
attack,  the  relief  is  complete,  and  the  voice  and  the  breathing  recover  their 


DISEASES  OF  THE  LARYNX  69 

normal  character.  Retro-pharyngeal  abscess  is  \asible  on  the  posterior  wall 
of  the  pharynx,  and  if  the  base  of  the  tongue  be  well  depressed,  a  swelling 
which  may  fluctuate  and  is  of  a  deeper  colour  than  the  surrounding  tissues 
is  discovered.  (Edema  of  the  larynx  being  recognized,  its  cause  must  be 
diagnosed.  The  oedema  may  be  primary,  but  before  we  admit  the  existence 
of  primary  oedema,  or  of  oedema  a  frvjore,  careful  search  must  be  made  for 
any  causes  or  the  lesions  which  may,  sooner  or  later,  give  rise  to  laryngeal 
oedema.  It  is  important  to  exclude  Bright's  disease  and  syphilis,  which 
are  the  two  chief  causes  of  oedema  of  the  larynx. 

I  shall  not  go  into  the  treatment,  which  has  already  been  studied  in  each 
special  case. 

IX.  SPASM  OF  THE  GLOTTIS. 

Definition — etiology. — Spasm  of  the  glottis  results  from  tonic  contrac- 
tion of  the  constrictor  and  tensor  muscles  of  the  vocal  cords.  It  lasts  some 
seconds,  and  causes  suffocative  attacks,  which  may  result  in  death.  The 
spasm  is  either  symptomatic  or  idiopathic. 

The  symptomatic  spasm  arises  from  stimulation  of  the  recurrent  nerves 
by  a  neighbouring  tumour — e.g.,  aneurysm  of  the  arch  of  the  aorta,  tuber- 
cular or  cancerous  glands,  etc.  How  can  excitation  of  one  recurrent  nerve 
alone  provoke  spasm  of  the  glottis  ?  Krishaber  has  shown  experimentally 
that  stimulation  of  one  recurrent  nerve  acts  upon  both  lips  of  the  glottis, 
just  as  stimulation  of  one  vagus  arrests  or  slows  the  heart-beat.  Sympto- 
matic spasm  is  also  seen  in  certain  diseases  of  the  larynx,  such  as  croup, 
false  croup,  or  oedema  of  the  glottis,  and  it  is  remarkable  that  the  spasm  is 
intermittent,  although  the  exciting  cause  is  continvious.  This  intermittence 
is  met  witli  in  other  spasmodic  or  painful  actions  of  the  nervous  system 
(hepatic  and  renal  calculi,  neuralgia  in  cancer),  though  it  is  not  easy  to  give 
the  reason. 

Spasm  of  the  glottis  may  appear  alone,  or  be  associated  with  other 
laryngeal  troubles,  as  at  the  outset  or  during  the  course  of  locomotor  ataxia. 

Idiopathic  spasm  of  the  glottis  is  not,  like  the  preceding  form,  a  symptom 
appearing  in  the  course  of  another  disease,  but  a  real  morbid  entity  which 
occurs  in  children  from  four  to  eighteen  months  old,  and  it  is  this  form 
that  cliiefly  merits  description  here.  This  disease  has  been  improperly  called 
thymic  asthma,  because  it  was  thought  to  be  connected  ^vith  hypertrophy 
of  the  thymus.  It  is  really  a  neurosis,  which  may  be  independent  or  related 
to  dentition  or  to  digestive  troubles.  Heredity  may  play  some  part,  as 
several  infants  in  the  same  family  may  be  affected  (Romberg). 

Description. — Tlie  idiopathic  spasm  of  infancy,  whicli  may  or  may  not 
be  preceded  by  prodromata,  such  as  pains  in  the  back  and  hands,  or  convul- 


70  TEXT-BOOK  OF  MEDICINE 

sions,  begins  suddenly  in  the  middle  of  the  night,  hke  false  croup.  The 
glottis  closes  convulsively ;  the  breathing  becomes  more  and  more  difficult, 
and  is  soon  completely  suspended,  so  that  asphyxia  is  imminent.  The 
distress  is  extreme  ;  the  chest  is  immobile,  and  the  vesicular  murmur  can 
no  longer  be  heard.  The  face  is  cyanotic  and  bathed  in  sweat,  the  heart- 
beats are  tumultuous,  and  we  ask  ourselves  if  the  scene  is  not  about  to  end 
in  death.  After  fifteen  or  twenty  seconds  of  complete  apnoea,  "  the  child 
takes  a  quiet  breath  again,  and  the  attack  ends  by  a  high,  sonorous  inspira- 
tion that  is  quite  characteristic,  and  does  not  resemble  the  croupy  cough 
or  the  whoop  in  pertussis  "  (Tardieu).  It  is  more  like  a  shrill  and  very 
sharp  hiccough  (Herard), 

The  attacks  are  not  always  complete,  and  the  asphyxial  period  may  be 
wanting.  The  usual  duration  is  from  a  few  seconds  to  two  minutes,  but  in 
some  cases  they  recur  at  very  short  intervals,  and  are  prolonged  for  an 
hour  or  more  (Gaspari).  At  first  these  attacks  are  only  repeated  once  or 
twice  a  week  ;  later,  they  reappear  daily,  and  as  many  as  twenty- live  to 
fifty  have  been  counted  in  a  day  (Herard).  Between  the  attacks  the  child's 
health  is  good  ;  fever,  cough,  and  loss  of  appetite  do  not  occur,  and  cachexia 
does  not  appear  till  late.  The  total  duration  of  the  malady  is  very  variable, 
but  its  limits  He  between  a  few  weeks  and  several  months  (Herard).  The 
prognosis  is  most  gloomy,  and  recovery  is  the  exception. 

The  symptomatic  spasm  in  the  adult  presents  some  differences.  The 
shape  of  the  larynx  and  the  resistance  of  the  interarytenoid  glottis  explain 
why  the  spasms  are  less  formidable  than  in  the  infant,  and  also  why  the 
inspiration  is  wheezing,  some  air  being  able  to  pass  through  the  glottis. 

Diagnosis. — Stridulous  laryngitis,  wliich  also  results  from  a  spasmodic 
contraction,  resembles  spasm  of  the  glottis  ;  but  the  former  attacks  children 
from  one  to  six  years  old,  while  the  latter  is  seen  between  the  ages  of  tliree 
and  twenty  months.  The  former  is  preceded  or  accompanied  by  catarrh, 
hoarseness,  cough,  and  coryza  ;  the  latter  comes  on  so  suddenly  that  asphyxia 
threatens  in  a  few  seconds. 

Hereditary  syphilis  often  produces  in  young  children  laryngeal  troubles 
which  are  so  like  spasm  of  the  glottis  that  I  am  convinced  that  in  many 
cases  (treatment  proves  the  point)  syphilis  is  the  cause. 

Treatment. — In  the  attack  the  face  should  be  sprinkled  with  cold  water 
and  friction  to  the  body  should  be  employed.  The  spasm  often  yields  when 
the  child  is  forced  to  breathe  through  the  nose.  Antispasmodics  are  indi- 
cated. Change  of  air  and  a  stay  in  the  country  are  advisable.  The  possi- 
bihty  of  hereditary  or  acquired  syphiHs  must  be  thought  of,  and  mercury 
and  iodides  employed. 


DISEASES  OF  THE  LARYNX  71 


X.  PARALYSIS  OF  THE  MUSCLES  OF  THE  LARYNX. 

Laryngeal  paralysis  may  be  classed  as  of  peripheral,  bulbar,  or  cerebral 
origin,  according  to  the  seat  of  the  lesion. 

Peripheral  Lesions. — The  laryngeal  nerves  may  be  directly  injured  by 
traumatism  (Neumann),  by  surgical  intervention,  and  by  compression. 
Compression  is  more  frequent  in  men  than  in  women,  and  afEects  the  left 
recurrent  nerve  more  often  than  the  right  (AvelUs).  It  may  be  due  to 
tumours  of  the  thyroid  body  or  of  glands,  abscess,  cancer  of  the  oesophagus, 
aneurysms  of  the  great  vessels  of  the  mediastinum  and  the  root  of  the  neck, 
pericarditis,  and  pleural  effusions.  Tumours  of  the  base  of  the  skull  and 
fractures  may  compress  or  injure  the  vagus  and  the  spinal  accessory  nerves. 
Tabes  and  diphtheria  are  accompanied  by  lesions  of  the  laryngeal  nerves, 
and  the  same  holds  good  in  certain  intoxications  and  infections  (alcoholism, 
saturnism,  morphinism,  syphilis,  and  diabetes).  Finally,  more  or  less  lasting 
paralysis  of  the  muscles  of  the  larynx  may  be  set  down  to  extra-  or  intra- 
cervical  action  of  cold. 

Bulbar  Lesions. — The  nuclei  of  the  spinal  accessory  nerves  may  be 
affected  by  the  following  lesions :  Syphilitic  growths,  tumours,  caries, 
softening,  hemorrhage,  acute  or  chronic  inflammation  of  the  bulb,  pachy- 
meningitis, disseminated  sclerosis,  amyotrophic  lateral  sclerosis,  labio- 
glosso-laryngeal  paralysis,  and  tabes. 

Cerebral  Lesions. — The  foot  of  the  third  frontal  convolution  (Garel),  the 
subjacent  white  matter  (Dejerine),  the  external  part  of  the  internal  capsule 
(Garel  and  Dor),  the  caudate  nucleus,  and  the  claustrum  (Picot  and  Hobbs), 
have  been  found  diseased  in  cases  of  laryngeal  palsies.  The  same  troubles 
may  be  due  to  hysteria,  or  may  be  provoked  by  suggestion. 

The  palsies  may  attack  several  groups,  a  single  group,  or  a  single  muscle.* 

Paralysis  of  the  Dilators. — Isolated  paralysis  of  the  posterior  crico- 
arytenoid muscles  is  very  rare  (Ziemssen),  though  it  has  recently  been  noted 
in  laryngeal  phthisis  (Gougenheim).  When  both  muscles  are  paralyzed,  the 
vocal  cords  no  longer  open,  but  fall  together  during  inspiration  from  the 
action  of  the  constrictor  muscles,  and,  since  very  little  air  enters  through 
the  glottis,  intense  dyspnoea  results.  Vocal  effort  is  possible,  and  tlie 
voice  is  slightly  altered  through  imperfect  fixation  of  the  arytenoids.  If  the 
paralysis  is  unilateral,  the  immobihty  of  the  vocal  cord  at  the  moment  of 
inspiration  may  be  seen  with  the  mirror. 

Paralysis  of  the  Constrictors. — Paralysis  of  the  constrictors  is  much  more 
common  tlian  the  preceding  form.  It  may  be  bilateral  (hysteria  and  diph- 
theria), but  is  more  often  unilateral,  and  almost  always  consecutive  to  a 

*  To  complete  this  study,  sco  p.  23  et  seq. 


72 


TEXT-BOOK  OF  MEDICINE 


direct  lesion  of  the  recurrent  or  of  the  spinal  accessory  nerves.  The  length 
of  the  course  and  the  relations  of  the  recurrent  nerves  explain  the  relative 
frequency  of  tliis  palsy.  The  causes  of  the  lesion  include  aneurysm  of  the 
carotid  artery  (Mackenzie),  double  paralysis  from  a  cancerous  tumour  at  the 
posterior  lacerated  foramina  (Tiirck),  cancer  of  the  recurrent  nerve  (Heller), 
double  paralysis  by  aneurysm  of  the  subclavian  and  innominate  vessels 
(Ziemssen),  aneurysm  of  the  arch  of  the  aorta  (numerous  cases),  cancer  of  the 

t 


Pig.   8. — Normal  Larynx  :  Appearance  of  the  Glottis  dttring  Deep 

Inspiration. 

E,  Epiglottis  ;  L,  base  of  the  tongue  ;  B,  ventricular  bands  ;  V,  ventricle  of  Mor- 
gagni  ;  R,  aryteno-epiglottic  fold  ;  A,  interarytenoid  region  (distended) ;  S,  cartilage 
of  Santorini  ;  W,  cartilage  of  Wrisberg  ;  C,  vocal  cords,  opened  to  their  maximum  ; 
F,  hyoid  fossa  ;  T,  trachea,  with  superposed  rings  ;  D,  bifurcation  of  the  bronchi. 


Fjg.  9. — Normal  Larynx  :  Appearance  of  the  Glottis  during  Phonation. 

The  vocal  cords  are  tense,  and  nearly  touching  in  their  anterior  two-thirds.  The 
cartilages  of  Wrisberg  and  of  Santorini  are  approximated,  and  the  interarytenoid  region 
is  partially  effaced.  The  epiglottis  is  straightened,  and  the  larjmx  is  elongated  in  the 
anteroposterior  direction. 

oesophagus  (Braune),  chronic  pleurisy  of  the  right  apex  (Gerhardt),  chronic 
'pericardial  effusions  (Baiimler),  and  mediastinal  tumours (Gueneau  de  Mussy). 
In  paralysis  of  the  constrictor  muscles  the  glottis  is  constantly  open,  so 
that  respiration  is  easy;  but  the  voice  is  lost,  and  effort  is  incomplete. 
These  symptoms  are  less  marked  when  the  paralysis  is  unilateral.  The 
laryngoscope  shows  that  both  cords  (or  one  of  them,  according  to  the  case) 
remain  immobile,  and  do  not  come  together. 


DISEASES  OF  THE  LARYNX 


73 


Paralysis  of  the  Crico-Thyroidei. — These  muscles  are  supplied  by  the 
external  lar\nigeal  nerve.  The  paralysis  induces  no  respiratory  trouble, 
because  the  dilator  muscles  are  intact.  Effort  is  complete,  because  the 
constrictors  are  healthy,  and  the  voice  is  not  completely  lost,  because  the 
other  muscles  of  phonation  are  intact ;  but  the  voice  is  altered,  and  dysphonia 
is  present,  because  the  tension  of  the  vocal  cords  is  insufficient,  and  thei' 


Fig.  10.- 


-Paralysis  of  the  Adductors  dttring  an  Effort  op 
Phoxation. 


The  lateral  cricoarytenoid  muscles  and  the  ary-arytenoid  muscles  are  paralyzed. 
The  vocal  cords  are  relatively  tense,  but  they  cannot  approximate  to  the  middle  line. 
The  orifice  of  the  glottis  is  triangular. 


Fig.  11. — Paralysis  of  the  Tensors:  Appearance  of  the  Glottis  dxtrinq  an 

Effort  of  Phonation. 

The  vocal  cords  appear  curved,  and  sometimes  beaded  at  their  free  edge,  and  the 
glottis  gapes  slightly.  This  appearance  corresponds  to  paralysis  of  the  cricothyroid 
muscle,  or  to  paralysis  of  the  elevator  muscles  of  the  larynx. 


vibration  is  incomplete  during  the  emission  of  sound.  This  paralysis  occurs 
in  hysteria.  It  comes  on  after  great  vocal  effort,  and  often  follows  a  chill, 
like  paralysis  of  the  facial  or  of  the  radial  nerve. 

Paralysis  of  the  Elevators. — In  order  that  the  crico-thyroid  muscles  may 
produce  the  tension  of  the  vocal  cords  necessary  for  phonation,  the  tiiyroid 
cartilage  must  be  fixed  above  and  in  front  by  the  elevators  of  the  larynx — 
i.e.,  genio-hyoid,  mylo-hyoid,  digastric,  stylo-hyoid,  and  thvro-hvoid  muscles. 
If  these  muscles,  wliich  are  chieHy  ititiervated  by  the  hypoglossal  nerve,  are 
paralyzed,  the  larynx  remains  depressed,  the  tension  is  incomplete,  and  the 


74 


TEXT-BOOK  OF  MEDICINE 


aphonia  is  almost  absolute.  The  voice  has  a  low,  monotonous  tone, 
due  to  the  passive  tension  of  the  vocal  cords  under  the  strain  of  the 
expired  air. 

Diagnosis — Prognosis — Treatment. — Laryngoscopic  examination  sim- 
plifies the  diagnosis  of  paralysis  of  the  larynx,  and  the  discovery  of  the 
paralysis  may  give  a  clue  to  its  cause.  Mediastinal  tumours  may  at  first  give 
no  symptoms  save  vocal  troubles  due  to  paralysis  of  one  vocal  cord  (compres- 
sion of  the  recurrent  nerve).  We  are  not  liable,  thanks  to  direct  examina- 
tion, to  mistake  paralysis  of  the  dilators  for  spasm  of  the  constrictors, 


Fig.  12. — Paralysis  of  the  Left  Recttbrent  Nerve:  Appearance  of  the 
Glottis  during  an  Effort  of  Inspiration. 

The  left  cord  reaches  beyond  the  middle  line,  being  pulled  over  by  the  overaction 
of  the  muscles  supphed  by  the  right  recurrent  nerve. 


Fig.  13. — ^Paralysis  of  the  Left  Recurrent  Nerve  :  Appearance  of  the 
Glottis  during  an  Effort  of  Phonation, 

The  left  vocal  cord  remains  in  the  cadaveric  position.    The  right  vocal  cord  passes 
slightly  beyond  the  middle  line,  and  is  alone  tense. 


although  in  both  cases  the  respiratory  troubles  are  almost  similar.  Again, 
paralysis  of  the  muscles  of  phonation  will  not  be  confounded  with  atrophy 
of  the  vocal  cords,  or  ankylosis  of  the  arytenoid  articulations,  though  the 
vocal  troubles  present  great  analogy.  For  similar  reasons,  laryngeal 
phthisis,  cancer,  and  polypi  of  the  larynx  can  be  excluded.  The  diagnosis 
between  paralysis  of  the  crico-thyroid  muscles  and  catarrhal  laryngitis  has 
been  given  in  the  description  of  the  latter  malady. 


DISEASES  OF  THE  LARYNX  75 

The  prognosis  is  only  grave  in  paralysis  of  the  dilator  muscles  (pos- 
terior crico-arytenoidei),  when  dyspnoea  may  be  so  acute  as  to  necessitate 
tracheotomy. 

Treatment  varies  with  the  cause  of  the  paralyses.  When  they  are 
primary,  electricity  is  the  best  curative  agent,  especially  in  paralysis  of  the 
crico-th}Toid  muscles.  The  voice  often  reappears  at  the  first  sitting.  Cure 
is  obtained  by  applying  the  electrodes  over  the  region  of  the  larynx,  or  even 
at  any  two  parts  of  the  body  (Kjishaber). 


CHAPTER  III 
DISEASES  OF  THE  BRONCHI 

I.  ACUTE  BRONCHITIS 

Acute  bronchitis  is  a  catarrhal  inflammation  of  the  large  and  medium-sized 
bronclii.  It  is  often  associated  with  inflammation  of  the  trachea,  and, 
indeed,  in  some  cases  tracheitis  is  the  chief  trouble.  Tracheo-bronchitis  is 
often  preceded  by  laryngitis,  and  "  The  cold  has  settled  on  the  chest "  is 
quite  a  common  saying. 

Inflammation  of  the  bronchioles  will  be  studied  later,  under  capillary 
bronchitis. 

Description. — Acute  bronchitis  shows  different  degrees  of  severity. 
Thus,  the  slight  form,  commonly  called  a  cold  on  the  chest,  is  almost  apyretic, 
and  is  only  accompanied  by  slight  malaise  and  headache.  The  cough  at 
first  is  painful,  dry,  and  spasmodic,  and  the  expectoration  is  serous  and 
greyish ;  but  later  the  cough  becomes  loose,  the  sputum  is  thick,  and  in  a 
week  the  illness  is  at  an  end. 

In  the  severe  form  bronchitis  begins  with  general  malaise,  shivering, 
and  fever,  which  rises  at  night.  The  patient  complains  of  headache  and 
loss  of  appetite.  The  breathing  is  wheezing  and  painful.  The  cough, 
which  is  at  first  dry,  causes  acute  pain  in  the  intercostal  muscles  and 
the  diaphragm,  and  is  often  followed  by  the  vomiting  of  mucus  or  of 
food. 

On  percussion,  the  resonance  of  the  chest  is  normal ;  on  auscultation, 
snoring  and  sibilant  rhonchi  are  heard  during  inspiration  and  expiration  on 
both  sides  of  the  chest  (because  bronchitis  is  always  double),  and  are  trans- 
mitted in  different  directions. 

These  initiatory  symptoms  last  from  three  to  five  days,  and  coincide 
with  the  immature  stage.  When  secretion  from  the  bronchial  mucosa 
(called  the  mature  stage)  replaces  the  dry  swelling  of  the  immature  stage, 
the  fever  falls,  the  breathing  becomes  easier,  the  cough  is  loose,  the  sputum 
thick  and  yellowish-green,  and  the  column  of  air,  instead  of  being  broken 
up  against  the  rough,  dry  mucosa,  meets  the  liquid  bronchial  secretion. 

76 


DISEASES  OF  THE  BRONCHI  77 

As  a  result,  the  rhonchi  change  to  rales,  which  acquire  the  timbre  of  bubbles 
bursting  in  a  liquid,  and  are  known  as  bubbling,  mucous,  or  SUbcrepitant. 
Mucous  rales  in  a  large  bronchus  may  simulate  the  gurgling  of  a  cavity  ; 
subcrepitant  rales  are  finer,  and  have  their  origin  in  the  smaller  bronchi. 
Unlike  rhonchi,  the  moist  rales  may  disappear  at  certain  spots  after  a  fit  of 
coughing  has  freed  the  bronchi  from  the  obstructing  mucus. 

The  second  stage  lasts  about  a  week,  during  which  improvement  gradually 
supervenes,  and  resolution  is  complete  in  about  a  fortnight.  The  urine  now 
becomes  abundant,  and  contains  much  sediment.  Slight  diarrhoea  often 
completes  the  crisis.  The  disease  may  become  chronic,  or  change  to  capillary 
bronchitis.  In  old  people  who  cannot  cough  up  the  secretion  bronchiti-; 
may  turn  to  suffocative  catarrh. 

^Etiology. — Acute  bronchitis  is  a  disease  of  cold  and  damp  weather,  and 
in  certain  predisposed  persons  it  appears  on  the  least  chill,  or  at  the  approach 
of  winter.  It  is  one  of  the  chief  elements  in  measles  and  influenza.  It  is 
less  frank  in  whooping-cough,  asthma,  and  hay-fever,  where  the  nervous 
element  is  so  much  in  evidence  that  the  inflammatory  element  is  much  less 
marked.  The  broncliitis  present  at  the  commencement  of  typhoid  fever  is 
rather  hypergemic  than  inflammatory,  though  it  may  turn  to  true  catarrh, 
and  become  a  troublesome  complication. 

Bronchitis  in  Bright's  disease  is  not  a  genuine  one,  and  its  special  char- 
acters depend  on  pulmonary  oedema  or  urajmic  dyspnoea.  The  same  remark 
applies  to  pseudo-bronchitis,  which  is  associated  with  heart  disease,  and  is 
especially  characterized  by  signs  of  congestion  and  stasis  in  the  lungs. 
Dust  and  irritating  vapours  may  produce  an  inflammation  of  the  bronchi, 
usually  associated  with  lesions  in  the  lungs. 

I  make  special  mention  of  syphilitic  bronchitis.  The  erythema  and  the 
catarrh,  so  frequent  in  the  larynx  during  the  first  years  of  infection,  also 
affect  the  trachea  and  the  large  bronchi.  This  subacute  tracheo-bronchitis 
is  Hable  to  relapse  from  exposure  to  cold.  Many  syphilitics,  formerly 
immune  to  chills,  complain  that  they  take  cold  easily,  and  suffer  from 
laryngitis  and  bronchitis.  They  are  always  liable  to  erythema  and  specific 
catarrhs  of  the  larynx,  the  trachea,  and  the  bronchi — catarrhs  which  are 
readily  excited  by  chills. 

Bronchitis  in  young  children  deserves  special  mention.  It  seems  some- 
times to  be  associated  with  teething  and  digestive  troubles,  and  in  this 
connection  the  Barillm  coli  has  been  said  to  play  a  prominent  part.  Even 
the  most  trifling  forms  of  bronchitis  in  young  children  may  be  compUcated  by 
congestion  of  the  lung.  The  temperature  rises,  and  we  hear  at  the  bases 
of  the  lungs  fine  rales,  which  lead  us  to  fear  the  onset  of  capillary  bronchitis. 
All  symptoms  subside,  however,  after  one  or  two  days  (Cadet  de  Gassi- 
court). 


78  TEXT-BOOK  OF  MEDICINE 

Diagnosis. — It  is  not  enough  to  diagnose  bronchitis,  for  that  is  quite 
simple ;  but  it  must  be  distinguished  from  conditions  which  may  simulate 
it ;  above  all,  its  cause  must  be  made  out,  as  the  different  forms  require 
absolutely  different  treatment.  SyphiUtic  bronchitis,  to  wit,  demands 
treatment  with  mercury  and  iodides  ;  bronchitis  in  Bright' s  disease  only 
improves  with  milk  diet ;  bronchitis  in  cardiac  cases  yields  to  the  treatment 
suitable  for  heart  diseases.  Bronchitis  in  tuberculous  patients  cannot 
always  be  diagnosed  by  a  study  of  the  symptoms  alone.  Its  tubercular 
origin  is  in  some  cases  doubtful  until  bacilli  are  found  in  the  sputum. 

Speaking  broadly,  apparent  broncliitis  which  does  not  begin  in  a  regular 
manner  must  be  suspected  ;  a  bronchitis  which  begins  with  fever  is  often 
spurious.  On  the  other  hand,  we  must  be  equally  suspicious  of  so-called 
bronchitis  in  which  cough  is  the  cliief  symptom,  to  the  exclusion  of  fever 
and  of  expectoration.  Because  an  individual  coughs  much,  we  must  not 
at  once  suppose  that  he  is  suffering  from  tracheo-bronchitis.  Hysterical 
persons  suffer  from  frequent  and  incessant  cough  mthout  having  bron- 
chitis. We  find  people  in  whom  the  taenia  and  other  worms  provoke  a 
cough  that  is  quite  wrongly  styled  bronchitis.  After  expulsion  of  the  tsenia 
the  cough  disappears. 

Bacteriology. — Bacteriology  cannot  help  us  in  classifying  bronchitis. 
The  microbes  which  inhabit  the  healthy  air-passages,  and  include  the 
Staphylococcus  alhus  and  aureus,  the  Streptococcus  pyogenes,  the  pneumo- 
coccus  and  the  pneumobacillus,  may  all  be  found  iii  bronchitic  sputa,  and 
are  in  no  way  specific.  Besides  these  microbes,  the  sputum  in  bronchitis 
often  contains  a  bacillus  identical  with  the  Bacillus  coli,  a  fungus  of  the 
genus  O'idium,  and  microbes  which  give  the  sputum  its  yellowish  or  greenish 
colour. 

Treatment. — In  sHght  cases  we  should  induce  sweating  by  diaphoretic 
drinks.  We  must  give  soothing  inhalations,  and  quiet  the  pain  and  the 
fits  of  cough  by  the  following  draught : 

R  Orange-flower  water    , .  . .         . .  . .  . .      iv. 

Syrup  of  chloral     1  oo  -«• 

a  c  I,-      "    •  •         •  •         •  •         •  •         • .     aa  qV. 

feyrup  or  morphia  j 

Cherry-laurel  water      . .  . .  . .  • .  . .     §u. 

Dose  :  For  an  adult,  a  tablespoonful  every  two  hours. 

In  the  severe  form  we  should  employ  stimulating  apphcations  (mustard- 
plasters  and  bUsters)  and  dry-cupping  to  the  chest.  If  the  bronchi  is 
much  choked,  especially  in  old  people,  emetics  must  be  given. 


DISEASES  OF  THE  BRONCHI  79 


II.  CAPILLARY  BRONCHITIS— BRONCHO-PNEUMONIA— 
LOBULAR  PNEUMONIA 

Discussion. — Should  the  temperature  rise,  the  respiration  become 
panting,  and  auscultation  show  fine  subcrepitant  rales  on  both  sides  of  the 
chest,  on  the  sixth,  seventh,  or  eighth  day,  in  a  child  sufiering  from  measles 
complicated  by  ordinary  bronchitis,  capillary  bronchitis  has  set  in.  The 
thermometer  soon  registers  104°  F.,  the  dyspnoea  becomes  acute,  and  the 
respiration  rate  rises  to  60,  while  dullness  and  tubular  breathing  are  found 
over  one  lung  or  at  both  bases.     Broncho-pneumonia  has  supervened. 

Another  child  has  reached  the  stationary  stage  of  whooping-COUgh 
without  accident.  In  spite  of  the  convulsive  cough,  fever  is  shght  or 
absent,  and  but  few  bronchitic  rales  are  heard  in  the  intervals  of  the  fits. 
Fever  then  appears ;  the  temperature  rises ;  the  character  of  the  cough 
changes,  being  more  continuous  and  less  convulsive ;  the  breathing  becomes 
panting,  and  on  auscultation  fine  scattered  rfdes  are  audible  on  both  sides 
of  the  chest.  Capillary  bronchitis  has  begun.  The  thermometer  now 
registers  104*^  F.,  the  cough  becomes  incessant,  the  dyspnoea  is  extreme, 
percussion  and  auscidtation  show  one  or  several  pneumonic  patches. 
Broncho-pneumonia  has  developed. 

In  another  cliild  suffering  from  croup,  who  has  or  has  not  been  operated 
upon,  the  situation  appears  quite  favourable.  The  fever  is  very  moderate, 
no  toxic  symptoms  are  present,  and  the  prognosis  is  good  ;  but  suddenly 
the  temperature  rises,  the  dyspnoea  grows  worse,  and  is  no  longer  of  laryngeal 
but  of  bronchial  origin.  Auscultation,  although  difficult,  because  of  the 
laryngeal  sounds,  reveals  fine  rales  in  the  chest.  This  condition  means 
capillary  bronchitis.  Then  the  thermometer  rises,  and  the  dyspnoea 
becomes  excessive.  The  dreaded  broncho-pneumonia  of  diphtheria  has 
set  m. 

In  an  infant  suffering  from  teething  or  from  gastro-intestinal  troubles 
a  broncliitis,  which  may  or  may  not  be  due  to  chill,  begins.  On  auscultation, 
large  broncliitic  rales  are  heard,  yet  so  far  there  is  little  fever  or  dyspnoea. 
The  fever  suddenly  increases,  the  dyspnoea  grows,  the  rales  become  fine  and 
scattered.  Capillary  bronchitis  is  beginning.  The  temperature  reaches 
104°  F.  ;  the  intensity  of  the  dyspnoea  becomes  acute  ;  auscultation  shows 
tubular  breathing  at  both  bases.     Broncho-pneumonia  has  supervened. 

In  an  adult  who  has  had  an  apparently  normal  influenza,  with  moderate 
fever,  broncliitis,  and  catarrhal  expectoration,  the  temperature  rises,  the 
dyspiKjea  grows  worse,  the  expectoration  becomes  muco-purulent,  and  on 
auscultation  rAles  of  all  kinds  are  audible.  These  symptoms  indicate 
influenzal  capillary  bronchitis.    A  step  further,  and  bronchial  breathing  is 


80  TEXT-BOOK  OF  MEDICINE 

perceptible  in  different  spots — or  at  both  bases.     Broncho-pneumonia  is 
present. 

These  different  examples  prove  that  we  find  not  a  "  single  broncho- 
pneumonia," but  "  broncho-pneumonias,"  which,  strictly  speaking,  may 
all  follow  bronchitis  from  cold,  though  they  most  often  supervene  in  the 
specific  infections  of  measles,  whooping-cough,  diphtheria,  influenza,  tuber- 
culosis, typhoid  fever,  erysipelas,  etc. 

In  some  cases  the  capillary  bronchitis  is  the  trouble,  especially  in  adults 
and  the  lobular  pneumonia  is  of  less  importance.  In  other  cases,  on  the 
contrary,  the  capillary  bronchitis  is  not  important,  but  has  joined  hands 
with  broncho-pneumonia,  which  is  then  the  chief  lesion. 

Bacteriological  research  in  broncho- pneumonia  permits  in  some  cases 
the  isolation  of  such  specific  bacilli  as  those  of  diphtheria,  typhoid  fever,  or 
tuberculosis,  but  these  specific  microbes  alone  are  not  sufficient  to  cause 
broncho-pneumonia.  They  are  not  always  found  in  the  foci  of  broncho- 
pneumonia, while  other  microbes  normally  present  in  the  mouth  or  the  air- 
passages  are  always  found.  These  microbes,  which  are  the  true  cause  of 
broncho-pneumonia,  are  the  Staphylococcus  alhus  and  aureus,  the  Strepto- 
coccus, the  Pneumococcus ,  the  Pneumobacillus ,  and  sometimes  the  Bac- 
terium coli.     They  increase  the  danger  and  make  the  prognosis  worse. 

We  can  now  begin  the  detailed  study  of  capillary  bronchitis  and  of 
broncho-pneumonia. 

Definition — History. — When  inflammation  affects  the  bronchioles,  the 
bronchitis  is  said  to  be  capillary.  In  ordinary  bronchitis  the  larger  bronchi 
are  alone  attacked,  and  therefore  the  air  can  circulate  freely,  in  spite  of  the 
lesions  present.  In  capillary  bronchitis,  on  the  contrary,  where  the  small 
bronchi  are  inflamed,  the  narrowness  of  the  tubes,  the  tliickening  of  their 
mucosa,  and  the  obstruction  by  morbid  products  prevent  the  free  passage 
of  air,  and  produce  dyspnoea,  which  too  often  ends  in  asphyxia.  This 
dyspnoea  is  such  a  marked  symptom  that  it  gained  for  the  malady  the  name 
of  suffocative  catarrh  at  a  time  when  neither  the  seat  nor  the  nature  of  the 
lesion  was  known  Avith  certainty.  Under  the  terms  "  suffocative  catarrh," 
"  peripneumonia  notha,"  and  "  false  inflammation  of  the  chest,"  Sydenham 
had  confused  bronchitis,  asthma,  and  emphysema.  His  successors  followed 
the  same  track,  and  Home,  all  through  his  work  on  membranous  exudates, 
found  the  explanation  of  every  kind  of  suffocative  bronchitis  in  the  false 
membranes.  Laennec  put  an  end  to  the  confusion,  and  showed  that  suffoca- 
tive catarrh  is  a  phlegmasia  of  the  bronchi,  but  he  attributed  its  extreme 
gravity  only  to  the  extent  of  the  lesions.  Andral  substituted  the  more 
correct  idea  of  the  seat  of  the  phlegmasia,  and  localized  the  lesions  of 
capillary  bronchitis  in  the  bronchioles.  The  works  of  Gendrin,  RilHet 
and  Bathez,  Fauvel,  Legendre,  and  Barrier  then  appeared,  and  it  may  be 


DISEASES  OF  THE  BRONCHI  81 

said  that  capillary  bronchitis,  as  now  established,  was  the  work  of  the 
French  school. 

Capillary  bronchitis,  however,  rarely  exists  in  a  pure  form.  More  often 
in  children — we  might  say  always — the  pulmonary  lobules  participate  in  the 
inflammation,  and  the  disease  takes  the  name  of  broncho-pneumonia 
(Seiffert),  or  of  lobular  pneumonia.  This  disease  often  follows  measles, 
whooping-cough,  and  diphtheria. 

Pathological  Anatomy. — In  a  child  who  has  died  of  capillary  bronchitis 
and  broncho-j^neumoma  we  see,  after  opening  the  thorax,  that  the  lungs  do 
not  collapse.  The  edges  and  the  apices  are  emphysematous.  The  posterior 
and  lower  part  of  the  lungs  is  bluish  or  brownish,  and  in  these  regions,  which 
are  dark  and  violet-coloured,  isolated  or  confluent  nodules  of  lobular  pneu- 
monia are  perceptible  both  to  sight  and  to  touch. 

Whether  capillary  bronchitis  exist  alone,  which  is  rare,  or  be  associated 
with  inflammation  of  the  pulmonary  lobules,  which  is  the  usual  condition, 
the  inflammation  of  the  small  bronchi  determines  two  kinds  of  lesions. 
The  former  affects  the  bronchi,  the  latter  the  corresponding  pulmonary 
lobules.  The  mucosa  of  the  bronchioles  is  swollen  and  smooth,  instead  of 
being  folded  longitudinally,  as  in  the  normal  state.  The  vessels  are  engorged 
with  blood,  and  allow  the  white  corpuscles  to  pass  out.  The  epitheUal  cells 
lose  their  cilia,  and  become  vesiculated  ;  they  desquamate  or  become  seg- 
mented, and  give  birth  to  new  elements.  The  glands  increase  in  size,  and 
allow  epitheUal  cells  and  muco-pus  to  escape  by  their  ducts.  The  sub- 
epitheUal  connective  tissue  is  infiltrated  with  leucocytes,  and  in  the  bron- 
chioles near  the  lobule  the  muscular  fibres  disappear,  owing  to  the  invasion 
of  embryonic  tissue. 

The  inflamed  bronchioles  are  enlarged  in  calibre.  These  acute  dilata- 
tions cliiefly  invade  the  smaller  bronchi,  and  we  see  broncliioles  which 
measure  a  centimetre  instead  of  1  to  2  millimetres  in  diameter.  The  dilata- 
tions are  usually  cylindrical,  sometimes  ampullary,  and  appear,  when  the 
lung  is  cut,  as  cavities  which  are  filled  with  pus.  They  may  be  isolated  or 
may  communicate  with  one  another.  These  dilatations  are  due  partly  to 
the  mechanical  action  of  secretions  driven  back  by  the  inspired  air,  but 
chiefly  to  the  diminished  resistance  of  the  inflamed  tissue,  which  is  deprived 
of  its  muscular  elements.  They  exist  in  the  broncho-pneumonia  of  young 
children,  but  may  disappear  with  the  cure  of  the  disease.  The  inflammatory 
products,  including  cells,  leucocytes,  and  fibrinous  exudate,  accumulate  in 
the  bronchi,  which  are  "  filled  or  almost  obhterated  from  the  branches  of 
the  second  size  to  the  smallest  ramiflcations  by  a  yellowish-white  sub- 
stance "  (Hardy  and  Behier). 

'J'his  obliteration  of  tli(!  small  bronchi  induces  changes  in  the  corre- 
sponding pulmonary  lobules.  These  changes  have  been  explained  as  follows: 

G 


82  TEXT-BOOK  OF  MEDICINE 

The  inspired  air  cannot  reach  the  lobules,  because  the  small  bronchi  are 
choked  with  inflammatory  products.  During  expiration,  however,  by  the 
help  of  coughing,  the  air  previously  contained  in  the  lobules  can  overcome 
the  resistance  of  the  plugs  which  act  as  valves,  and  close  the  lumen  of  the 
bronchi.  As  a  result,  the  infundibula  empty  themselves  of  the  contained 
air,  and,  as  this  air  is  not  renewed,  the  lobules  collapse,  and  cause  the  col- 
lapsed parts  to  look  hke  the  lung  of  a  foetus  which  has  never  breathed, 
whence  the  name  of  foetal  state  appUed  to  this  lesion  (Legendre).  There  is 
no  proof  of  the  absolute  truth  of  this  theory,  and  it  may  be  asked  if  the  air 
in  the  alveoli  is  not  simply  absorbed  there.  This  fact  would  explain  the 
production  of  the  foetal  state. 

The  foetal  state,  also  called  atelectasis,  or  pulmonary  collapse,  is  chiefly 
met  with  at  the  edges  and  the  base  of  the  lungs  in  young  subjects  with 
broncho-pneumonia.  The  collapsed  parts  are  bluish,  brownish,  or  violet- 
coloured,  and  do  not  crepitate  on  pressure.  The  cut  section  is  smooth  and 
miiform.  They  do  not  float  in  water,  and  although  they  may  have  this 
character  in  common  with  lobar  pneumonia,  they  differ  totally  in  that  they 
can  be  blown  out.  Under  the  microscope,  the  alveoh  are  seen  to  be  intact, 
but  the  vessels  are  gorged  with  blood.  This  stasis  causes  oedema,  and 
atelectasis  is  often  the  first  stage  of  splenization.  So  far,  having  in  view  only 
the  changes  proper  to  capillary  bronchitis,  I  have  described  two  lesions : 
the  first  active — that  of  the  bronchus  ;  the  second  partly  mechanical — the 
fcBtal  state  of  the  lung.     Let  us  study  the  lesions  of  broncho-pneumonia. 

The  diversity  of  the  lesions  complicates  the  description.  There  is  not 
one  lesion,  as  in  pneumonia,  and  the  morbid  process  is  not  homogeneous, 
but  comprises  bronchitis,  congestion,  hepatization,  splenization,  atelectasis, 
emphysema,  etc.  Sometimes  splenization,  at  other  times  hepatization,  is 
the  chief  factor,  and  as  these  expressions  will  often  recur,  it  will  be  well  to 
explain  their  meaning.  We  already  know  the  signification  of  atelectasis, 
or  the  foetal  condition.  Hepatization,  so  called  because  of  its  coarse  resem- 
blance to  liver  tissue,  is  the  result  of  the  inflammatory  process  which  affects 
certain  parts  of  the  lung.  Splenization,  so  called  because  of  its  coarse  resem- 
blance to  spleen  tissue,  results  from  lesions  which  are  rather  congestive  than 
inflammatory,  and  is  a  kind  of  epithehal  pneumonia.  Carnlfication,  so 
called  because  of  its  rough  likeness  to  muscular  tissue,  is  a  condition  of  the 
pulmonary  lobide  described  under  Chronic  Broncho-Pneumonia. 

More  exact  knowledge  as  to  the  structure  of  the  lung  has  led  us  to 
abandon  the  idea  that,  as  regards  structure  and  circulation,  the  bronchiole 
was  quite  independent  of  the  pulmonary  lobule.  Extension  of  inflam- 
mation from  the  one  to  the  other,  which  was  formerly  supposed  to  be  the 
exception,  is  really  the  rule,  so  that  any  lobular  pneumonia  may  be  pre- 
ceded or  accompanied  by  capillary  bronchitis.      The  bronchus,  so  to  say, 


DISEASES  OF  THE  BRONCHI  83 

carries  the  inflammation  to  the  lobule.  Inflammation  of  the  small  bronchi 
sometimes  precedes  the  outbreak  of  the  lobular  pneumonia ;  at  other  times 
their  appearance  is  almost  simultaneous.  Lobular  pneumonia,  or  broncho- 
pneumonia, was  called  catarrhal  when  it  was  supposed  to  comprise  only 
surface  lesions.  This  designation  is  insufficient,  for  the  lesions  of  lobular 
pneumonia  are  in  some  cases  deep  and  parenchymatous. 

The  lesions  affect  both  lungs,  and  by  choice  the  lower  lobes  and  their 
posterior  part.  The  islets  of  broncho -pneumonia  may  be  diffuse  or  con- 
fluent. In  the  former  event,  they  vary  in  size  from  a  pea  to  a  walnut,  and 
contain  one  or  several  inflamed  pulmonary  lobules.  They  are  scattered 
here  and  there  in  the  middle  of  lung  tissue,  which  may  be  healthy,  con- 
gested, bluish,  violet- coloured,  collapsed,  or  emphysematous.  This  form  is 
called  disseminated  lobular  pneumonia.  In  the  latter  event,  the  lesion 
involves  a  large  number  of  lobules,  and  may  even  affect  an  entire  lobe. 
The  disease  then  takes  the  name  of  confluent,  or  pseudo-lobar,  pneumonia. 
Besides  the  principal  lesion,  some  scattered  islets  are  also  found. 

In  the  disseminated  form  the  nodules,  which  are  of  variable  size,  and 
often  lozenge-shaped,  are  prominent,  hard,  and  red  in  the  congestive  period  ; 
they  are  greyish  in  the  next  stage,  because  of  the  pus  cells  in  the  alveoli, 
and  finaUy  become  yellowish  and  caseous. 

The  pseudo-lobar  form  differs  from  the  preceding  in  the  confluence  of 
the  nodules,  which  present  various  changes.  Near  a  nodule  in  which  pus 
is  forming  nodules  which  are  simply  congested  or  splenized  may  be  seen  ; 
consequently,  the  bulk  of  the  lung  presents  diversity  of  colour  and  of 
consistence. 

The  inflamed  lobules  are  often  superficial,  and  infundibula,  fiiUed 
with  beads  of  pus,  which  have  been  termed  purulent  graulations 
(Fauvel)  and  vacuoles  (Barrier),  are  sometimes  seen  on  their  surface. 
These  granulations  are  yellowish,  rounded,  as  large  as  a  pin's  head,  and 
most  common  on  the  surface  of  the  lung.  The  vacuoles,  which  have  the 
same  origin,  also  contain  pus,  but  are  larger,  because  the  alveolar  septa  are 
destroyed. 

On  section,  the  cut  surface  presents  a  less  granular  appearance  than  in 
lobar  pneumonia.  As  regards  the  minute  structure,  if  we  choose  a  well- 
inflamed  lobule,  and  make  the  section  at  right  angles  to  the  intralobular 
bronchus,  we  see  under  the  microscope — ■ 

1.  In  the  centre  the  bronchus  is  dilated  and  choked  with  cells  and  pus. 
The  walls  are  in  part  infiltrated  with  embryonic  cells,  and  have  lost  almost 
all  their  muscular  tissue.  These  points  are  best  seen  in  very  young  chiidi-en, 
but  the  lesion  is  curable.  The  bronchial  dilatation,  however,  does  not 
always  disappear,  and  broncho-pneumonia  may  lead  to  chronic  bronchi- 
ectasis. 

6—2 


84  TEXT-BOOK  OF  MEDICINE 

2.  Around  the  intralobular  bronchus  and  its  artery  a  zone  of  inflamed 
alveoli  and  ducts  is  found.  This  is  the  zone  of  hepatization,  also  called 
the  peribronchial  nodule  (Charcot). 

In  this  nodule  the  phases  of  engorgement,  and  of  red  and  grey  hepatiza- 
tion, can  be  seen.  The  lesions  of  engorgement  are  as  follows  :  Cut  surface 
smooth,  tissue  spongy,  red,  and  uniform ;  crepitation  has  disappeared ; 
tissue  sinks  in  water  ;  mider  the  microscope,  the  intralobular  bronchus  is 
seen  surrounded  by  distended  vessels,  which  are  crammed  with  red  cor- 
puscles ;  the  alveoH  contain  red  corpuscles  and  fibrino-albuminous  fluid. 
The  lesions  of  red  hepatization  are  as  follows :  On  section,  mottled  surface ; 
around  the  bronchus,  granulations  hke  those  of  lobar  pneumonia ;  under 
the  microscope,  alveoli  filled  with  leucocytes  and  fibrino- purulent  exudate ; 
walls  of  the  alveoh  infiltrated  with  leucocytes.  The  lesions  of  grey  hepatiza- 
tion are  :  Nodule  is  less  firm  on  section,  dry,  and  mottled  with  red  ;  fibrinous 
exudate  is  replaced  by  pus  ;  intralobular  connective  tissue  infiltrated  with 
leucocytes  ;  tissue  of  the  bronchus  and  the  peribronchial  nodule  often 
blended  in  a  puriform  sheet,  in  the  midst  of  which  the  pulmonary  artery 
appears  as  a  landmark.  The  peribronchial  abscess,  which  is  never  peri- 
lobular, is  formed  in  this  way. 

3.  Around  the  peribronchial  nodule  is  the  zone  of  splenization,  which 
is  smooth  on  section.  Splenization  is  characterized  by  lesions  wliich  are 
less  inflammatory  than  those  of  hepatization.  The  alveoh  contain  a  fibrinous 
exudate,  with  leucocytes  and  epithehal  cells,  derived  from  the  alveolar  walls, 
wliich  have  proliferated.  This  is  the  zone  of  epithelial  pneumonia  (Charcot). 
The  walls  of  the  alveoh  at  first  undergo  no  change  of  structure.  The  peri- 
lobular spaces  are  well  marked  by  the  inflammation,  but  the  suppuration 
does  not  affect  them. 

I  have  just  described  splenization  in  its  relations  to  hepatization  of  the 
pulmonary  lobule,  but  splenization  is  sometimes  the  chief  lesion  in  broncho- 
pneumonia, especially  in  the  pseudo-lobar  form,  nodules  of  hepatization 
being  absent.  The  splenized  lung  is  red,  cedematous,  heavy,  resistant, 
smooth  on  section,  and  filled  with  muco-pus,  wliich  comes  from  the  bronchi. 
"  This  splenization,  wliich  is  a  kind  of  epithelial  pneumonia,  might  well  be 
consecutive  to  the  obliteration  of  the  bronchi  "  (Charcot).  The  epithehal 
cells  of  the  alveoh  swell  and  desquamate,  the  congestion  is  intense,  albu- 
minous exudate  occurs  both  inside  and  outside  the  alveoli,  and  if  the  lesion 
persists  for  some  time  the  alveolar  epithelium  tends  to  become  cubical,  and 
the  peri-alveolar  connective  tissue  is  thickened.  Certain  parts  of  the  lung 
are  affected  by  inflammation  and  congestion,  independent  of  any  pneumonic 
process. 

The  peribronchial  nodule,  or  zone  of  hepatization,  is  associated  with 
phlegmonous  inflammation  of  the  intralobular  bronchus,  while  the  lesions 


DISEASES  OF  THE  BRONCHI  85 

of  splenization  are  associated  with  obliteration  of  the  bronchi  in  the  splenized 
areas. 

Whatever  be  the  form  of  the  broncho-pneumonia,  the  congestion  in 
generally  intense  in  both  sets  of  vessels,  though  it  is  most  marked  in  the 
bronchial  vessels.  Hsemorrhage  also  occurs  in  the  interior  of  the  pneu- 
monic nodules.  The  entire  lymphatic  system  may  be  involved,  the  bronchial 
glands  are  enlarged  and  congested,  the  intralobular  spaces  are  thickened, 
and  the  lymphatic  spaces  are  filled  with  white  corpuscles. 

Visceral  pleurisy  is  frequently  met  with  over  the  superficial  nodules  of 
lobular  pneumonia,  and  subpleural  haemorrhages  have  often  been  observed 
by  Parrot. 

Lastly,  in  those  who  have  died  from  broncho-pneumonia  emphysema  is 
often  seen,  especially  at  the  upper  lobes  and  the  anterior  borders  of  the 
lungs.  This  lesion,  joined  with  the  congestion,  explains  why,  post  mortem, 
the  lungs  appear  cramped  in  the  thorax.  Such,  then,  are  the  many  lesions 
of  broncho-pneumonia.  Changes  in  the  small  bronchi,  atelectasis,  spleniza- 
tion, hepatization,  haemorrhage,  emphysema,  combine  in  different  degrees 
to  produce  the  various  anatomical  types  which  I  have  just  described. 

Experimental  Broncho-Pneumonia. — While  lobar  pneumonia  is  difficult 
to  reproduce  in  animals,  broncho- pneumonia  may  be  readily  caused  in 
them. 

The  introduction  of  ammonia,  essence  of  turpentine,  and  perchloride  of 
iron  through  an  opening  in  the  trachea  produces  capillary  bronchitis  and 
broncho-pneumonia  in  animals.  The  same  result  is  obtained  by  section  of 
the  vagi  in  the  dog,  an  operation  which  favours  the  entrance  of  foreign 
bodies  into  the  bronclii  (Traube),  and  also  that  of  pathogenic  microbes. 
When  the  experiment  has  been  quite  successful,  the  lungs  of  the  animal 
present  all  the  lesions  previously  described  :  obstruction  of  the  inflamed 
bronchioles,  atelectasis,  splenization,  nodules  of  lobular  pneumonia,  and 
emphysema. 

Bacteriology. — Microbes  are  the  active  agents  in  broncho-pneumonia. 
It  has  been  found  possible  to  produce  broncho-pneumonia  in  animals  by 
injecting  into  the  trachea  cultures  of  different  microbes.  Several  species 
of  microbes  may  give  rise  to  broncho-pneumonia  in  man. 
table  gives  their  relative  frequency  in  adults  (Netter)  : 


Pneumococcus 
Streptococcus 
Encapsuled  bacillus 
Staphylococcus  pyogenes    . . 

These  various  microbes  are  often  associated.     The  pneumococcus  is  most 
important  in  adults,  the  streptococcus  in  children. 


The  following 

Per  Cent. 

38-47 

30-77 

2308 

7-68 

86  TEXT-BOOK  OF  MEDICINE 

Mosny  believes  that  the  anatomical  varieties  of  broncho-pneumonia 
correspond  to  the  particular  microbe — streptococcus  in  the  lobular,  pneumo- 
coccus  in  the  pseudo-lobar  form.     Netter  does  not  hold  this  opinion. 

These  different  microbes  are  often  found  in  the  mouths,  the  nasal  fossae, 
and  the  bronchi  of  healthy  persons.  Why  do  they  become  virulent  at 
certain  times  ?     I  do  not  know,  and  I  refrain  from  theories. 

In  broncho-pneumonia,  which  supervenes  in  the  course  of  diphtheria 
and  of  typhoid  fever,  the  specific  bacillus  of  these  maladies  may  be  found 
in  the  diseased  lung,  or  may  be  absent,  while  the  broncho-pneumonic  focus 
always  contains  the  other  microbes  previously  quoted.  The  specific  bacillus 
of  diphtheria,  of  typhoid  fever,  and  the  as  yet  unknown  microbes  of  other 
diseases,  do  not  therefore  appear  to  be  capable  'per  se  of  causing  broncho- 
pneumonia. Their  associates  must  be  present,  and  these,  the  real  cause  of 
broncho-pneumonia,  are  the  microbes  of  which  I  have  spoken  above.  It 
has  been  asked  if  bacteriological  examination  of  the  sputum  would  not 
throw  light  upon  the  prognosis  of  broncho-pneumonia  by  establishing  a 
scale  of  gravity  according  as  the  chief  pathogenic  agent  be  the  pneumo- 
coccus,  the  pneumobacillus,  or  the  streptococcus  ;  but  the  researches  under- 
taken on  this  subject  have  as  yet  given  no  positive  resu.lt. 

Symptoms — (a)  Capillary  Bronchitis. — The  symptoms  of  invasion — i.e., 
the  fever  and  the  elevation  of  temperature — are  more  marked  than  in 
simple  bronchitis.  The  fits  of  coughing  are  more  painful,  and  are  often 
followed  by  vomiting  of  mucus  or  of  food.  Dyspnoea,  which  is  rapid  in  its 
appearance,  is  the  chief  symptom  ;  indeed,  it  is  not  seen  with  such  severity 
in  any  other  acute  inflammation  of  the  bronchi  or  of  the  lung.  The  dyspnoea 
is  as  severe  as  the  suffocation  produced  by  the  false  membrane  of  croup  or 
by  oedema  of  the  glottis,  and,  indeed,  the  mechanism  is  much  the  same, 
for  in  both  cases  it  is  a  question  of  foreign  bodies  which  prevent  the  free 
passage  of  air :  only  in  disease  of  the  larynx  "  the  obstacle  occupies  the 
common  trunk  of  the  air- passages ;  in  capillary  bronchitis  it  is  diffused  in 
the  terminal  ramifications  of  the  tree  "  (Jaccoud).  The  dyspnoea  is  con- 
tinuous and  progressive.  It  is  not  interrupted  by  suffocative  attacks  and 
by  remissions,  as  in  the  diseases  of  the  larynx  to  which  I  have  alluded,  and 
soon  reaches  its  acme,  so  that  the  respiration  rate  may  be  50  in  an  adult 
and  80  in  a  child.  The  extreme  distress,  the  small  irregular  pulse,  the 
jerky  voice,  the  working  of  all  the  inspiratory  muscles,  the  violet  tint 
of  the  Ups,  the  pallor  of  the  face,  and  the  coldness  of  the  extremities,  bear 
witness  to  the  increasing  asphyxia. 

During  the  asphyxial  period  the  scene  is  heartrending.  The  patient 
sits  up  in  bed  ;  his  face  is  pale  and  covered  with  cold  sweat ;  his  body  is  bent 
forward  and  propped  up  by  his  arms  behind ;  he  tries  instinctively  to  help 
his  respiratory  muscles,  but  yet,  in  spite  of  all  Ids  efforts,  hsematosis  is 


DISEASES  OF  THE  BRONCHI  87 

imperfect,  and  the  blood  is  loaded  with  carbonic  acid  (anoxaemic  poisoning). 
This  toxic  stage  is  characterized  by  cardiac  weakness.  The  pulse  is  small 
and  intermittent,  the  face  becomes  livid,  the  urine  is  scanty,  and  delirium 
appears. 

When  capillary  bronchitis  ends  favourably,  recovery  is  announced  by 
the  ease  in  expectoration  ;  the  sputum  becomes  more  abundant,  yellowish, 
and  viscid  ;  the  fever  falls,  and  the  dyspnoea  gradually  diminishes.  Remis- 
sions, however,  must  be  mistrusted,  for  they  sue  sometimes  temporary,  and 
may  be  followed  by  fresh  inflammation. 

The  physical  signs  are  as  follows  : 

Percussion  of  the  chest  yields  normal  resonance.  Auscultation,  both 
during  inspiration  and  expiration,  gives  fine  subcrepitant  rales  scattered 
in  front  and  behind  over  both  sides  of  the  chest.  The  large  rales  of  ordinary 
bronchitis  are  often  heard.  Recamier  gave  the  name  bruit  de  tempSte  to 
these  sounds,  which  form  a  perfect  tumult.  The  sputum  is  composed  of 
the  tliick  purulent  exudate  from  the  small  bronchi,  and  of  a  frothy  secretion 
from  the  larger  bronchi.  In  children  there  is  no  sputum.  In  some  cases 
the  secretion  is  so  abundant  that  the  patient  repeatedly  fills  his  spittoon 
with  pus,  as  though  he  vomited  it. 

It  has  been  asked  if  capillary -bronchitis  can  be  quite  independent  of 
broncho-pneumonia.  It  may  be,  especially  in  an  epidemic.  Whether  the 
cause  be  cold,  influenza,  or  measles,  capillary  bronchitis  may  be  unaccom- 
panied by  broncho-pneumonia.  It  is,  however,  always  accompanied  by 
emphysema  of  the  antero-superior  parts  of  the  lung  and  by  splenization  of 
the  postero-inferior  parts.  We  may  also  find  yellow  granules,  subpleural 
ecchymoses,  and  congestive  foci  which  would  have  ended  in  broncho- 
pneumonia if  death  had  not  been  so  prompt. 

(6)  Broncho-Pneumonia. — This  malady  behaves  so  differently,  according 
to  age,  that  it  must  be  studied  separately  in  adults  and  in  children.  Broncho- 
pneumonia in  the  adult  presents  some  of  the  symptoms  which  have  just 
been  mentioned  under  capillary  bronchitis.  To  this  description  the  follow- 
ing symptoms  must  be  added:  The  temperature  rises  to  104:°  F.,  and  the 
sputum  may  be  streaked  with  blood,  but  is  not  rusty.  If  the  inflammation 
only  attack  isolated  lobules,  the  signs  on  auscultation  are  but  little  changed. 
If,  however,  tlio  lesion  occupy  a  large  surface,  and  especially  if  it  assume 
the  form  of  pseudo-Iobar  pneumonia,  dullness,  tubular  breathing,  and 
bronchophony  appear  simultaneously  at  the  seat  of  the  lesions,  although 
these  signs  are  not  so  severe  as  in  lobar  pneumonia. 

As  the  pneumonic  lesions  vary  in  intensity,  rough  bronchial  breathing 
may  be  heard  at  one  point  and  faint  tubular  breathing  at  another.  These 
lesions  are  usually  multiple,  and  invade  in  succession  several  regions  in  one, 
or  both  lungs,  but  es[)ecially  the  posterior  and  inferior  parts.     The  sibilant 


88  TEXT-BOOK  OF  MEDICINE 

and  the  mucous  rales  are  more  or  less  fine,  numerous,  and  scattered,  accord- 
ing to  the  concomitant  changes  in  the  bronchi.  In  children  broncho- 
pneumonia  is  frequent,  and  is  usually  a  very  serious  disease.  As  we  shall 
see  under  ^Etiology,  it  is  rarely  primary,  and  usually  supervenes  in  the  course 
of  simple  bronchitis,  or  appears  as  a  complication  of  measles,  whooping- 
cough,  diphtheria,  or  influenza.     In  infants  it  is  very  often  tubercular. 

As  a  rule,  high  temperature,  quick  pulse,  and  severe  dyspnoea  indicate 
the  invasion  of  broncho -pneumonia.  Dullness  and  more  or  less  harsh, 
tubular  breathing  indicate  the  part  of  the  lung  invaded.  If  the  lesion  is 
inflammatory,  it  takes  some  days  to  run  its  course ;  if,  however,  it  is 
congestive,  it  may  disappear  by  the  next  day,  and  reappear  at  another 
point,  which  fact  gives  to  broncho-pneumonia  an  appearance  of  mobility. 
Moreover,  as  the  inflammatory  and  hypersemic  lesions  of  the  lung  are 
differently  combined,  numerous  clinical  varieties  may  be  observed. 

Broncho-pneumonia  usually  matures  by  successive  outbreaks.  Some- 
times one  part  of  the  lung  is  attacked  before  another  part  has  cleared  up ; 
at  other  times  the  new  outbreak  supervenes  after  two  or  three  days  of  im- 
provement, which  made  recovery  appear  probable.  On  auscultation,  the 
tubular  breathing  is  in  part  masked  by  subcrepitant  rales.  It  is  not  rare 
to  find  several  foci  of  broncho-pneumonia.  They  are  usually  present  on 
both  sides,  and  more  often  at  the  base  or  the  middle  of  the  lung.  The 
existence  of  a  rub  or  of  aegophony  indicates  concomitant  pleurisy.  The 
little  patient,  who  is  breathless  and  excited,  utters  plaintive  cries,  and  the 
continual  working  of  the  alae  nasi  indicate  the  violence  of  the  dyspnoea. 
The  respiration  rate  may  reach  50,  60,  or  even  80  a  minute.  The  cough 
is  constant  and  overpowering,  the  face  is  pale,  the  lips  are  blue.  When 
broncho-pneumonia  is  of  moderate  intensity,  it  lasts  from  a  fortnight  to 
three  weeks,  and  ends  in  recovery.  We  see,  however,  cases  in  which  it 
carries  children  off  in  less  than  a  week,  and  also  fulminant  forms  wliich  are 
fatal  in  two  or  three  days. 

In  the  aged,  broncho-pneumonia  affects  different  forms.  In  the  acute 
form,  which  much  resembles  the  variety  in  an  adult,  we  find  violent  cough, 
progressive  dyspnoea,  muco- purulent  or  muco-sanguinolent  expectoration, 
with  multiple  rales  and  tubular  breathing.  In  the  suffocating  form  (suffoca- 
tive catarrh)  the  dyspnoea  rapidly  becomes  alarming  ;  the  expectoration  is 
scanty,  viscid,  and  sometimes  quite  airless  ;  the  pulse  is  small  and  irregular  ; 
the  vital  forces  quickly  fail ;  the  extremities  become  cold,  a  clammy  sweat 
appears,  and  the  patient  dies  in  delirium  or  coma. 

Course — Duration — Prognosis. — The  course  of  capillary  bronchitis  and 
of  broncho -pneumonia  has  been  divided  into  two  periods — the  one  dyspnoeic, 
the  other  asphyxial — while  the  two  together  may  last  from  one  to  three 
weeks.     This  division,  however,  is  artificial.     The  prognosis  is  most  grave. 


DISEASES  OF  THE  BRONCHI  89 

Death  is  common  in  children  and  old  people,  especially  when  the  disease 
occurs  in  an  epidemic  form,  and  when  it  breaks  out  in  a  children's  hospital 
as  a  sequel  to  whooping-cough,  measles,  and  diphtheria.  I  have  twice 
remarked  that  in  children  suffering  from  capillary  bronchitis  with  measles 
the  bronchitic  symptoms  improved  on  the  appearance  of  pneumonia,  as  if 
under  the  influence  of  a  natural  revulsive.  The  fine  scattered  rales  partly 
disappeared,  as  if  the  inflammatory  process  were  about  to  concentrate  itself 
at  certain  points.  It  seems  at  first  sight  as  though  the  localized  lesions 
could  be  easily  controlled,  but  new  foci  of  lobular  pneumonia  develop,  and 
after  several  alternations  in  the  course  of  events  the  termination  is  too  often 
fatal. 

In  favourable  cases  the  dyspnoea  mends,  the  fine  rales  disappear,  and 
improvement  is  gradually  established.  Sometimes  broncho-pneumonia 
shows  a  subacute  course,  and  may  finally  become  chronic.  This  course, 
although  it  be  rare,  is  especially  seen  in  the  pseudo-lobar  form,  where 
splenLzation  is  the  chief  lesion,  I  shall  refer  to  it  under  Clu-onic  Pneu- 
monia. 

Diagnosis. — The  diagnosis  between  capillary  bronchitis  and  acute 
tuberculosis  in  the  adult  is  given  later,*  Let  us  at  present  differentiate 
capillary  bronchitis  from  simple  bronchitis,  pseudo-membranous  bronchitis, 
pulmonary  oedema,  and  congestion  of  the  lung. 

The  sonorous  rhonchi  and  the  mucous  rales  of  simple  bronchitis 
show  no  resemblance  to  the  sharp,  fine  rales  of  capillary  bronchitis  ; 
the  slight  distress  in  the  former  is  quite  unlike  the  terrible  dyspnoea  of 
the  latter.  The  appearance  of  these  signs,  however,  in  the  course  of  a 
simple  catarrh  indicates  the  change  from  ordinary  to  capillary  bronchitis. 
Pseudo-membranous  l)ronchitis  may  occur  without  membranes  in  the 
larynx  and  the  pharynx.  The  membranes  which  line  the  ramifications  of 
the  bronchi  cause  fits  of  dyspnoea,  similar  to  those  of  capillary  bronchitis ; 
but  as  the  patient  i)rings  up  long,  branched  membranes,  tlie  diagnosis  is 
obvious.  (Edema  of  the  lung  alone,  or  associated  with  passive  congestion, 
is  seen  in  Bright's  disease,  in  mitral  and  tricuspid  lesions,  and  in  all  cases 
where  the  pulmonary  circulation  is  impeded.  Auscultation  reveals  fine 
subcrepitant  rales,  which  are  most  abundant  at  both  bases  ;  fever  is  absent, 
the  dyspn(JDa  is  intense,  and  the  expectoration  is  frothy,  albuminous,  and 
rosy,  when  the  case  is  one  of  superacute  oedema  of  the  lung. 

The  diagnosis  of  broncho-pneumonia  from  lobar  pneumonia  is  easy. 
Lobar  pneumonia,  as  a  rule,  appears  suddenly  in  healthy  persons,  and 
begins  with  stitch  in  the  side  and  shivering  ;  while  broncho-pneumonia  most 
often  develops  in  those  wjio  are  already  ill  (measles,  whooj>ing-r<»ugli, 
diphtheria,  influenza).  Lobar  pneumonia  is  nearly  always  unilateral  and 
*    Vide  Chapter  IV.,  Section  Hi. 


90  TEXT-BOOK  OF  MEDICINE 

characterized  by  crepitant  rales  and  tubular  breathing,  while  broncho- 
pneumonia affects  both  sides  of  the  chest  at  multiple  centres,  which  are 
more  or  less  extensive,  and  characterized  by  blowing  breathing  and  multiple 
rales.  In  lobar  pneumonia  the  cough  is  dry,  and  the  sputum  in  adults  is 
rusty ;  in  broncho-pneumonia  it  is  loose,  incessant,  overpowering,  and  the 
sputum  is  muco-purulent.  Genuine  pneumonia  usually  ends  from  the 
fifth  to  the  ninth  day,  and  its  termination  is  almost  always  favourable  in 
children ;  broncho-pneumonia  is  much  more  formidable,  and  lasts  week» 
or  even  months. 

If  the  reader  will  turn  to  the  chapter  on  Asthma,  he  will  see  that  certain 
febrile  forms  of  asthma,  especially  in  children,  may  at  first  sight  simulate 
capillary  bronchitis. 

The  diagnosis  of  broncho-pneumonia  from  acute  tuberculosis  is  often 
very  difficult.  Both  may  supervene  in  the  course  of  another  disease 
(measles,  whooping-cough) ;  in  both  we  find  extreme  dyspnoea,  high  tem- 
perature, early  cyanosis  of  the  face,  with  subcrepitant  rales  and  blowing 
breathing.  The  predominance  of  the  lesions  at  the  apices  and  the  presence 
of  blood  in  the  sputum  are .  presumptive  signs  in  favour  of  tuberculosis, 
and  the  presence  of  bacilli  is  a  certain  sign.  Sero-diagnosis  gives  valuable 
information. 

iffitiology. — Capillary  bronchitis  alone  is  hardly  ever  seen  except  in 
adults ;  broncho- pneumonia  is  especially  a  disease  of  infancy  and  old  age. 
Measles,  whooping-cough,  influenza,  diphtheria,  typhoid  fever,  erysipelas, 
cholera,  and  tuberculosis  in  infancy,  are  the  affections  in  which  broncho- 
pneumonia usually  appears.  I  refer  to  these  different  diseases  for  the 
study  of  the  special  characters  which  broncho -pneumonia  assumes  in  each. 
It  often  occurs  after  tracheotomy.  It  is  more  frequent  in  cold  weather, 
and  sometimes  assumes  an  epidemic  form. 

Suppurative  and  infectious  lesions  of  the  nasal  fossae  and  of  the  tlu'oat 
may  cause  broncho-pneumonia  by  descending  infection.  The  pathogenic 
agents  pass  through  the  larynx  and  the  bronchi  to  the  lungs  ;  in  some  cases 
the  lung  is  affected,  although  the  intermediary  air-passages  appear  free. 

Simjile  bronchitis  may  in  some  circumstances  be  followed  by  capillary 
bronchitis  and  broncho-pneumonia. 

Epidemics  of  broncho-pneumonia  have  been  noted  in  workmen  employed 
in  crushing  slag  diu*ing  the  manufacture  of  steel.  The  dust  and  the 
microbes  which  are  present  both  take  their  share  in  the  pathogenesis. 

Let  us  also  note  the  broncho-pulmonary  lesions  secondary  to  such  con- 
ditions of  the  nervous  system,  as  cerebral  hsemorrhage,  softening,  general 
paralysis,  mental  affections,  etc. 

Treatment. — In  capillary  bronchitis  and  broncho-pneumonia  the  indi- 
cations are  identical.     We  must  reduce  the  broncho-pulmonary  inflamma- 


DISEASES  OF  THE  BRONCHI  9J 

tion  and  favour  the  expulsion  of  the  secretions  which  block  the  bronchi. 
The  first  indication  will  be  attained  by  means  of  revulsives,  blood-letting, 
dry-  and  wet-cupping,  and  application  of  leeches.  Kermes,  repeated  emetics, 
ipecacuanha  alone,  or  with  tartar  emetic,  fulfil  the  second  indication. 

For  a  child  : 

I^t  Syrup  of  ipecacuanha  . .  . .  . .  . .     ^ii. 

Powdered  ipecacuanha       . .  . .  . .  . .     gr.  xv. 

Give  a  teaspoonful  or  a  dessertspoonful  every  five  minutes  till 
vomiting  occurs. 

For  an  adult : 

I^  Ipecacuanha  . .  . .  . ,  . .  . .     gr.  xx. 

Tartar  emetic  . .  . .  , .  . .  . .     gr.  i. 

Divide  into  two  doses,  give  at  five-minute  intervals,  and  make  the 
patient  drink  tepid  water  to  assist  vomiting. 

For  the  fits  of  coughing  and  the  pain  the  following  draught  will  be  useful : 
For  an  adult : 

J^  Orange -flower  water  . .          . .          . .          . .     5iii- 

Syrup  of  chloral   1  

byrup  oi  morphiaj 

Cherry-laurel  water  . .          . .          . .          . .      3ii. 

A  tablespoonful  to  be  taken  every  three  hours. 

Inhalations  of  oxygen  are  of  some  use  in  asphyxia.  Lastly,  the  strength 
of  the  patient  must  be  carefully  supported  by  broths,  tonics,  and  alcohol. 
A  child  two  years  old  can  take  during  the  day  a  draught  containing 
25  grammes  of  sherry  and  15  centigrammes  of  acetate  of  ammonia. 

Baths,  both  cold  and  hot,  have  been  extolled  (Renaut).  This  treatment 
cannot,  and  ought  not,  to  be  systematic.  In  a  case  with  marked  fever, 
very  high  temperature,  and  an  ataxic  tendency,  baths  at  75°  F.  are  to  be 
used.  In  a  case  with  great  broncliial  embarrassment,  much  dyspnoea,  and 
an  adynamic  tendency,  hot  baths  are  preferable. 

Injections  of  serum,  in  amount  appro]iriate  to  the  age  of  the  patient, 
may  be  used  with  advantage  {vide  appendix  on  Therapeutics). 

Prophylactic  treatment  must  not  bo  neglected,  and  children  who  are 
predisposed  to  colds  and  bronchitis  must  not  be  allowed  to  come  near  those 
suffering  from  broncho-pneumonia. 

III.  CHRONIC  BRONCHITIS. 

etiology — Description.—  Altliough  chronic  bronchitis  may  be  primary, 
it  is  often  associated  with  constitutional  maladies.  In  lymphatic  and 
scrofulous  subjects,  in  gouty  persons,  and  those  affected  with  skin  Icsioas, 


92  TEXT-BOOK  OF  MEDICINE 

and  in  old  people,  bronchitis  may  be  chronic  from  the  first,  or  follow  upon 
more  or  less  acute  attacks.  Clironic  bronchitis  is  most  prevalent  during 
cold,  damp  weather,  and  chills  provoke  acute  attacks,  which  have  a  very- 
bad  effect  upon  the  disease. 

Chronic  bronchitis  is  characterized  by  long  and  painful  fits  of  coughing, 
which  are  frequently  repeated,  especially  in  the  morning  and  the  evening. 
Animated  conversation  or  a  quick  walk  may  bring  on  a  fit  which  is  often 
followed  by  abundant  expectoration.  The  sputum  is  thick,  greenish- 
yellow,  and  often  mixed  with  froth.  More  rarely  the  expectoration  is 
scanty,  and  the  balls  of  sputum  have  the  consistence  of  starch  (dry  catarrh). 
The  breathing  is  wheezing  and  difficult.  On  auscultation,  snoring  and  sibi- 
lant rhonchi  and  large  bubbling  rales  are  heard  over  both  sides  of  the  chest ; 
they  may  be  so  abundant  as  to  simulate  the  gurgling  of  a  cavity.  There  is 
no  fever,  the  appetite  is  scarcely  affected,  and  the  dyspnoea  is  slight,  apart 
from  the  fits  of  coughing.  Chronic  bronchitis  has  no  fixed  course  ;  it  lasts 
several  months,  improves  in  fine  weather,  but  reappears  with  the  first 
cold. 

In  artlu-itics  subject  to  skin  lesions,  such  as  eczema  or  lichen,  it  is  not 
rare  to  see  a  certain  alternation  between  the  cutaneous  and  the  bronchitic 
troubles. 

Chronic  bronchitis  usually  leaves  behind  it  pulmonary  emphysema,  but 
the  patient  may  live  indefinitely  till  complications  change  the  situation. 

These  complications  are  of  various  kinds.  Some,  sudden  in  their  appear- 
ance, comprise  pulmonary  congestions,  which  cause  attacks  of  dyspnoea  and 
acute  broncho-pulmonary  inflammations,  which  create  immediate  danger  ; 
others,  slow  in  their  development,  are  pulmonary  emphysema  and  lesions 
of  the  right  heart,  which  give  rise  to  increasing  difficulty  in  breathing, 
cyanosis,  and  general  oedema. 

Dilatation  of  the  bronchi  is  also  one  of  the  consequences  of  chronic 
bronchitis.  In  feeble  subjects,  especially  elderly  ones,  who  have  no  longer 
strength  to  expel  the  secretion  in  the  bronchi,  clu-onic  catarrh  may  change 
into  a  suffocative  one. 

In  the  course  of  bronchitis  the  breath  and  the  expectoration  may  some- 
times become  foetid.  This  foetor,  which  may  last  weeks  and  months,  is 
due  to  decomposition  of  the  bronchial  secretions,  to  the  presence  of  butyric 
acid  (Laycock),  or  to  gangrene  of  the  mucosa,  which,  however,  is  not  so 
serious  as  gangrene  of  the  lung. 

Certain  persons  suffering  from  chronic  bronchitis  may  bring  up  for 
months  and  years  branched,  and  often  cylindrical,  membranes.  These  may 
measure  from  4  to  6  inches  in  length,  are  whitish,  elastic,  and  chiefly  com- 
posed of  mucine.  They  must  not  be  confused  with  diphtheria  of  the 
bronchi. 


DISEASES  OF  THE  BRONCHI  93 

Diagnosis. — Chronic  catarrh  of  the  bronchi  must  not  be  confounded 
with  spurious  bronchial  inflammation,  which  is  only  an  episode  in  the 
course  of  some  other  disease.  In  people  suffering  from  cardiac  disease 
(mitral  lesions),  the  broncho-pulmonary  circulation  is  easily  impeded,  and 
congestion  and  oedema  of  the  respiratory  passage  are  the  result.  Multiple  rales 
are  heard  on  auscultation,  and  the  distress  sometimes  takes  the  form  of  fits. 
If  the  cardiac  lesion  is  not  recognized,  these  different  troubles  are  set  down 
to  chronic  bronchitis  until  other  symptoms  call  attention  to  the  true  cause. 

The  same  remark  applies  to  bronchitis  in  patients  with  Bright's  disease. 
A  patient  complains  of  distress  and  suft'ocation,  accompanied  by  cough  and 
expectoration.  On  listening,  we  find  mucous  rales  on  both  sides  of  the 
shest,  usually  most  abundant  at  the  bases.  A  superficial  examination 
would  readil}  lead  to  the  idea  of  subacute  or  chronic  catarrh,  but  a  minute 
interrogation  reveals  other  important  signs.  The  patient  has  frequent 
micturition,  his  eyelids  are  puffy,  the  heart  is  hypertrophied,  and  we  find 
a  gallop  rhythm  (Potain) ;  the  urine  is  albuminous ;  and,  in  short,  the 
so-called  bronchitis  is  only  an  episode  in  Bright's  disease. 

We  shall  see  later  that  chronic  bronchitis  is  often  associated  with  asthma, 
dilatation  of  the  bronchi,  and  emphysema.  It  precedes  or  follows  them, 
and  may,  especially  in  asthmatics,  become  the  chief  trouble,  so  as  to 
mask  the  real  nature  of  the  disease. 

Pathological  Anatomy. — The  diseased  bronchi  are  thickened,  and  the 
connective  tissue  of  the  mucosa  is  mvaded  by  fibrous  tissue,  which  some- 
times forms  prominent  vegetations.  It  is  not  rare  to  meet  with  superficial 
ulcerations  at  the  glandular  openings.  Emphysema  Ls  often  seen  as  a 
complication. 

Treatment. — The  end  in  view  is  to  dry  up  the  secretion  and  modify 
the  secreting  parts.  CVeosote  (Bouchard),  iodoform  (See),  aijd  essence  of 
turpentine  give  good  results.  These  different  medicaments  may  be  ad- 
ministered by  the  respiratory  passages  as  vapours  (inhalation-rooms),  and 
sprays  (atomizers),  or  by  the  digestive  tract. 

The  following  formulae  relate  to  the  adminLstration  of  these  remedies  : 

Capsules  of  creosote,  each  containing  1  minim.  Dose,  4  to  8  with  each 
meal. 

Perles  of  essence  of  turpentine,  each  containing  4  minims.  Dose,  4  to  G 
with  each  meal. 

Pills  of  iodoform,  each  containing  1  grain.  One  pill  to  be  taken  with 
each  meal. 

Capsules,  containing  4  minims  of  copaiba  and  4  minims  of  tar.  Dose, 
J  to  8  with  each  meal. 

Terpenc  may  be  employed,  givhig  daily  G  to  13  pills,  each  containing 
]  ^  minims,  amounting  to   from   10  to    15  minims  in  twenty-four  hours. 


94  TEXT-BOOK  OF  MEDICINE 

Good  results  may  be  obtained  with  eucalyptol,  given  in  doses  of  from  4  to 
10  capsules  daily. 

Arsenic  and  sulphur  should  be  used  with  these  different  remedies.  The 
sulphur  cures  of  Saint-Sauveur,  Luchon,  and  Cauterets,  and  the  arsenical  ones 
of  Mont-Dore  and  La  Bourboule,  will  be  of  much  service.  I  often  prescribe 
Labassere  water,  taken  in  the  morning,  fasting.  The  dose  is  4  table- 
spoonfuls  in  hot  milk.  In  old  people  especially  the  blocking  of  the  bronchi 
by  secretion  must  be  carefully  watched,  and  combated  by  means  of  repeated 
emetics. 

The  patient  who  suffers  from  chronic  bronchitis  should  avoid  chills  and 
pass  the  winter  in  a  temperate  cUmate. 

IV.  DILATATION  OF  THE  BRONCHI— BRONCHIECTASIS. 

Pathological  Anatomy. — When  we  read  the  chapter  which  Laennec 
devoted  to  dilatation  of  the  bronchi,  and  consider  that  this  subject  was 
previously  untouched,  we  are  astonished  at  his  great  accuracy. 

The  lesions  fomid  post  mortem  are  usually  multiple,  because  dilatation 
of  the  bronchi  is  accompanied  by  chronic  broncho-pneumonia,  fibrosis  of 
the  lung,  chronic  pleurisy,  with  adhesions  and  pulmonary  emphysema — 
lesions  which  are  more  or  less  marked  according  to  the  case.  On  openmg 
the  chest,  the  lungs  do  not  collapse  ;  in  certain  parts  they  are  indurated, 
carnified,  and  hepati^ed,  and  their  surface  is  mottled  and  cyanotic.  In 
some  cases  a  lobe  is  atrophied  and  cirrhotic.  The  lesions  of  recent  acute 
broncho-pneumonia  are  not  rare.  In  some  cases  the  dilatations  appear  on 
the  surface  of  the  Imigs  ;  in  others  they  are  only  seen  on  section  in  the  depth 
of  the  organ.  The  large  bronclii  are  rarely  dUated ;  bronchiectasis  occurs 
chiefly  in  the  third  and  fourth  order  of  bronchi,  which  are  2  to  3  millimetres 
in  diameter. 

The  pathological  anatomy  of  the  dilated  bronchi  comprises  their  shape, 
structure,  and  situation. 

The  shape  is  variable.  Uniform  dilatation,  the  rarest  form,  affects 
the  whole  length  of  the  bronchus,  the  calibre  alone  being  altered.  Monili- 
form  dilatation  (Cruveilhier),  by  its  successive  swellings,  gives  the  bronchus 
the  appearance  of  a  string  of  beads.  Ampullary  dilatation  is  the  commonest 
form,  and  is  made  up  of  cavities  which  may  be  isolated,  like  a  cyst,  or 
commmiicate  with  neighbouring  dilatations.  In  the  latter  case,  the  invaded 
area  resembles  the  auricle  of  the  heart,  or  an  alveolar  mass  in  which  the 
septa  are  formed  by  the  atrophied  and  fibrous  lung  tissue. 

Ampullary  dilatation  has  different  forms,  accordmg  as  the  enlargement 
invades  the  lateral  parts  of  the  bronchus,  or  an  entire  segment.  These 
enlargements,  or  bronchial   aneurysms,  have  been   compared  to   aortic 


DISEASES  OF  THE  BRONCHI  95 

aneurysms — a  comparison  which  is  the  more  justified  as  it  is  the  change 
in  the  bronchial  wall  which  is  chiefly  responsible  for  the  swelling.  The 
dilatations  vary  in  size  from  a  pea  to  a  pigeon's  egg  ;  the  peripheral  portion 
of  the  bronchus,  which  is  usually  atrophied,  terminates  in  a  cul-de-sac,  but  it 
may  in  exceptional  cases  be  dilated  into  a  kind  of  cyst  on  the  surface  of  the 
lung  (Gombault).  The  different  forms  which  I  have  described  may  be 
found  combined  in  the  specimen. 

The  structure  of  the  dilated  bronchus  varies  according  to  the  stage  of 
the  lesion.  Where  the  lesion  is  but  little  advanced,  the  mucosa  of  the 
cavity  is  almost  healthy,  and  is  continuous  with  that  of  the  bronchus  ; 
the  cylindrical  epithelium  remains  ;  the  glands  are  atrophied  ;  the  submucous 
connective  tissue  has  lost  some  of  its  elastic  folds ;  and  the  muscular  fibres 
are  much  separated,  but  rarely  destroyed. 

When  the  lesion  is  very  advanced,  the  bronchi  have  quite  lost  their 
normal  structure  ;  the  mucosa  is  no  longer  wrinkled,  because  the  elastic 
fibres  have  disappeared  ;  the  cylindrical  epithelium  (jjropulsive)  is  replaced 
by  pavement  (protective)  epithelium ;  the  mucosa  is  covered  with  villi, 
wliich  are  composed  of  embryonic  tissue  and  vessels.  The  muscular  layer 
is  converted  into  embryonic  tissue  with  new  vessels  ;  the  cartilages  also 
return  to  the  embryonic  state,  and  are  infiltrated  with  calcareous  salts. 
The  elastic  fibres  of  the  connective  tissue  are  broken  up,  and  no  longer  form 
a  complete  ring  around  the  bronchus.  The  connective  tissue  forms,  so  to 
speak,  the  skeleton  of  the  diseased  bronchi.  The  capillary  vessels  are  number- 
less, tortuous,  and  dilated  ;  they  present  swellings  of  every  shape,  and  project 
into  the  cavity  of  the  bronchus.  This  capillary  network  is  especially  de- 
veloped in  the  villi  and  in  the  layers  adjoining  the  lumen  of  the  bronchus. 
The  vessels  anastomose  in  every  direction  and  form  a  cavernous  tissue. 

In  the  lesions  of  bronchiectasis  there  are,  then,  two  kinds  :  the  one — 
neo-formative — ends  in  the  development  of  embryonic  and  vascular  tissue  ; 
the  other — destructive — causes  a  loss  of  normal  tissue  (Hanot). 

In  certain  cases  ulceration  occurs,  and  the  surface  of  the  cavity  may  be 
attacked  with  "  a  superficial  curable  gangrene,  which  is  analogous  to  the 
death  of  connective  tissue  in  phlegmon."  The  liquid  in  the  dilated  bronchi 
is  composed  of  mucus  and  pus  in  variable  proportions  ;  it  contains  crystals 
of  margarine  and  of  cholesterine,  and  its  mawkish  odour  becomes  foetid  in 
cases  of  gangrene.  When  a  dilatation  has  lost  its  connections  with  the  parent 
bronchus,  it  becomes  filled  with  a  caseous  mass,  and  looks  like  an  isolated  cyst. 

Bronchiectasis  chiefly  affects  the  apex  of  the  lung  wlien  the  dilatation 
is  nioniliform,  while  it  more  often  occurs  at  the  periphery  when  the  swelling 
is  anipullary.  The  dilatations  are  more  frequent  on  the  left  side  than  on 
the  right,  and  affect  one  lung  only  in  the  proportion  of  20  to  4  (Bjirth). 
Bronchiectasis  is  always  accompanied   by  clu'onic  inflammation  of    the 


96  TEXT-BOOK  OF  MEDICINE 

tissues — i.e.,  peribronchitis,  fibrosis  of  the  lung,  and  chronic  pleurisy — but 
the  origin  of  these  tissues  of  new  formation  has  not  been  completely  eluci- 
dated. According  to  recent  researches,  the  tissue  of  the  chronic  pneumonia 
which  accompanies  bronchiectasis  is  said  to  arise  solely  in  the  fibro- 
vascular  framework  of  the  lung,  while  the  epithelium  of  the  parenchyma 
takes  no  part,  and  the  pulmonary  tissue  itself  disappears  by  reason  of  the 
marked  diapedesis  which  gives  rise  to  the  new  fibrous  tissue.  "  The 
parenchyma  of  the  lung  is  transformed  into  granulation  tissue,  which  finally 
forms  adult  connective  tissue,  more  or  less  studded  with  vascular  neoplasms, 
according  to  the  age  of  the  lesions.  According  to  their  more  or  less  advanced 
organization  into  fibrous  tissue,  we  may  see  the  splenization,  the  carnification, 
and  the  areolar  state  of  the  parts  of  the  lung  which  surround  the  dilated 
bronchus."  Emphysema  often  accompanies  bronchiectasis.  Hypertrophy  of 
the  bronchial  glands  is  sometimes  seen,  and  tuberculosis,  which  was  regarded 
as  rare  (Barth),  appears  to  be  fairly  often  associated  with  bronchiectasis 
(Grancher). 

etiology. — Bronchiectasis  is  a  disease  of  middle  and  advanced  age.  It 
may  result  from  acute  bronchitis  or  broncho-pneumonia,  but  more  often  it 
follows  clironic  bronchitis,  or  broncho-pneumonia  which  has  not  cleared  up, 
and  is  consecutive  to  measles,  whooping-cough,  mfluenza,  or  typhoid  fever. 
In  some  cases  the  aetiology  completely  escapes  our  grasp. 

The  chief  theories  of  the  pathogenesis  of  bronchiectasis  are  : 
Laennec :  Accumulation  of  secretion  in  the  bronchi,  and  consequent 
enlargement  of  these  channels. 

Andral :  Alteration  in  nutrition  and  diminished  elasticity  of  the  walls 
of  the  bronchi. 

Corrigan  :  Fibrosis  of  the  lung,  the  retractile  tissue  of  which  puUs  upon 
the  walls  of  the  bronchi. 

Stokes  :  Paralysis  of  the  muscular  fibres  and  diminution  in  the  resistance 
of  the  bronchi. 

Mendelssohn:  Pressure  exerted  by  the  air  upon  the  diseased  bronchi 
during  fits  of  coughing. 

Gonbault  admits  the  union  of  these  different  processes. 
Barth  adds    chronic    pleurisy,  acting,  like  pulmonary  fibrosis,  by  its 
retractile  tissue. 

Which  of  these  theories  are  we  to  adopt  ?  Any  morbid  state  capable  of 
producing  faulty  nutrition  of  the  bronchi  (acute  and  chronic  bronchitis), 
and  any  formation  of  extrabronchial  fibrous  tissue,  might  favour  or  produce 
bronchiectasis.*  I  admit  the  fact,  but  we  must  assign  the  proper  value  to 
each  of  these  factors. 

*  Paludism  appears  to  act  in  this  way  in  developing  interstitial  pneumonia.  The 
cases  of  Frerichs,  Lanceieaux,  and  Grasset,  are  quite  conclusive  (These  de  Grasset, 
MontpeUier,  ISTi). 


DISEASES  OF  THE  BRONCHI  97 

It  seems  to  me  that  we  have  exaggerated  the  role  of  chronic  pneumonia 
and  of  pleurisy — in  short,  of  fibrous  tissues — when  we  look  on  them  as 
retractile,  and  capable  of  producing  bronchiectasis  by  mechanical  action. 
There  are  cases,  it  is  true,  in  which  the  action  of  the  extrabronchial  fibrous 
tissue  appears  evident  ;  perhaps,  too,  the  bronchial  and  extrabronchial 
lesions  develop  on  parallel  lines,  but  the  present  tendency  is  to  admit  that 
the  pulmonary  lesion  which  accompanies  the  bronchial  dilatation  is  most 
often  the  consequence,  and  not  the  cause,  of  the  lesions  in  the  bronchus. 

The  phlegmasia  begins  in  the  bronchus  ;  it  then  extends  around  the 
bronchus,  reaches  the  neighbouring  pulmonary  tissue,  and  thus  gives  rise 
to  a  systematic  fibrosis.  The  proof  that  events  mast  follow  this  course  is 
that  chronic  lobar  pneumonia  is  not  accompanied  by  bronchial  dilatation, 
because  the  bronchus  does  not  take  part  in  the  morbid  process  (Charcot), 
while  bronchial  dilatations  are  found  in  lobular  or  broncho- pneumonia, 
because  the  bronchus  is  always  much  altered.  Therefore,  whether  there 
may  or  may  not  be  pulmonary  or  pleural  fibrosis,  the  lesion  of  the  bronchus 
is  the  necessary  fact  that  is  indispensable  to  the  production  of  bronchi- 
ectasis. By  reason  of  the  bronchial  lesion  the  bronchus  loses  its  normal 
elements,  the  elastic  and  muscular  fibres  give  place  to  embryonic  and 
vascular  tissue  which  have  no  resisting  power,  and  the  bronchus  dilates  at 
its  weak  spot  like  an  artery,  the  altered  wall  of  which  permits  the  formation 
of  an  aneurysm. 

It  has  been  asked  if  there  might  not  be  some  special  condition  capable  of 
preparing  the  way  for  enlargement  of  the  diseased  bronchus,  and  arterio- 
sclerosis of  the  bronchial  arteries  has  been  suggested.  In  a  case  recently 
reported  by  Hanot  arterio-sclerosis  of  the  bronchial  arteries  was  very 
marked. 

Symptoms. — Bronchiectasis  shows  itself  by  the  following  symptoms  : 
The  cough  is  fretjuent  and  spasmodic,  as  in  chronic  bronchitis,  which  often 
precedes  dilatation.  The  expectoration  becomes  abundant,  so  that  patients 
brmg  up  daily  4  to  12  ounces  of  muco-purulent  fluid,  with  a  mawkish  and 
sometimes  fcetid  smell  (bronchorrhoea).  If  the  sputum  is  examined  in  the 
spittoon  when  its  superficial  layer  alone  is  visible,  it  is  frothy  and  aerated ; 
but  if  it  is  put  in  a  measure-glass,  it  will  be  seen  to  have  an  opaque  lower 
layer,  which  contains  pus  corpuscles,  epithelial  cells,  and  crystals  of  chole- 
sterine  or  oi  margarine.  The  expectoration  may  be  uniformly  divided 
through  the  course  of  the  day.  Some  patients,  however,  empty  their 
dilated  bronchi  three  or  four  times  daily  ;  they  are  seized  by  fits  of  coughing 
or  straining,  like  a  fit  of  vomiting,  and  bring  up  each  time  2  or  3  ounces  of 
muco-purulent  liquid.  This  fluid,  which  smells  like  fresh  plaster,  may 
become  hxitid  from  decomposition  of  the  fluid  or  from  gangrene  of  the  cavity. 
The  breath  then  acquires  such  a  stench  that  a  whole  ward  may  be  tainted. 


98  TEXT-BOOK  OF  MEDICINE 

This  foetor,  which  is  very  tenacious,  may  exist,  witli  or  without  remissions, 
for  months  and  years,  and  the  unhapjjy  sufferer  avoids  all  company,  and 
dare  not  show  himself  in  public. 

HaBmoptysis  is  frequent  m  bronchiectasis.  In  some  cases  it  can  be  set 
down  to  tuberculosis,  which  may  be  associated  with  bronchiectasis,  but  m  a 
large  immber  of  cases  there  is  no  question  of  tuberculosis.  The  haemoptysis 
depends  solely  on  the  bronchiectasis,  and  the  bleeding  is  due  to  rupture  of 
the  tortuous,  dilated  capillaries  (angiomata)  which  are  present  in  the  newly- 
formed  bronchial  and  extrabronchial  tissue.  These  forms  of  haemoptysis 
are  a  fresh  source  of  difficulty  in  diagnosis.  In  some  cases  they  have  been 
the  cause  of  death. 

In  most  cases  dilatation  of  the  bronchi  exists  on  one  side  only,  and 
affects  the  apex  of  the  lung  as  often  as  the  base.  We  find,  on  examination 
of  the  chest,  a  depression,  which  corresponds  to  the  site  of  the  dilatation, 
and  is  especially  marked  when  bronchiectasis  is  associated  with  chronic 
pleurisy.  This  depression  is  frequently  found  at  the  middle  and  back  part 
of  the  thorax.  Percussion  shows  dullness,  correspondmg  to  the  diseased 
region.  On  auscultation  the  signs  of  a  cavity  are  fomid,  but  the  signs 
vary  accordmg  to  the  size  and  number  of  the  cavities,  and  according  as 
they  are  empty  or  full.  They  are  sometimes  masked  by  pleurisy,  or  by 
chronic  pneumonia.  Thus,  m  some  patients  the  breathmg  is  blowing, 
cavernous,  and  even  amphoric,  and  may  or  may  npt  be  accompanied  by 
gurglmg  ;  while  bronchophony  or  pectoriloquy  may  be  heard. 

Course — Duration — Termination. — When  bronchiectasis  is  not  asso- 
ciated with  tuberculosis,  the  general  symptoms  are  benign  for  a  long  while. 
There  is  no  fever  ;  many  patients  ret  am  their  appetite,  and  contmue  to  attend 
to  their  busmess,  and  m  those  who  are  not  attacked  by  foetid  bronchitis  life 
is  fairly  comfortable,  save  that  expectoration  is  abundant  and  dyspnoea 
may  cause  an  mcreasing  distress.  In  short,  we  are  surprised,  says  Trousseau 
— and  this  is  also  Laennec's  opinion — by  the  apparent  innocence  of  the 
disease  up  to  almost  its  final  stage. 

In  some  cases  death  is  the  result  of  such  complications  as  acute  pneu- 
monia, acute  broncho -pneumonia,  gangrene  of  the  lung,  haemoptysis,  cerebral 
abscess,  purulent  pleurisy,  pneumothorax,  tuberculosis,  or  pyaemia  with 
articular  and  visceral  abscesses.  In  other  cases  death  comes  more  slowly, 
from  the  progress  of  the  disease  and  from  concomitant  pulmonary  troubles, 
which,  after  many  years,  are  complicated  by  lesions  of  the  right  heart,  or  by 
consumption.  The  absorption  of  microbic  products  from  the  surface  of 
the  bronchial  cavities  produces  a  true  septicaemia.  The  wasting,  the  hectic 
fever,  the  diarrhoea,  the  cachectic  oedema,  and  the  clubbed  fingers,  recall  the 
picture  of  pulmonary  phthisis. 

Bacteriology. — The  fluid  from  the  cavities  contams  numerous  microbes, 


DISEASES  OF  THE  BRONCHI  99 

including  the  Streptococcus  pyogenes,ihePneumococcus,  and  the  Staphylococcus 
aureus,  as  well  as  saprogenic  microbes,  such  as  the  Bacillus  pyogenes  fcctidus. 

These  microbes  perhaps  play  some  part  in  the  destruction  of  the 
bronchial  tissues  which  favour  dilatation,  but  they  certainly  play  an  im- 
portant one  in  most  of  the  complications.  These  complications  are  not  due 
solely  to  the  toxines  elaborated  by  the  microbes,  but  also  to  the  direct 
passage -of  certain  microbes  into  the  blood  and  the  organs.  The  acute 
septicaemia  which  sometimes  supervenes  m  bronchiectasis,  the  suppurative 
artln-itis,  the  infarcts,  and  the  cerebral  abscesses  are  due  to  different  strepto 
cocci  {Streptococcus  pyogenes,  Streptococcus  septic  us  liquefaciens)  which  have 
their  original  focus  in  bronchiectasis. 

Infective  endocarditis  with  abscess  in  the  liver  and  the  kidney  has  been 
seen.  It  was  consecutive  to  infection  by  the  Staphylococcus  aureus,  from 
an  infected  bronchial  dilatation. 

Diagnosis. — Pulmonary  phthisis,  foetid  bronchitis,  and  pleural  vomica 
have  many  signs  in  common  with  bronchiectasis.  Let  us  first  distinguish 
bronchial  dilatation  from  tuberculous  cavities  in  the  lung,  and  let  us  take 
a  well-marked  case,  in  which  bronchiectasis  is  not  associated  with  tuber- 
culosis. The  site  of  the  lesion  furnishes  no  distinctive  sign,  since  bronchi- 
ectasis is  as  often  unilateral  as  bilateral  (twenty-six  times  m  forty-three  cases), 
and  as  frequent  at  the  apex  as  at  the  base  (Barth).  Haemoptysis,  cough, 
and  clubbed  fingers  are  also  seen  in  both  diseases.  Lastly,  cavernous  breath- 
ing, gurgling,  and  pectoriloquy  show  in  both  cases  the  existence  of  cavities, 
but  give  no  information  as  to  their  nature.  Upon  what  points,  then,  can 
an  affirmative  diagnosis  be  based  ?  The  expectoration  in  bronchiectasis  is, 
it  is  true,  more  diffluent,  more  aerated  and  abundant  than  in  phthisis ;  but 
this  distinction  is  not  sufficient,  and  the  true  distinction  lies  in  the  different 
course  of  the  two  diseases.  The  patient  affected  only  with  bronchiectasis 
has  for  five,  eight,  or  ten  years  suffered  neither  fever  nor  marked  wastmg, 
but  has  simply  coughed  up  abundant  and  sometimes  foetid  sputum,  with  or 
without  dyspnoea.  Such  is  not  the  course  of  tuberculosis.  Fever,  wastuig, 
dyspepsia,  loss  of  strength,  sweats,  diarrhoea,  are  symptoms  which  coincide 
with  the  formation  of  cavities,  and  gradually  increase  with  the  spread  of 
the  lesion.  Lastly,  all  doubts  can  be  removed  by  examination  of  the 
sputum  ;  the  presence  of  bacilli  therein  being  a  sure  sign  of  tuberculosis. 

In  foetid  bronchitis,  which  is  characterized  by  sloughing  of  the  mucosa 
in  the  bronchioles  (Lasegue),  we  find  foctor  of  the  breath  and  of  the  sputum, 
whi(;h  is  profuse,  as  in  bronchiectasis ;  l)ut  the  signs  of  a  cavity  are  wanting. 

Between  dilatation  of  the  bronchi  and  vomica*  of  the  pleui-a  diagnosis  is 
difficult.  I  am  not  referrbig  to  a  vomica  of  the  great  pleural  cavity  occurring 
in  piurulent  pleurisy,  the  evolution  of  which  we  have  followed  out.     It  is 

♦    Vide  Chapter  V.,  Section  15. 

7—2 


100  TEXT-BOOK  OF  MEDICINE 

evident  that  in  such  a  case  the  abundance  of  fluid,  its  sudden  appearance 
by  way  of  the  bronchi,  and  the  signs  of  a  large  cavity  replacing  those  of 
effusion,  leave  no  doubt  as  to  the  diagnosis.  I  allude  to  those  interlobar 
varieties  (pleuro-pulmonary  cysts)  which  differ  from  effusions  of  the  great 
pleural  cavity,  in  that  the  symptoms  are  obscure  and  the  fluid  is  scanty. 
A  patient  coughs  up  for  some  time  10  to  15  ounces  of  foetid  muco-purulent 
fluid  daily.  On  inspection,  the  thorax  is  found  to  be  flattened  in  the  sub- 
scapular region.  At  the  same  level  impaired  resonance  exists.  On  auscul- 
tation, the  signs  of  the  cavity  may  be  recognized.  The  condition  is  just 
like  dilatation  of  the  bronchi.  How,  then,  can  we  diagnose  between  this 
condition  and  a  vomica  ?  We  must  investigate  the  course  of  events. 
Peter  and  I  followed  this  course  in  a  case  similar  to  one  described  by  Trous- 
seau.* The  signs  in  bronchiectasis  appear  gradually,  while  the  course  of 
events  is  more  sudden  in  interlobar  pleurisy  followed  by  vomica.  The 
pleuritic  phase  is  succeeded  quite  suddenly  by  the  vomica,  and  the  evacuated 
fluid  is  at  first  abundant,  but  diminishes  during  the  next  few  days. 

Treatment. — The  remedies  employed  to  dry  up  the  secretion  from  the 
dilated  bronchi  are  practically  those  used  in  chronic  bronchitis.  Terpene 
may  be  prescribed,  6  to  10  pills  daUy.  Good  results  may  be  obtained  with 
eucalyptol,  given  in  doses  of  from  4  to  10  capsules  daily.  Turpentine, 
iodoform,  and  creosote  will  also  find  their  indications.  Inhalations  and  sprays 
of  sulphurous  and  arsenical  waters  sometimes  give  go,od  results.  Revulsives, 
blisters,  and  the  cautery  must  not  be  neglected.  For  the  foetor  of  the 
breath  and  of  the  sputum,  Paquelin's  thermo-cautery  should  be  employed. 
I  have  several  times  caused  foetor  to  disappear  for  several  days  by  multiple 
applications  over  the  diseased  region. 

As  medical  treatment  too  often  fails,  it  is  recognized  that  resort  must 
be  made  to  surgical  measures.  I  am  not  speaking  solely  of  antiseptic 
injections  into  the  diseased  bronchi.  I  allude  to  pneumotomy.  I  am  well 
aware  that  the  published  results  are  not  very  encouraging,  and  the  pul- 
monary haemorrhage  which  supervenes  during  the  operation  is  a  source  of 
danger.  Boswell  Park,  in  his  statistics,  had  nine  deaths  in  twenty-five  cases. 
These  figures  are  not  as  yet  very  favourable  to  surgical  attempts,  but  yet, 
when  we  thmk  of  the  almost  fatal  prognosis  of  bronchiectasis,  we  confess 
that  the  hope  of  rational  treatment  lies  in  surgery. 

V.  PSEUDO-MEMBRANOUS  BRONCHITIS. 

This  disease  may  have  various  origins.  Sometimes  the  false  membrane 
contains  Loffler's  bacillus,  and  mcreases  the  gravity  of  the  prognosis  in 
diphtheria  of  the  larynx  or  pharynx ;  sometimes  the  false  membrane  is 

*  "  Dilatation  de  Bronches  "  ("  Le9ons  de  Clinique  Medicale,"  tome  i.,  p.  588). 


DISEASES  OF  THE  BRONCHT  101 

consecutive  to  pneumonia,  especially  massive  pneumonia  (Grancher),  and 
the  cause  is  the  pneumococcus.  Finally,  in  much  rarer  cases,  we  sometimes 
see  after  tuberculosis,  measles  (Jaeger),  heart  lesions,  and  ordinary  bron- 
chitis, cases  of  pseudo-membranous  bronchitis  which  are  difficult  to  classify. 
Pseudo-membranous  bronchitis  does  not  always  show  a  well-defined 
course.  The  bronchitis  is  only  an  episode  of  the  disease  which  it  happens 
to  complicate.  It  is  not  so  m  the  case  of  chronic  pseudo-membranous 
bronchitis,  in  which  the  course  and  the  symptoms  are  quite  characteristic 
(Paul-Lucas  Championniere). 

Chronic  Pseudo-Membranous  Bronchitis. 

etiology. — This  form  is  chiefly  seen  in  adult  and  elderly  persons.  It  is 
more  frequent  in  men  than  in  women.  Pulmonary  affection  and  arthritism 
in  the  patient's  ancestors  appear  to  predispose  to  it.  It  may  follow  ordinary 
bronchitis,  or  be  a  complication  of  pulmonary  tuberculosis.  It  is  sometimes 
associated  with  the  Aspergillus  fmnigatus. 

Pathological  Anatomy. — Post  mortem  the  bronchial  mucosa  is  seen  to 
be  slightly  red  and  thickened.  The  false  membranes  are  found  in  the 
trachea,  the  large  bronchi,  but  especially  in  the  smaller  bronchi.  The  false 
membranes  are  branched  like  a  tree  or  a  piece  of  coral  and  form  exact  casts 
of  the  bronchi.  These  casts  may  be  coughed  up  in  small  fragments,  or  in 
branching  pieces  4  or  5  inches  in  length.  The  substance  which  forms  them 
is  white  or  rosy,  and  is  often  disposed  in  concentric  lamina).  In  the  large 
bronchi  the  membranes  are  hollow,  and  show  a  central  lumen  ;  in  those  of 
small  calibre  the  casts  are  solid.  The  structure  of  these  membranes  varies. 
They  may  be  composed  of  firm  mucus,  coagulated  albumin  (Grancher), 
fibrin  (Caussade),  ur  fat  (Model).  Charcot-Leyden  crystals  and  eosinophile 
cells  are  at  times  found  in  them.  In  a  case  published  by  Claisse  membranous 
bronchitis  was  associated  with  the  streptococcus.  In  Griffon's  case  the 
pneumococcus  was  the  pathogenic  agent. 

Symptoms. — The  affection  generally  begins  as  acute  bronchitis,  which 
may  be  accompanied  by  the  expectoration  of  false  membranes,  and  then 
gradually  becomes  chronic.  The  membranes  may  not  appear  till  long  after 
the  disappearance  of  the  acute  bronchitis.  In  some  subjects  the  affection 
is  chronic  from  the  start. 

The  course  is  neither  continuous  nor  progressive  ;  it  is  characterized  by 
attacks.  At  more  or  less  lengthy  intervals  the  patients  are  seized  with  intense 
dyspncjea,  retrosternal  pain,  and  convulsive  cough.  At  first  they  bring  up 
abundant  shreddy  matter,  and  then  false  membranes,  which  may  take  the 
form  of  isolated  fragments,  or  be  rolled  up  in  balls  which  unfold  in  water. 
In  some  cases  an  entire  bronchial  tree  is  brought  up.  Haemoptysis  is  very 
rare.     After  the  expulsion  of  the  membranes  the  dyspncca  ceases.     During 


102  TEXT-BOOK  OF  MEDICINE 

the  attacks  the  vesicular  murmur  is  often  diminished.  We  sometimes  find 
a  focus  of  crepitant  rales  which  may  be  long  persistent  (Hyde  Salter),  or  a 
hruit  de  drapeau,  as  in  croup.     The  attack  is  generally  apyretic. 

At  the  Necker  Hospital  I  saw,  in  1891,  a  man,  fifty  years  of  age,  with  pseudo- 
membranous bronchitis.  For  twelve  months  membranes  were  absent ;  then  he  coughed 
them  up  every  week  for  a  month.  The  attack  was  preceded  by  certain  symptoms  the 
day  before.  He  used  to  feel  depressed,  and  would  next  day  cough  up  large  casts. 
He  never  had  haemoptysis,  and  I  found  no  signs  on  percussion  and  auscultation.  He 
improved  rapidly  under  iodide  of  potash,  although  he  was  not  syphilitic. 

The  duration  of  the  disease  is  unlimited.  A  case  of  twenty-five  years' 
duration  has  been  quoted  (Kirsch).  The  prognosis,  not  unlike  that  of  simple 
chronic  bronchitis,  is  only  grave  in  a  tubercular  subject. 

Diagnosis. — The  diagnosis  rests  entirely  upon  the  examination  of  the 
sputum.  When  false  membranes  are  discovered,  histological  and  especially 
bacteriological  exammations  must  be  made,  in  order  to  ascertain  if  it  be  a 
case  of  diphtheria,  pneumonia,  or  of  chronic  bronchitis,  with  or  without 
tuberculosis. 

Rational  treatment  consists  in  the  exhibition  of  iodide  of  potash,  mercury, 
terpene,  and  creosote. 

VI.  TRACHEO-BRONCHIAL  SYPHILIS. 

As  Mauriac  justly  remarks,  the  trachea  and  bronchi  are  simple  con- 
ductors of  air,  and  play  a  purely  passive  part,  which  cannot  be  compared 
with  the  many  functions  of  the  larynx.  The  symptoms  of  tracheo-bronchial 
syphiKs  are  therefore  respiratory,  but  are  more  serious  than  in  the  larjmx, 
because  tracheotomy  is  not  applicable  when  the  lesion  is  situated  in  the 
trachea  or  at  its  bifurcation. 

1.  Secondary  Troubles. 

Description. — Erythema,  catarrh,  and  erosions  exist  as  secondary  mani- 
festations in  the  trachea  and  the  large  bronchi ;  but  while  vocal  troubles  and 
laryngoscopy  readily  reveal  these  secondary  troubles  if  they  are  seated  in 
the  larynx,  they  can  only  be  suspected  when  located  in  the  trachea  or  the 
large  bronchi.  In  certain  cases,  however,  laryngoscopy  may  reveal  them, 
although  they  are  in  the  trachea. 

The  symptoms  are  those  of  ordinary  tracheo-bronchitis — viz.,  cough, 
slight  dyspnoea,  and  expectoration.  Their  syphilitic  origin  may  in  many 
cases  be  affirmed,  because  they  often  coincide  with  mucous  or  cutaneous 
syphilides,  and  because  they  improve  rapidly  under  treatment. 

Acute  or  subacute  syphilitic  tracheo-bronchitis  is  more  common  than 
we  think.  A  case  of  tracheo-bronchitis  which  has  lasted  a  long  time,  has 
been  rebellious  to  other  treatment,  or  has  been  set  down  to  tobacco, 
artliritism,  or  chills,  yields  rapidly  to  mercury  and  iodide  of  potash. 


DISEASES  OF  THE  BRONCHI  103 

2.  Tertiary  Troubles. 

Pathological  Anatomy. — In  the  trachea  and  the  large  bronchi,  as  else- 
where, the  syphiloma  may  be  circumscribed  or  diffuse.  The  lesion  spreads 
either  in  the  thickness  of  the  mucosa  or  below  it.  Its  action  is  not  limited 
to  the  soft  parts,  and  it  invades  the  cartilages,  the  fibrous  tissue,  and  the 
muscle.  The  gumma  may  be  of  large  size,  and  the  thickenings  are  more 
or  less  extensive. 

These  tertiary  growths  usually  end  in  circumscribed  ulceration  in  the 
case  of  gumma,  and  serpiginous  ulceration,  which  has  a  phagedaenic  tendency, 
in  the  diffuse  syphiloma. 

The  ulceration  may  occupy  a  segment  or  the  whole  circumference  of  the 
trachea  ;  the  phagedsena  may  attack  the  perichondrium  and  the  cartilages, 
and  perforate  the  trachea  or  furrow  it  from  above  downwards. 

In  some  cases  the  perichondritis  and  the  chondritis  are  primary,  the 
walls  of  the  trachea  bemg  indurated  and  converted  into  a  rigid  narrow  tube. 

Tracheo-stenosis  and  broncho-stenosis  are  the  result  of  these  lesions. 
The  narrowing  of  the  trachea  may  take  place  slowly  or  rapidly.  The 
gummata  and  the  ulcerations,  with  the  resultmg  oedema,  narrow  the  trachea 
and  the  bronchi.  The  fibrous  tissue  forms  longitudinal,  oblique,  transverse, 
or  annular  bands,  and  causes  most  marked  constrictions.  The  fibrous  scars 
produce  two  kinds  of  deformity  in  the  trachea  and  bronchi,  which  diminish 
both  in  length  and  in  breadth.  The  trachea,  which  is  normally  about 
f  inch  in  diameter,  is  reduced  to  a  third  or  a  quarter  of  its  size.  The  con- 
striction is  rarely  circular,  like  a  diaphragm,  but  takes  the  form  of  an 
irregular,  anfractuous  channel,  with  superposed  stages.  The  length  of  the 
trachea  diminishes  in  proportion  to  the  number  of  rings  destroyed.  The 
firmness  of  its  framework  is  destroyed  by  the  substitution  of  fibrous  tissue 
for  cartilage,  and  the  consequent  flattening  during  inspiration  may  cause 
asphyxia. 

The  tracheo-bronchial  syphiloma  is  nearly  always  accompanied  or  pre- 
ceded by  pharyngeal  or  laryngeal  syphilis.  In  sixty-five  cases  collected  by 
Mauriac,  in  six  only  was  the  pharynx  or  larynx  unaffected.  The  lower 
fourth  of  the  trachea,  with  or  without  the  participation  of  one  or  both 
bronchi,  is  the  most  frequent  seat  of  syphiloma.  The  traclieo  -  bronchial 
glands  iiTCi  almost  always  enlarged. 

Description. — The  cough  and  slight  dyspnoea  of  the  onset  make  us  think 
at  first  of  simple  bronchitis,  but  otlier  symptoms  soon  a|)pear  ;  obstinate 
spasmodic  cough,  the  sensation  of  a  foreign  body,  the  feeling  of  constriction 
in  the  neck,  pain  behind  the  sternum,  noisy  breathing,  stridor,  continuoas 
and  paroxysmal  dyspnoea,  indicate  stenosis  of  the  trachea.  Respiration  is 
often  quiet  when  the  patient  is  at  rest,  but  movement  brings  on  aruito 


104  TEXT-BOOK  OF  MEDICINE 

dyspnoea ;  attacks  of  oppression,  due  to  reflex  spasm  of  the  glottis,  super- 
vene night  and  day,  and  cause  extreme  distress. 

These  attacks  of  oppression  are  one  of  the  most  salient  characteristics 
of  tracheal  syphilis  (Mauriac).  I  verified  the  truth  of  this  assertion  in  a 
patient  whom  I  saw  with  Dr.  Poyet. 

The  expectoration  is  frothy,  but  sometimes  the  patient  brings  up  pieces 
of  gummatous  tissue,  and  even  fragments  of  cartilage.  The  larynx,  which 
normally  rises  during  deglutition,  is  often  fixed  by  scar-tissue  in  tracheal 
syphilis.  Laryngoscopic  examination  may  show  the  tracheal  lesion  even 
as  far  down  as  the  bifurcation. 

When  cure  has  not  been  obtained,  or  treatment  has  not  been  carried 
out  in  time,  slow  asphyxia,  syncope,  sudden  death,  perforation  of  the  gullet, 
of  the  vessels,  or  of  the  mediastinum,  with  consecutive  abscess,  broncho- 
pneumonia and  gangrene  of  the  lung,  are  possible  terminations.  We  must 
not  mistake  laryngo-bronchial  syphilis  for  ordinary  bronchitis,  asthma,  or 
tracheo-bronchial  adenitis,  lest  we  see  the  patient  succumb  for  want  of 
active  treatment. 

Retrosternal  pain,  feeling  of  strangulation  behind  the  sternum,  tracheal 
stridor,  immobility  or  lowering  of  the  trachea  during  deglutition  and 
preservation  of  the  voice,  together  with  the  dyspnoeic  troubles  I  have  de- 
scribed, show  that  the  trachea  is  stenosed. 

Several  lesions  in  the  larynx,  as  well  as  paralysis-  of  the  posterior  crico- 
arytenoid muscles,  may  cause  similar  dyspnoea  ;  but  the  stridor  is  laryngeal, 
the  voice  is  generally  affected,  and  the  laryngoscope  removes  all  doubts. 

The  trachea  may  be  compressed  by  an  aortic  aneurysm,  in  which  case  the 
signs  of  aneurysm  are  found. 

The  trachea  is  sometimes  depressed  by  tumours  of  the  mediastinum, 
but  other  symptoms,  such  as  dysphagia,  oedema  of  the  face  and  neck, 
deformity  of  the  sterno-clavicular  region,  dullness,  according  to  the  extent 
of  the  tumour,  and  swelling  of  the  supraclavicular  glands,  are  usually 
present,  and  indicate  the  nature  of  the  lesion. 

If  syphilis  of  the  trachea  is  recognized,  or  even  suspected,  mercury  and 
iodide  of  potassium  must  be  given  in  large  doses.  I  prefer  injections  of  bin- 
iodide  of  mercury.  This  treatment  must  be  carried  out  thoroughly.  Most 
active  treatment  may  cause  no  improvement  for  a  fortnight. 

VII.  WHOOPING-COUGH. 

Description.— Whooping-cough  is  a  contagious  and  epidemic  disease, 
which  is  probably  microbic,  attacks  the  young  especially,  and  confers 
almost  absolute  immunity.  It  is  composed  of  a  double  element :  the  one 
inflammatory,  catarrh  of  the  bronchi ;  the  other  nervous,  the  fit  of  coughing. 

It  is  customary  to  describe  three  stages  in  whooping-cough,  but  we  may 


DISEASES  OF  THE  BRONCHI  105 

add  the  period  of  incubation,  which  extends  from  the  moment  of  contagion 
to  the  outburst  of  the  attack,  and  varies,  according  to  Roger,  from  seven 
to  ten  days. 

In  the  first  stage  the  catarrh  resembles  simple  bronchitis.  The  child  has 
fever  and  cough,  as  in  ordinary  catarrh ;  but  yet  certain  fine  distinctions 
already  indicate  the  specific  nature  of  the  disease  :  the  cough  is  more 
obstinate  and  frequent,  and  the  fever  Ls  more  stubborn  than  in  a  simple  cold. 
This  stage  lasts  from  three  days  to  a  fortnight,  and  passes  insensibly  into 
the  stationary  stage. 

In  this  stage— that  of  convulsive  cough — the  fever  falls  back,  and  the 
nervous  element  takes  the  lead.  The  cough  is  less  incessant  than  formerly, 
but  the  expiratory  jerks  succeed  each  other  so  rapidly  that  the  patient  makes 
at  first  eight  to  ten,  then  fifteen  to  twenty,  expirations  without  being  able 
to  take  breath.  The  fit  is  now  established,  and  the  crisis  shows  the  symptoms 
so  graphically  described  by  Trousseau  that  I  cannot  do  better  than  repro- 
duce his  picture : 

A  child  is  at  play.  Some  moments  before  the  advent  of  the  crisis  he  stops ; 
his  mirth  gives  place  to  sadness.  If  he  should  be  in  the  company  of  his  playmates,  he 
stands  aside  and  tries  to  avoid  them.  He  meditates  his  crisis,  feels  it  coming,  and 
experiences  that  pricking  and  tickhng  in.  the  larynx  which  announces  it.  At  first  he 
tries  to  avert  the  paroxysm.  Instead  of  breathing  naturally  and  expanding  his  lungs 
to  the  full,  as  he  was  doing  just  before,  he  holds  his  breath,  for  it  seems  to  him  that  the 
full  current  of  air,  by  entering  his  larynx,  •vvill  produce  the  exhausting  cough  of  which 
he  has  had  a  sad  experience  ;  but,  I  repeat,  whatever  he  may  do,  he  T^-iU  not  prevent, 
and  at  most  he  will  only  be  able  to  delay,  the  fit.  The  fit  takes  place.  You  at  once 
see  the  patient  look  around  for  a  support  to  which  he  may  cling.  If  he  is  a  child  at 
the  breast,  he  throws  himself  into  the  arms  of  his  mother  or  of  his  nurse.  If  he  is 
older  and  standing  up,  you  notice  him  stamping,  in  a  state  of  complete  distress.  If  he 
is  lying  down,  he  sits  up  quickly  and  clutches  hold  of  the  bed-curtains  or  of  the  rails. 
The  attack  leaves  him  with  a  swollen  face,  and  this  swelling,  which  at  times  lasts  for 
three  weeks,  may  in  some  cases  be  quite  enough  to  cause  a  practised  physician  to  sus- 
pect the  existence  of  whooping-cough. 

Let  us  return  to  the  fit.  The  fit  commences  with  a  sudden,  noLsy 
expiration,  followed  by  a  series  of  short,  aphonic,  convulsive,  and  more  or 
less  hurried  expirations.  At  this  moment  a  pause,  which  may  last  ten  to 
fifteen  seconds,  occurs,  and  the  chest  remains  motionless  in  the  position  of 
full  expiration.  During  this  phase  of  the  fit  the  air  expelled  from  the  chest 
is  not  renewed  ,  consequently,  the  patient,  whose  eyes  are  injected  and 
streaming,  lips  cyanosed  and  face  bloated,  is  in  a  state  of  distress  bordering 
upon  asphyxia.  Then  comes  a  long,  singing,  convulsive  inspiration, 
whicli  ends  the  fit,  and  brings  a  short  spell  of  rest. 

A  second  fit,  however,  occurs  at  once,  and  is  followed  by  several  otiiers, 
which  decrease  in  severity ;  the  inspiration,  instead  of  being  singing,  be- 
comes aphonic,  showing  that  the  spasm  of  the  glottis  is  less.  The  attack 
may  then  be  said  to  be  at  an  end.    The  series  of  fits  constitutes  the  attack. 


106  TEXT-BOOK  OF  MEDICINE 

During  the  fits  the  child  brings  up  slireds  of  glairy  mucus,  which  stick  to 
the  mouth.  The  end  of  the  attack  is  often  marked  by  the  vomiting  of  glairy 
material  or  of  food-stuffs. 

These  attacks,  which  vary  in  duration  from  some  seconds  to  ten  or 
twelve  minutes,  are  more  frequent  at  night  than  in  the  day,  and  occur  as 
often  as  sixty  times  in  twenty-four  hours.  When  this  number  is  exceeded, 
the  child's  life  is  in  danger  (Trousseau).  Between  the  attacks  the  patient 
has  no  cough  to  speak  of ;  the  fit  sums  up  the  whole  disease.  During  the 
catarrhal  period,  bronchitic  rales  are  heard  in  the  chest.  As  soon  as  the 
spasmodic  period  begins  they  disappear. 

In  the  third  stage  all  the  symptoms  improve.  The  fits  are  less  frequent, 
the  inspiratory  stridor  is  less  marked,  and  the  glairy  mucus  is  replaced, 
especially  in  adults,  by  the  thick  sputum  of  bronchial  catarrh. 

Herff  examined  the  larynx  both  in  himself  and  in  others,  after  ansesthe- 
tizing  the  part  with  cocaine.  He  has  shown  that  during  the  whole  disease 
the  mucosa,  especially  in  the  interarytenoid  and  arytenoid  regions,  is  inflamed. 

During  the  attack  mucus  accumulates  in  this  region.  If  this  mucus  is 
removed  by  a  probe,  the  attack  can  be  stopped  ;  but  if  the  same  region  is 
tickled,  the  fits  can  be  reproduced.  Touching  other  parts  of  the  larynx  does 
not  produce  the  same  effect.  The  reflex  which  provokes  the  fit  originates, 
therefore,  in  the  interarytenoid  region. 

Course — Duration. — Whooping-cough  usually  shows  three  stages.  The 
convulsive  cough  very  rarely  appears  at  first,  but  is  preceded  by  the 
catarrhal  period. 

In  some  patients  the  fits  are  replaced  by  attacks  of  sneezing  (Roger), 
and  I  have  seen  two  examples  of  this  in  children  of  asthmatic  parents.  The 
fit,  says  Trousseau,  sometimes  ends  by  sneezing.  AVhooping-cough  has  an 
average  duration  of  six  to  eight  weeks.  Some  patients,  however,  have  fits 
of  spasmodic  cough  for  months,  as  though  the  malady  had  passed  into  a 
chronic  state. 

The  diagnosis  of  whooping-cough  is  indicated,  even  in  the  catarrhal  stage, 
by  the  obstinacy  of  the  cough  and  the  tenacity  of  the  fever.  In  the 
stationary  stage  the  fit  and  the  whoop  are  quite  characteristic. 

Sometimes  certain  tumours  of  the  mediastinum  provoke  a  cough,  termed 
"  pertussoid  "  (Gueneau  de  Mussy),  which  somewhat  resembles  the  true  fit 
of  whoopmg-cough. 

It  is  important  m  diagnosis  to  recognize  the  different  forms  of  defaced* 
whooping-cough.  I  have  already  said  that  the  fit  may  be  replaced  by 
attacks  of  sneezing. 

*  The  term  "  fruste  "  (defaced)  was  applied  by  Trousseau  to  cases  of  scarlatina, 
in  which  certain  symptoms  were  absent.  In  archaeology  it  refers  to  an  inscription, 
part  of  which  is  missing. 


DISEASES  OF  THE  BRONCHI  107 

At  Chantilly  I  saw  an  olderly  latly  (her  daughter  had  whooping-cough)  who  waa 
seized  with  spasms  of  the  glottis  and  inspiratory  stridor  which  lasted  some  seconds, 
and  recurred  repeatedly  in  the  form  of  attacks,  day  and  night.  In  tliis  defaced  form 
the  fit  of  whooping-cough  was  reduced  to  an  inspiratory  spasm  of  the  glottis,  and  the 
other  elements  were  quite  wanting.  Similar  cases  have  been  published — two  by 
Trousseau  and  one  by  Blache. 

Prognosis  —  Complications. — Whooping-cough  per  se  is  not  a  serious 
malady,  and  the  gravity  comes  from  the  complications.  Thus,  the  catarrh 
of  the  early  period,  which  usually  improves  at  the  beginning  of  the  spasmodic 
period,  may  invade  the  smaU  bronchi.  Fever  then  lights  up,  the  dyspnoea 
becomes  intense,  and  the  tubular  breathing  of  broncho-pneumonia  or  the 
fine  rales  of  capillary  bronchitis  are  heard  in  the  chest.  This  serious  com- 
plication, which  may  arise  in  all  the  stages,  is  chiefly  seen  in  the  stationary 
stage.  The  appearance  of  the  inflammatory  process  often  causes  the 
nervous  element  to  disappear — sfasmos  febris  accedens  solvit.  "  When  in 
a  child  with  whooping-cough  you  find  that  the  fits,  which  numbered  fifty 
or  sixty  in  the  twenty-four  hours,  cease  suddenly,  although  the  disease  may 
be  still  in  the  stationary  stage,  beware,  for  you  will  find  yourself  face  to 
face  with  an  inflammatory  complication  "  (Trousseau).  In  an  adult  these 
inflammatory  complications  may  take  the  form  of  pleurisy  or  lobar  pneu- 
monia. 

Whooping-cough  predisposes  to  tubercular  disease  of  the  bronchial 
glands  and  to  tuberculosis.  In  some  cases  we  find  meningitis  or  miliary 
tuberculosis ;  in  others,  it  runs  the  course  of  chronic  pulmonary  tuber- 
culosis. 

The  nervous  element  is  connected  with  complications  of  another  kind. 
Spasm  of  the  glottis  is  frequent  and  very  serious  in  children  under  four 
years  of  age.  Convulsions  may  come  on  during  the  attacks  or  in  the 
interval,  and  are  very  serious  in  infants.  The  fits  cause  a  vesicular  emphy- 
sema which  in  exceptional  cases  has  become  interlobular  by  rupture  of  air- 
cells  in  the  lung.  The  repeated  congestions  excited  by  the  fits  induce 
epistaxls,  haemoptysis,  bleeding  from  the  ear  (rupture  of  the  membrana 
tympani),  subconjunctival  ecchymosis,  and  cerebral  congestion,  with  attacks 
of  eclampsia. 

Furthermore,  the  vomiting  of  food  is  due  to  the  fits  of  coughing,  and 
leads  to  malnutrition  if  often  repeated.  The  exaggerated  contraction 
of  the  expiratory  muscles  causes  involuntary  evacuations  and  hemic©,  and 
the  rubbing  of  the  tongue  upon  the  incisor  teeth  causes  ulccnitioit  of  tlie 
fr»num  (Bouchut). 

etiology. — Whooping-cough  is  an  epidemic  and  contagious  disciisc 
which  chiefly  affects  children  between  the  ages  of  two  and  seven  years.  Tiie 
contagion  is  so  virulent  that  an  infant  may  be  infected  after  being  a  few 
minutes  in  the  company  of  a  patient  suffering  from  whooping-cougli.     In 


108  TEXT-BOOK  OF  MEDICINE 

the  sporadic  state  it  follows  the  usual  course  which  we  have  described,  but 
it  assumes  different  characters  in  the  epidemic  form.  Thus,  in  the  epidemic 
of  Dillingen,  in  1811,  patients  were  carried  off  by  eclampsia  ;  in  the  Geneva 
epidemic,  in  1850,  capillary  bronchitis  was  the  chief  complication  (Rilliet)  ; 
in  other  epidemics  the  catarrhal  stage  was  very  short,  and  the  spasmodic 
one  appeared  almost  from  the  start  (Trousseau).  Epidemics  of  whooping- 
cough  and  of  measles  sometimes  follow  each  other  so  closely  as  to  indicate 
a  causal  relation  between  them. 

Bacteriology. — Afanassief  thought  that  he  had  discovered  the  bacillus 
of  whooping-cough.  This  microbe — Bacillus  tussis  convnlsivcB — is  said  to 
be  small,  slender,  and  disposed  in  groups  or  colonies. 

Quite  recently  Bordet  and  Gengou  claim  to  have  obtained  the  specific 
organism  of  whooping-cough  in  pure  cultures.  It  is  a  small  bacterium 
of  ovoid  form,  and  presents  the  same  appearance  both  in  the  sputum  and 
in  cultures.  The  presence  of  haemoglobin  is  necessary  for  its  growth.  It 
is  specially  abmidant  in  the  exudate  during  the  first  fits. 

The  broncho-pneumonia,  however,  which  occurs  as  a  complication  is 
usually  due  to  the  streptococcus,  the  staphylococcus,  the  pneumococcns,  etc. 

Treatment. — The  indications  must  be  directed  to  the  inflammatory  and 
the  spasmodic  elements.  The  former  is  relieved  by  emetics  ;  for  the  latter 
we  employ  opium,  aconite,  belladonna,  and  bromide  of  potash.  The  use  of 
alkalies  has  been  advised  (Labadie-Lagrave).  Revulsives  and  blisters 
should  be  reserved  for  the  inflammatory  complications.  Anaesthesia  of  the 
interarytenoid  region,  induced  by  means  of  cocaine,  has  given  good  results. 
Fumigation  with  sulphur  has  been  extolled.  The  patient  enters  the  fumi- 
gating chamber,  the  windows  having  been  opened  after  the  fumigation. 

H.  de  Rothschild  has  obtained  good  results  with  chloroform.  It  should 
not  be  given  in  severe  cases,  where  the  patient  is  weakened  by  vomiting  and 
insomnia.  Acute  bronchitis  and  broncho-pneumonia  are,  of  course,  contra- 
indications. It  may  be  given  till  anaesthesia  is  complete,  or  may  be  inhaled 
during  the  fits  alone.  For  inhalation  10  to  20  drops  of  the  following  mixture 
are  sprinkled  on  lint : 

Anaesthetic  chloroform        . .  . .  . .  . .  . .     3iv. 

Essence  of  pine        . .  . .  . .         . .  . .  . .     3ii. 

Essence  of  eucalyptus         . .  . .         . .  . .  . .     3ii. 

This  measure  has  been  curative  in  some  cases  and  has  caused  great 
improvement  in  others. 

Hygiene  plays  a  large  part  in  the  treatment  of  whooping-cough.  The 
rooms  should  be  as  large  as  possible,  and  the  child  should  not  spend  day  and 
night  in  the  same  apartment.  At  the  beginning  of  defervescence  change 
of  air  is  most  useful  in  shortening  the  duration  of  the  disease. 


DISEASES  OF  THE  BRONCHI  109 

Prophylactic  treatment  is  essential.  The  patient  should  be  isolated 
from  other  children.  The  things  he  has  used  and  the  room  he  has  occupied 
should  be  thoroughly  disinfected. 

Till.  ASTHMA. 

The  attacks  of  dyspnoea  which  constitute  asthma  are  quite  charac- 
teristic ;  they  appear  suddenly,  weeks,  months,  or  even  years  apart.  They 
may  exist  as  a  pure  neurosis,  without  any  inflammation  of  the  bronchi,  but 
in  most  cases  they  are  complicated  by  a  catarrhal  element  of  variable 
intensity.  Catarrh  does  not  usually  accompany  first  attacks  of  asthma,  but 
is  associated  with  them  later.  Sometimes  it  plays  a  minor  part,  and 
appears  towards  the  end  of  the  attack  ;  at  other  times  it  begins  with  the 
attack  as  a  true  febrile  catarrh  ;  and  lastly,  in  other  cases,  it  is  so  marked 
that  the  nervous  element  is  of  secondary  moment. 

These  two  elements,  of  which  the  nervous  is  constant  and  the  catarrhal 
is  variable,  may  finally  give  rise  to  chronic  bronchitis  and  emphysema,  and 
form  a  morbid  cycle,  which  may  be  complicated  by  lesions  of  the  right  heart. 

Description. — The  attack  of  asthma  generally  begins  in  the  early  hours 
of  the  night,  without  prodromata.  ^  A  patient  who  has  gone  to  bed  quite 
well  wakes  up  suddenly  with  acute  distress.  He  feels  agonizing  constriction 
in  the  chest,  and  his  breathing  is  painful  and  wheezing.  He  gets  up  and 
opens  the  window  to  get  air,  putting  every  respiratory  muscle  into  play. 
Hoping  to  make  his  breathing  easier,  he  sits  on  his  bed  with  his  body  bent, 
kneels  upon  a  chair,  with  his  head  bent  forward,  or  props  himself  up  by 
leaning  with  his  elbows  on  a  piece  of  furniture.  He  strives  hard,  but  the 
distress  increases  in  spite  of  his  efforts.  Inspiration  is  imperfect ;  expira- 
tion Ls  slow,  wheezing,  and  convulsive.  His  distress  is  extreme,  and  seeing 
the  patient  with  face  bloated  and  covered  with  sweat,  with  starting  eyes  and 
cyanosed  lips,  we  might  think  that  asphyxia  was  imminent.  We  should  be 
wrong,  for  after  this  struggle  has  lasted  for  one  or  more  hours  the  breatliing 
becomes  easier,  the  air  enters  the  chest  better,  the  expiration  is  less  con- 
vulsive and  not  so  prolonged,  and  the  crisis  subsides. 

The  end  of  the  attack  Ls  sometimes  indicated  by  a  belching,  by  catarrhal 
expectoration,  or  the  emission  of  dry,  crepitant,  or  gelatinoas  sputum, 
which  takes  the  shape  of  vermicelli.  The  first  urine  voided  is  clear  and 
abundant  (nervous  urine),  and  sleep  returns.  Next  day  the  patient  feels 
tired,  and  has  a  disagreeable  sensation  of  thoracic  constriction,  with  balloon- 
nig  of  the  belly,  and  some  tendency  to  breathlessness. 

An  attack  of  asthma  is  rarely  single  ;  we  usually  see  a  series  of  attacks, 
wliich  are  repeated  for  several  days  or  weeks  ;  they  often  return  at  the  same 
hour — usually  at  night.     This  series  of  fits  forms  an  attack  of  asthma. 


110  TEXT-BOOK  OF  MEDICINE 

The  attacks  do  not  always  have  the  intermittent  form  just  described. 
In  some  asthmatics  the  distress  continues  throughout  the  whole  attack,  and 
the  paroxysms  reappear  day  and  night,  or  several  times  in  the  twenty-four 
hours,  allowing  no  rest. 

Analysis  of  the  attack  of  asthma  shows  that  the  dyspnoea  presents 
peculiar  characteristics.  A  respiration  rate  of  40  or  50  is  not  seen  in 
asthma,  as  in  broncho-pulmonary  inflammations  ;  the  number  of  respira- 
tions is,  on  the  contrary,  less  than  normal.  The  painful  and  wheezing 
inspiration  only  allows  an  insufficient  quantity  of  air  to  enter  the  chest,  and 
the  expiration,  which  is  still  more  painful,  and  three  or  four  times  as  long 
as  the  inspiration,  does  not  drive  out  the  inspired  air.  Let  me  add  that, 
even  at  the  height  of  suffocation,  we  do  not  see  sucking-in,  as  in  croup, 
because  in  asthma  the  chest  is  always  filled  to  its  maximum  with  air. 

During  the  attack  snoring  rhonchi  and  mucous  rales,  which  depend  on 
the  severity  of  the  catarrh,  are  heard  in  the  chest,  or  we  may  find  total 
absence  of  the  respiratory  murmur  in  places.  The  chest  is  bulging  and 
rounded,  the  diaplu-agm  is  depressed,  and  percussion  gives  the  exaggerated 
resonance  of  acute  emphysema. 

In  the  variety  of  asthma  above  described  the  nervous  element  is  almost 
alone  in  play ;  but  when  the  catarrhal  element  is  associated  with  it,  the 
clinical  picture  is  more  or  less  modified.  Some  asthmatics  during  or  towards 
the  end  of  the  attack  suffer  from  fatiguing  spasms  of  coughing,  and  bring 
up  catarrhal  sputum,  which  is  also  present  between  the  attacks.  The  ex- 
pectoration is  chiefly  composed  of  gelatmous  sputum,  which  is  vermiform, 
and  resembles  fragments  of  vermicelli,  or  consists  of  rounded  pellets, 
crepitant  to  the  touch,  and  known  as  Laennec's  paries.  The  sputum  often 
contains  Curschmann's  spirals,  octohedral  crystals  (Charcot-Leyden)  and 
eosinophile  cells  (Miiller),  which,  however,  are  not  characteristic  of  asthma. 
In  some  asthmatics  the  fever,  the  cough,  and  the  nature  of  the  sputum  prove 
that  bronchitis  is  present ;  but  the  dyspnoea  preserves  its  characteristic  type, 
and  appears  in  the  form  of  paroxysms.  In  some  persons,  however,  the 
bronchitis  becomes  clu-onic,  emphysema  appears,  and  from  that  time  it 
becomes  more  difficult  to  estimate  the  nervous  element. 

In  some  persons  the  attack  of  asthma  is  preceded  or  replaced  by  fits  of 
sneezing.  These  spasmodic  fits  may  occur  thirty  or  forty  times  in  a  few 
minutes,  and  reappear  night  and  morning  for  several  consecutive  days. 
During  the  attack  of  sneezing  the  eyes,  which  are  injected  and  weeping, 
often  itch  acutely ;  the  face  is  congested,  and  the  nose  runs  freely.  Every- 
thing then  returns  to  its  normal  state.  This  description  would  do  well  for 
hay-fever,  as  the  reader  will  no  doubt  notice.  In  those  affected  with  these 
sneezing  fits  it  has  been  possible  to  predict  asthma  several  months  or  years 
in  advance. 


DISEASES  OF  THE  BRONCHI  111 

Pathological  Anatomy. — The  theories  which  hold  that  asthma  is  con- 
secutive to  em^jhysema  (Louis  and  Rostan),  catarrh  of  the  small  bronchi 
(Beau),  catarrh  (Laennec),  or  pulmonary  congestion  (Bretonneau),  are 
erroneous,  as  in  the  main  they  mistake  the  effect  for  the  cause.  The  attack 
of  asthma  ls  certainly  produced  by  spasm  of  the  muscles  of  respiration.  A 
difficulty  beguis  when  we  try  to  decide  which  muscles  are  affected.  Some 
authors  (Biermer  and  Williams)  would  place  the  spasm  in  the  bronchial 
muscles  ;  the  contraction  of  the  bronchi  is  said  to  prevent  the  circulation  of 
the  air  and  the  lowering  of  the  diaphragm  to  be  consecutive  to  the  exag- 
gerated fullness  of  the  lung.  According  to  others  (See  and  Wintrick),  the 
bronchi  have  nothing  to  do  with  asthma,  and  the  spasm  pervades  m  turn  all 
the  extrinsic  muscles  of  inspiration,  including  the  diapliragm,  mtercostals, 
scalenis,  trapezius,  etc.,  which  re  mam  convulsed  tlirough  the  attack,  keep 
the  lung  in  a  position  of  constant  dilatation,  and  only  permit  a  scanty 
renewal  of  the  air  m  the  pulmonary  vesicles.  A  third  opmion  (Trousseau 
and  Jaccoud)  combines  the  two  preceding  ones,  and  admits  spasm  both  of 
the  extrinsic  and  of  the  intrnisic  muscles  of  respiration. 

I  share  the  last  opinion,  and  believe  that  the  number  and  the  species  of 
muscles  involved  depend  on  the  severity  of  the  attack.  In  violent  attacks 
both  extrinsic  and  intrinsic  muscles, are  involved  ;  in  slight  cases  the  spasm 
may  well  be  limited  to  the  muscles  of  the  bronchi,  or  only  encroach  on  the 
diaphragm.  In  all  cases  the  sphere  of  nervous  excitation  does  not  remain 
localized  to  the  muscles  of  inspiration;  it  also  attacks  the  muscles  of 
expiration,  and  the  rhythmic  spasm  of  the  expiratory  mascles  explains  the 
length  and  the  mteasity  of  each  expiration,  which  can  only  overcome  part 
of  the  resistance  of  the  inspiratory  muscles.  The  renewal  of  the  air  in  the 
lungs,  therefore,  is  very  incomplete,  and  dyspnoea  is  the  result. 

When  we  see  the  swelling  and  secretion  of  the  nasal  and  ocular  mucous 
membrane  in  some  asthmatics,  we  are  tempted  to  admit  that  like  swelling 
and  secretion  exist  in  the  mucosa  of  the  bronchi,  and  help  to  narrow  their 
calibre.  This  hypothesis  is  the  more  probable  in  that  Stark  has  seen 
swelling  of  the  tracheal  mucosa  with  the  laryngoscope. 

The  spasm  of  the  respiratory  muscles  and  the  phenomena  of  vaso- 
dilatation and  vaso-secretion  are  tliemselves  due  to  a  special  condition  of 
the  nerves  which  govern  these  functions.  This  state  of  irritability  Ls  some- 
times spontaneous,  or  at  least  apparently  so  ;  at  other  times  it  is  due  to  a 
reflex  act  which  starts  in  the  terminals  of  the  sensory  nerves  which  supjily 
the  bronchi  or  the  nasal  passages.  Many  theories  now  in  .vogue  woultl, 
indeed,  assign  the  chief  part  to  the  nasal  mucosa.  I  shall  speak  of  this  later, 
under  ^Etiology. 

Course—Duration — Termination . — First  attacks  of  asthma  are  generally 
benign,  and  leave  no  scquelic  ;  later,  if  catarrh  also  is  present,  and  more 


112  TEXT-BOOK  OF  MEDICINE 

especially  if  it  predominate,  the  patient,  even  in  the  intervals,  has  a  morbid 
condition,  which  is  analogous  to  chronic  bronchitis,  and  is  the  more  tenacious 
because  emphysema  may  also  be  present.  The  lesions  of  chronic  bronchitis 
and  of  emphysema  are  especially  seen  in  people  who  have  at  first  suffered 
from  asthma  alone.  Dilatation  of  the  right  heart  and  tricuspid  insufficiency 
may  finally  be  met  with.  Fortunately,  the  disease  does  not  always  follow  the 
same  course  ;  it  may  improve,  without  causing  such  complications,  or  may 
be  cured  by  well-directed  treatment.  As  a  matter  of  fact,  persons  may  have 
several  attacks  of  asthma,  which  finally  disappear. 

etiology. — Asthma  presents  all  the  caprices  of  a  neurosis  ;  it  may  be 
provoked  or  reawakened  by  the  most  insignificant  causes,  such  as  a  smell 
(Floyer),  the  fumes  of  a  sulphur  match,  the  dust  of  oats  (Trousseau),  or 
powdered  ipecacuanha  (Cullen).  A  man  who  suffers  from  asthma  in  the 
North  remains  well  when  he  resides  in  the  South.  A  patient  has  asthma  in 
Paris,  but  not  in  Versailles.  I  know  a  man  who  is  subject  to  severe  attacks 
m  Egypt ;  he  recovers  as  soon  as  he  is  at  sea.  Some  asthmatics  cannot 
enjoy  a  hearty  laugh  without  being  seized  with  a  slight  attack.  A  high 
altitude  and  life  in  the  mountains  are  often  prejudicial  to  asthmatics. 
Asthma  is  a  neurosis,  and,  further,  it  is  almost  always  a  diathetic  and 
hereditary  neurosis,  as  Trousseau  has  clearly  shown.  "  Skin  diseases, 
rheumatism,  gout,  haemorrhoids,  gravel,  and  migraine  are  affections  which 
asthma  may  replace,  and  which,  in  their  turn,  may  replace  asthma.  They 
are  different  expressions  of  the  same  diathesis."  A  gouty  father  begets 
children ;  while  young  they  have  migraine  or  piles,  and  later  gravel,  asthma, 
or  gout. 

The  alternation  of  asthma  and  urticaria  is  a  well-known  fact,  and  asthma 
has  been  called  "  bronchial  urticaria."  The  alternation  of  asthma  with  such 
neuroses  as  epilepsy,  hysteria,  hypochondria,  and  mania  has  also  been 
noted.     Asthmatics  may  have  relapsmg  or  cychcal  attacks  of  mania. 

Asthma  is  more  frequent  hi  men  than  m  women.  It  is  a  disease  of  all 
ages,  and  has  been  seen  even  in  children,  especially  m  the  latter  part  of 
childhood.  In  children,  asthma  may  behave  as  m  adults,  but  it  fairly  often 
assumes  the  features  of  capillary  bronchitis,  suffocative  catarrh,  or  broncho- 
pneumonia. The  disease  presents  a  grave  appearance,  and  correct  diagnosis 
is  most  important,  because  proper  treatment  gives  excellent  results. 
Trousseau  and  See  report  strikmg  examples  of  this  mfantile  asthma,  which 
must  be  recognized,  so  as  to  avoid  serious  mistakes. 

Diagnosii^. — Hay-fever  closely  resembles  asthma,  and  belongs  to  the 
same  family. 

Mediastmal  tumours,  enlargement  of  the  bronchial  glands,  and  aortic 
aneurysm  produce  attacks  of  dyspnoea,  which  must  not  be  confounded  with 
asthma. 


DISEASES  OF  THE  BRONCHI  113 

A  form  of  pulmonary  tuberculosis  simulates  asthma,  and  is  known 
as  pseudo-asthmatic.  I  am  not  speaking  of  acute  miliary  tuberculosis, 
which  Andral  compared  to  asthma  because  of  the  continuous  or  paroxysmal 
dyspnoea,  but  I  allude  to  ordinary  chronic  tuberculosis.  Certam  tubercular 
patients  at  the  outset,  or  during  the  course  of  their  malady,  suffer  from 
attacks  of  asthma,  and  the  tuberculosis  may  be  overlooked  if  we  forget  this 
pseudo-asthmatic  form. 

Diseases  of  the  heart,  especially  mitral  lesions,  often  provoke  dyspnoea. 
In  addition  to  this  dyspnoea,  the  patient  sometimes  experiences  attacks  of 
oppression,  which  are  more  frequent  at  night.  The  attacks  are  as  severe 
as  those  of  asthma,  and  the  dyspnoea  has  therefore  been  called  *'  cardiac 
asthma."  The  term  is  wrong.  Mitral  disease  does  not  produce  true 
asthma,  and  tiie  paroxysmal  dyspnoea  of  cardiac  disease  has  not  the  char- 
acters of  the  dyspnoea  in  asthma.  In  a  cardiac  case  the  breathing  is  rapid 
and  panting ;  both  inspiration  and  expiration  are  short  and  jerky ;  palpita- 
tion is  frequent ;  the  pulse  is  small ;  the  face  is  pale ;  and  the  lips  are  cyanosed. 
Asthma  presents  quite  a  different  picture.  The  breathing  is  not  quickened, 
inspiration  is  slow  and  difficult,  and  expiration,  which  is  wheezing  and 
spasmodic,  is  three  or  four  times  as  long  as  inspiration  ;  palpitation  is  absent, 
and  the  pulse  remains  regular.  In  some  cardiac  cases  attacks  of  dyspnoea 
are  the  chief  symptom,  and  mitral  disease  may  show  itself  at  first  solely  by 
attacks  of  cardiac  dyspnoea,  which  are  mistaken  for  asthma,  just  as  in 
patients  with  Bright's  disease  the  renal  lesion  shows  itself  by  attacks  of 
dyspnoea,  wrongly  called  asthma.  In  any  case,  cardiac  asthma  and  true 
asthma  must  not  be  confused. 

Lesions  of  the  aorta  are  also  accompanied  by  attacks  of  oppression,  which 
bear  some  slight  resemblance  to  those  of  asthma.  These  attacks  of  aortic 
dyspnoea,  however,  are  more  or  less  painful,  like  angina  pectoris.  In 
nowise  have  they  the  character  of  the  true  asthmatic  attack,  and  the  aortic 
lesion  quickly  decides  the  diagnosis. 

From  want  of  care  the  dyspnoea  of  Bright's  disease  may  be  taken  for 
asthma,  and  many  patients  with  Bright's  disease  arc  treated  for  asthma. 
This  dyspnoea  presents  forms  which  are  slightly  different.  In  the  first 
variety  the  patient  is  "  short  of  breath,"  especially  if  he  walks  upstairs 
too  quickly.  The  shortness  of  breath  may  be  mistaken  for  asthma,  but 
examination  reveals  pulmonary  oedema,  albumin  in  the  urine,  and  other 
symptoms  of  Bright's  disease. 

In  the  second  variety  the  threatening  asphyxia  is  due  to  superacute 
oedema  of  the  lung.  The  fcdema  rapidly  invades  the  lung,  the  dyspnoea 
becomes  acute,  fine  rales  are  heard  all  over  the  chest,  and  the  patient  coughs 
up  frothy,  rose-coloured,  albuminous  sputum,  which  is  characteristic  uf 
superacute  oedema. 

8 


114  TEXT-BOOK  OF  MEDICINE 

In  a  third  variety  the  dyspnoea  is  ursemic  and  toxic ;  it  may  show  thft 
character  of  Cheyne-Stokes  breathing.  This  dyspnoea  may  appear  in  the 
form  of  attacks,  which  patients  mistake  for  asthma.  The  attack  comes  on 
night  and  day,  rapidly  becomes  acute,  and  reappears  at  the  slightest  move- 
ment It  may  recur  several  times  in  the  twenty-four  hours,  or  disappear 
and  return  after  more  or  less  lengthy  intervals. 

Dyspnoea  comes  on  at  all  periods  of  Bright' s  disease,  but  we  must  never 
forget  that  it  may  be  the  first  symptom.  In  some  cases  it  appears  suddenly, 
like  an  attack  of  asthma ;  in  others  it  establishes  itself  gradually,  like  a  chronic 
bronchitis.  A  knowledge  of  these  facts  will  prevent  our  sending  patients  to 
Mont-Dore  or  to  Cauterets  for  bronchial  catarrh,  asthma,  or  emphysema, 
when  they  are  really  suffering  from  Bright's  disease. 

Much  attention  has  lately  been  paid  to  asthma  following  nasal  lesions. 
Voltolini  of  Breslau  in  1871  published  cases  of  asthma  in  patients  with 
nasal  polypi.  Removal  of  the  polypi  cured  the  attacks.  Hack  thinks  that 
the  pathological  reflex  has  its  origin  in  inflammation  of  the  erectile  tissue  of 
the  nose,  and  since  then  the  nose  has  been  accused  (polypi,  hypertrophy 
of  the  mucosa,  deviation  of  the  septum)  of  causing  most  cases  of  asthma,  and 
also  dyspnoea,  migraine,  cough,  oedema,  incontmence  of  urine,  etc.  The 
result  was  attempts  to  destroy  the  cause  of  so  many  ills  by  cutting  and 
burning  the  nasal  fossae. 

These  statements  are  much  exaggerated.  It  is  quite  true  that  the  nasal 
mucosa  plays  a  large  part  in  asthma.  Attacks  sometimes  appear  after 
certain  nasal  stimuli.  Sneezmg,  nasal  secretion,  and  swelling  of  the  mucosa, 
are  present  in  true  asthma,  in  hay-fever,  and  in  asthma  following  nasal 
polypi.  It  is  therefore  necessary  to  pay  attention  to  the  undoubted  part 
which  the  nasal  mucosa  plays  in  the  production  of  asthmatic  attacks.  It  may 
occasionally  be  necessary  to  deal  with  this  mucosa,  but  this  is  only  one  side 
of  the  question,  and  if  in  some  cases  the  nasal  mucosa,  by  its  special  excit- 
ability, be  the  origm  of  the  reflex  which  provokes  the  asthmatic  attack,  this 
special  excitability  is  often  present  elsewhere  (bronchi,  lungs,  or  centres  in 
the  medulla). 

Treatment. — We  may  first  consider  the  treatment  of  the  attack.  The 
attack  can  be  checked  or  much  modified  by  prompt  actioii.  Inhalation  of 
the  fumes  of  Datura  stramo7iium,  nitrate  paper,  Espic  cigarettes,  hypodermic 
injections  of  morphia,  inhalations  of  pyridine,  and  bromide  of  potash,  are 
of  service.  Nitrite  of  amyl  "  is  as  dangerous  as  it  is  difficult  to  handle  " 
(See). 

I  constantly  prescribe  stramonium,  smoked  in  a  pipe.  The  dry  leaves 
should  be  finely  cut  up  and  some  small  pieces  of  nitrate  paper  added. 

Pyridine  may  be  used,  either  by  inhalation  of  10  or  12  drops  on  a  hand- 
kerchief, or  by  allowing  the  drug  to  evaj)orate  slowly  near  the  patient. 


DISEASES  OF  THE  BRONCHI  115 

These  remedies  may  be  repeated  two  or  three  times  a  day,  and  when  em- 
ployed for  some  time  and  between  the  attacks  may  cause  marked  improvement. 
Iodide  of  potash,  however,  is  the  best  drug  for  asthma,  both  in  the  attack 
and  in  the  intervals  (Trousseau).  The  dose  depends  on  the  tolerance  of  the 
patient.  We  may  begin  with  10  grains  daily,  and  increase  to  30  grains,  or 
even  more  (See,  Jacc.oud).  The  drug  should  be  continued  for  a  long  while, 
care  being  taken  to  suspend  its  use  at  mtervals.  With  iodide  of  potash 
Trousseau  employed  tmcture  of  lobelia  in  small  doses. 

He  also  advises  the  use  of  belladonna  and  bromide  of  potassium,  replaced, 
as  the  case  may  be,  by  preparations  of  arsenic. 

I  usually  advise  the  following  regime  between  the  attacks.  During  the 
first  and  third  week  of  each  month  I  prescribe  10  to  15  grams  of  iodide  of 
potash  daily,  with  10  drops  of  tincture  of  lobelia. 

In  the  second  and  fourth  weeks  of  the  month  I  prescribe  bromide  of  potash, 
15  to  30  grains  a  day,  and  pills  of  extract  of  belladoima.  This  treatment 
should  be  continued  for  a  very  long  while. 

Between  the  attacks  iodide  of  codeine  has  been  extolled.  It  is  given  in 
sjTTup  (Labadie-Lagrave  and  Rollin),  and  the  dose  is  |  grain. 

The  cure  at  Mont-Dore  gives  very  good  results  (Tardieu). 

The  local  treatment  in  the  attack  consists  m  painting  the  nasal  mucosa 
with  a  5  per  cent,  solution  of  cocame.  The  nasal  fossae  must  always  be 
carefully  examined,  in  order  to  remove  polypi,  or  cauterize  the  mucous 
membrane,  if  necessary. 

IX.  SUMMER  ASTHMA— HAY-FEVER. 

This  disease  which  in  some  respects  resembles  true  asthma  has  been  called 
hay-fever,  summer  asthma,  or  spasmodic  rhino-bronchitis. 

The  term  "  hay-fever  "  is  not  good,  for  fever  is  usually  absent,  and  the 
disease  occurs  when  there  is  no  hay.  The  term  "  summer  asthma  "  is 
preferable ;  but  as  the  disease  is  equally  prevalent  hi  the  autumn,  the 
name  "  annual  asthma  "  is  better  still. 

This  disease,  which  is  most  common  m  the  Anglo-Saxon  race.  Is  not 
rare,  and  I  have  seen  a  good  many  cases. 

Description. — Annual  asthma  assumes  two  chief  forms  :  the  one  is 
called  oculo-nasal,  the  other  oculo-naso-thoracic. 

The  disease  appears  usually  about  the  15th  or  20th  of  May,  and  almost 
at  a  fixed  date.  A  person  who  Is  not  susceptible  at  other  seasons  is  seized 
with  a  kind  of  "  cold  in  the  head."  Sneezing,  obstruction  of  the  no.sc,  and 
supra-orbital  headache  are  present.  The  trouble  is  at  first  thought  to  bo  a 
cold. 

The  eyes,  however,  become  the  scat  of  pricking  and  intolerable  itcliing, 
chiefly  at  the  inner  canthus.    The  patient  rubs  hia  eyelids  vigorously.   The 

8—2 


116  TEXT-BOOK  OF  MEDICINE 

eyes  are  red,  swollen,  and  weeping  ;  the  conjunctiva  is  oedematous  :  th-Q 
tears  are  so  abundant  that  they  hamper  vision,  and  flow  over  the  cheeks  ; 
the  photophobia  is  intense,  so  that  the  patient  avoids  daylight. 

These  troubles  generally  disappear  or  improve  towards  evening.  In  the 
nose  we  find  the  following  symptoms :  unbearable  itching ;  violent  sneezing, 
repeated  ten,  twenty,  or  thirty  times  in  succession  ;  profuse  serous  discharge 
from  the  nose,  which  runs  "  like  a  fountain." 

The  nasal,  like  the  ocular,  symptoms  are  brought  on  agam  or  made  worse 
by  sunlight  and  heat ;  they  become  less  severe  under  the  influence  of  shade 
and  cold. 

Such  is  the  oculo-nasal  form  of  the  disease.  It  persists  for  weeks,  with 
alternating  improvement  and  aggravation.  The  symptoms  then  improve, 
and  recovery  is  complete  till  the  followhig  year.  In  the  other  variety, 
called  oculo-naso-thoracic,  in  addition  to  the  above  symptoms,  we  find 
dyspnoea,  like  that  of  asthma.  The  dyspnoea  begins  about  a  fortnight  after 
the  ocular  and  nasal  symptoms  ;  it  becomes  gradually  worse,  is  marked  by 
the  occurrence  of  fits,  and  is  complicated  by  catarrh,  in  which  the  patient 
coughs  and  brmgs  up  bronchitic  sputum.  Improvement  now  comes  on, 
and  recovery  is  complete  in  six  weeks,  till  the  next  year. 

Patients  have  usually  one  annual  attack.  The  prognosis  is  good,  for 
this  variety  of  asthma  does  not  lead  to  chronic  bronchitis  or  cardiac 
dilatation. 

In  my  opinion,  annual  asthma  should  be  included  in  the  family  of  true 
asthma.  It  forms  part  of  the  gouty  diathesis,  and  is  often  hereditary.  It 
may  recur  annually  for  a  great  number  of  years. 

This  asthma  is  nothing  but  the  spasmodic  exaggeration  of  the  defensive 
reflexes  of  the  respiratory  mucosa,  which  include  sneezing,  cough,  and 
serous  exudation  from  the  mucous  membrane.  Its  starting-point  seems  to  be 
irritation  of  a  submucous  nerve  filament  belonging  to  the  ethmoidal  branch 
of  the  oplithalmic  nerve,  which  is  particularly  sensitive  in  the  angle  formed 
by  the  nasal  septum  and  the  lateral  wall  at  its  upper  part.  Touching  this 
pomt  may  provoke  cough  alone,  sneeznig  and  laclirymation,  or  the  com- 
plete crisis.  This  point  must  be  burnt  with  the  galvano-cautery,  without 
troubling  about  the  malformations  or  the  various  lesions  of  the  nasal  fossae. 
Partial  or  total  relief  is  thus  obtained.  P.  Bonnier,  under  the  name  of 
**  rhino -laryngitis  sicca,"  has  described  an  inverse  form  of  hay-fever, 
which  appears  under  identical  conditions,  but  is  characterized  by  painful 
dryness  of  the  respiratory  mucous  membrane,  producing  aphonia. 

The  various  remedies  employed  are  less  efiicacious  in  this  variety  than 
in  true  asthma.     A  cool,  shady  room  is  a  good  measure. 


CHAPTER  rv 
DISEASES  OF  THE  LUNG 

I.  GENERAL  SURVEY  OF  THE  ANATOMY  OF  THE  LUNC4 

The  lung  is  made  up  of  lobules  of  a  polyhedral  form,  set  one  against  the  other,  and 
separated  by  connective  tissue.  These  lobules  are  well  seen  in  the  new-born,  because 
at  this  age  the  network  of  connective  tissue  which  surrounds  them  is  much  thickened. 
Later  the  dehmitation  is  less  apparent,  because  the  connective  envelope  loses  its  thick- 
ness. The  dehmitation  of  the  lobules,  however,  is  readily  seen  on  the  surface  of  the 
organ,  where  the  connective  sheaths  are  infiltrated  with  dark  material,  and  form  a  kind 
of  mosaic. 

The  pulmonary  lobule  represents  the  structure  of  the  whole  lung.  It  is  a  small 
and  spongy  polyhedral  or  conical  mass,  of  about  1  c.c.  in  size,  and  joined  to  the  rest 
of  the  organ  by  a  short  pedicle.  This  pedicle  contains  a  bronchiole,  which  is  given 
off  at  right  angles  from  a  large  bronchial  twig,  and  a  pulmonary  arteriole  and  vein,  with 
lymphatics  and  nerves,  the  whole  being  ensheathed  by  connective  tissue.  The  bronchus 
and  the  artery  penetrate  the  interior  of  the  lobule  at  the  hilum,  but  the  vein  ramifies 
over  the  lobule,  following  the  perilobular  connective  sheath. 

A  transverse  section  of  the  lobule  therefore  presents  two  connective-tissue  regions — 
a  central  one  (the  intralobular  space,  which  contains  the  bronchus  and  the  artery),  and 
a  peripheral  one  (the  perilobular  space),  containing  the  vein. 

When  the  bronchus  enters  the  lobule,  it  takes  the  name  of  intralobular,  and  parts 
company  with  the  vein,  but  is  accompanied  by  the  artery  as  far  as  its  farthest  ramifica- 
tions. The  intralobular  bronchus  traverses  the  lobule  without  diminution  in  size  ; 
it  forms  the  axis  of  tht;  lobule,  and  in  its  passage  gives  off  alternate  branches,  and  ends 
by  dividing  dichotomously.  Each  branch  derived  from  the  intralobular  bronchus 
passes  into  an  acinus,  and  takes  the  name  of  "  acinous  bronchus."    What  is  the  acinus  ? 

The  lobule  is  formed  by  a  number  of  acini,  and  each  acinus,  measuring  2  to  3  milli- 
metres in  each  direction,  forms  within  its  bronchus  a  small  system,  which  has  the 
following  arrangement : 

On  reaching  the  acinus,  the  branch,  after  a  short  course,  spreads  out  like  a  funnel, 
and  forms  a  kind  of  vestibule,  whence^  arise  three,  four,  or  five  alveolar  ducts,  which 
widen  out  to  form  infundibula.  The  infundibuluin  may  be  considered  as  the  expanded 
end  of  the  alveolar  duct.  All  these  parts,  except  the  acinous  bronchus,  are  lined  by 
the  alveoli. 

The  alveoli  are  air-cells  in  which  liiiiuatosis  goes  on.  They  resemble  shallow  cups  in 
the  walls,*  and  in  the;  dried  section  of  an  acinus  api)ear  as  oval  or  rounded  cavities, 
separated  by  partitions,  hke  a  beehive.  The  interalveolar  septa  form  the  skeleton  of 
the  acinus,  and,  like  it,  are  composed  of  a  connective  membrane  and  elastic   fibres. 

*  Frey,  "  Traite  d'Histologie,"  p.  rA'.i.  The  opening  of  the  alveolus  into  the 
infunclibulum  is  narrower  than  the:  fundus  of  the  alveolus. 

117 


118  TEXT-BOOK  OF  MEDICINE 

This  fibro-elastic  skeleton  permits  the  extension  and  the  retraction  of  the  alveoli. 
supports  the  capillary  network,  and  "  gives  a  foundation  to  the  pavement  epithelium 
of  the  lung  "  (Ranvier). 

The  capillary  network  of  the  lobule  arises  from  the  artery,  and  projects  into  the 
interior  of  the  alveoli,  when  they  are  not  too  dilated. 

Lymphatic  vessels  are  everywhere  present,  and  surround  the  alveoli,  infundibula, 
acini,  and  lobules  (Grancher). 

Each  disease  of  the  lung  alters  the  infundibulum,  the  acinus,  and  the  lobule,  in  a 
particular  way.  In  lobar  pneumonia  the  lobule  is  filled  with  an  exudate  rich  in 
fibrin,  and  the  projection  of  the  acini  on  the  surface  of  the  section  explains  the  granular 
appearance  of  red  hepatization.  In  disseminated  or  confluent  broncho -pneumonia 
the  inflammation  spreads  from  lobule  to  lobule.  The  lobular  bronchus  is  primarily 
invaded.  Around  the  bronchus  we  find  the  peribronchial  inflammatory  nodule  or 
zone  of  hepatization,  and  farther  out  the  zone  of  splenization.  The  exudate  is  poor  in 
fibrin,  but  rich  in  pus  cells.  In  emphysema  the  lobule  is  distended  to  its  maximum, 
and  the  alveolar  septa  are  often  atrophied  or  perforated.  In  pulmonary  fibrosis  the 
dense  and  fibroid  interstitial  tissue  partly  blocks  the  alveoli  and  the  acini.  In  certain 
occupation  pneumonias  (miners,  founders)  the  walls  of  the  alveolus,  the  connective 
tissue,  and  the  lymphatics  are  loaded  with  coloured  particles  (anthracosis).  In  tuber- 
culosis the  walls  of  the  alveoli,  of  the  small  vessels,  and  of  the  bronchial  ramifications 
contribute  to  the  formation  of  the  tubercles. 

11.  PULMONARY  CONGESTION. 

Congestion  of  the  lungs  may  be  divided  into  two  chief  classes — active, 
produced  by  afflux  of  blood  ;  passive,  resulting  from  blood-stasis. 

1.  Active  Congestion. 

Active  congestion  of  the  lung  is  caused  by  inhalations  of  irritant 
vapours ;  by  the  sudden  passage  from  a  warm  to  a  cold  atmosphere,  or  vice 
versa  ;  by  pathological  neoplasms,  especially  tubercle.  It  accompanies  the 
eruptive  fevers — principally  typhoid  fever — in  which  it  often  makes  the 
prognosis  worse.  It  may  be  due  to  malaria,  gout,  and  rheumatism,  and 
is  provoked  by  the  suppression  of  normal  or  accidental  haemorrhage  (piles, 
menstruation).  Some  forms  have  a  nervous  origin  (hysteria),  arise  from 
reflex  action  (large  burns),  and  accompany  cerebral  lesions  (haemorrhage 
and  softening). 

The  symptoms  are  in  harmony  with  the  severity  and  the  extent  of  the 
hyperaemia.  As  a  general  rule,  pulmonary  congestion,  if  pushed  to  its 
extreme  limit,  may  terminate  in  haemorrhage,  with  or  without  haemoptysis, 
and,  indeed,  cases  of  rapid  death  have  been  quoted  (Devergie).  Dyspnoea, 
cough,  pain  in  the  side,  may  be  seen  in  the  congestion  of  malarial,  gouty, 
or  rheumatic  origin. 

In  articular  rheumatism  this  complication  arises  suddenly :  the  expec- 
toration is  streaked  with  blood,  the  breathing  is  uneasy.  On  auscultation  all 
the  signs  of  broncho-pulmonary  congestion,  with  oedema,  are  found,  and 
death  may  occur  in  a  few  hours. 


DISEASES  OF  THE  LUNG  119 

2.  Passive  Congestion. 

Passive  congestion  is  due  to  blood-stasis,  caused  by  cardiac  diseases 
(mitral  and  tricuspid  lesions),  degeneration  of  the  cardiac  muscle,  and 
prolonged  decubitus  (hypostasis). 

Passive  congestion  is  slow  in  its  course,  and  is  always  accompanied 
by  oedema  of  the  lung. 

The  capillaries  allow  the  transudation  of  a  highly  coloured  fluid,  and 
pigmentation  of  the  alveolar  walls  and  of  the  epithelial  cells  is  the  result. 
Chronic  hyperaemia  often  goes  on  to  splenization — a  condition  in  which 
the  tissue  of  the  lung  is  firm  and  reddish,  like  the  pulp  of  the  spleen.  This 
morbid  state  has  been  called  hypostatic  pneumonia,  although  there  is  no 
pneumonia  in  the  true  sense  of  the  word.  The  exudate  is  poor  in  fibrin 
and  cellular  elements.  At  the  seat  of  the  lesion  percussion  shows  more  or 
less  complete  dullness,  and  on  auscultation  the  breathing  is  almost  tubular. 

Treatment. — Bleeding  and  cupping  should  be  reserved  for  acute  con- 
gestion. The  treatment  of  passive  congestion  forms  a  part  of  the  treatment 
of  the  cardiac  disease.  When  the  congestion  is  hypostatic,  the  position  of 
the  patient  should  frequently  be  changed. 

III.  INFLAMMATION  OF  THE  CHEST. 

Discussion. — When  I  began  to  study  medicine  at  Toulouse,  my  first 
teachers,  former  pupils  of  the  Paris  and  Montpelier  schools,  and,  con- 
sequently, rather  eclectic  than  absolute,  taught  us  that,  besides  pulmonary 
congestion  and  genuine  inflammations  of  the  broncho-pulmonary  apparatus, 
there  exist  bastard  phlegmasiae,  called  inflammations  of  the  chest,  wherein 
hyperemia  and  inflammation  exist  in  irregular  combinations. 

The  term  ''  inflammation  of  the  chest "  has  to-day  almost  ceased  to 
exist.  Treatises  on  pathology,  the  publications  and  the  theses  of  our 
faculty,  are  for  the  most  part  silent  on  the  subject.  We  speak  of  pulmonary 
congestion,  pneumonia,  and  broncho-pneumonia,  but  not  of  "  inflammation 
of  the  chest,"  which  seems  to  have  lost  all  its  claims  as  a  distinct  morbid 
condition. 

I  do  not  hold  this  view.  I  believe  that  inflammation  of  the  chest  should 
have  a  place  in  our  nosology.  Besides  the  genuine  inflammations  of  the 
respiratory  apparatus,  such  as  pneumonia,  broncho- pneumonia,  pleurisy, 
and  bronohitis.  wo  find  othor  bastard  morliid  stato>^.  in  which  the  hypersemic 
and  inflammatory  elements  are  differently  combined,  and  whicli,  by  huit 
accord,  have  been  called  "  fluxions." 

It  is,  moreover,  remarkable  that,  while  the  plilogmasijin  fix  voluntarily  upon 
certain  parts  of  the  respiratory  apparatus  so  that  they  might  he  culled 
*•  systematic,"  an  epithet  employed  in  diseases  of  the  spinal  cord  (Vulpian), 


120  TEXT-BOOK  OF  MEDICINE 

tlie  fluxions,  on  the  contrary,  are  naturally  difEuse  and  multiple.  Inflam- 
mation (fluxion)  is  rarely  localized  to  the  lung  or  to  the  pleura  without 
affecting  other  parts  of  the  respiratory  apparatus.  It  may  touch  or  strike 
the  lung,  the  bronchi,  the  pleura,  and  the  muscular  layers  of  the  thorax — in 
a  word,  all  the  superimposed  layers  of  the  chest,  and  hence  custom  termed 
it  "  inflammation  of  the  chest." 

Cruveilhier  was  pertitient  m  describing  pleurodynia,  accompanied  by 
fftver  and  pleural  friction  sounds,  and  Peter,  in  his  "  Clinical  Lectures  " 
tells  us  :  "  Inflammation,  if  it  be  intense,  may  not  remain  limited  to  the 
muscles,  but  may  invade  all  the  superposed  planes  of  the  thorax,  including 
even  the  pleura."  A  step  farther,  and  Peter  would  have  come  to  inflamma- 
tion of  the  chest. 

Description. — Inflammation  of  the  chest  is  a  morbid  state  of  variable 
intensity  and  nature.  It  is  neither  abortive  pneumonia  nor  broncho- 
pneumonia, but  another  entity.  Sometimes  it  spreads  its  action  over  all 
the  parts  of  the  respiratory  apparatus  ;  at  other  times  it  leaves  some  parts 
almost  untouched,  and  concentrates  its  action  on  the  lung,  the  bronchi,  or 
the  pleura. 

As  examples — 

An  individual  is  seized  with  a  sharp  pain  in  the  side  ;  he  has  slight  rigors,  cough,  and 
fever.  On  examination,  we  find  pleurodynia,  w4th  or  without  cutaneous  hyperaesthesia. 
The  pains  affect  not  only  the  intercostals,  but  all  the  muscles  of  the  part.  The  abdo- 
minal and  lumbar  muscles  may  also  be  involved.  Friction  sounds  over  the  painful 
area,  and  bronchitic  rales,  scattered  over  both  sides  of  the  chest,  are  heard.  In  this 
case  the  skin,  the  muscles,  the  pleura,  and  the  bronchi  have  been  affected.  The  pleurisy 
is  in  the  incomplete  stage,  and  no  effusion  appears.  The  bronchitis  is  but  shght,  and 
the  patient  will  be  well  in  a  few  days. 

In  another  person  the  inflammation  involves  the  bronchi  and  iung  to  a  slight 
degree,  but  concentrates  its  action  on  the  pleura,  and  effusion  is  found.  To  this  category 
belong  certain  bastard  pleurisies,  obscured  by  the  inflammation  of  the  lung  and  of  the 
bronchi. 

In  another  case  the  clmical  picture  presents  some  difference. 

The  illness  has  commenced  with  fever  ;  the  musculature  of  the  thorax  may  or  may 
not  be  painful.  On  auscultation  we  find  fairly  severe  bronchitis  and  pleuritic  rubs, 
and  at  one  part  of  the  chest  we  recognize  dullness  and  blowing  breathing,  Mith  broncho- 
phony, which  are  evidence  of  marked  pulmonary  congestion.  From  the  onset  the 
sputum  is  streaked  with  blood,  the  dyspnoea  is  fairly  acute,  and  the  temperature 
102°  F.  or  more.  What  name  is  to  be  given  to  this  disease  ?  It  is  not  pleurisy,  for  the 
pleural  lesion  is  but  incomplete.  It  is  not  bronchitis,  although  the  bronchi  have  been 
attacked.  It  is  not  pneumonia  in  the  true  sense  of  the  word.  It  is  a  case  of  inflam- 
mation of  the  chest  which  has  concentrated  its  action  upon  the  lung. 

Lastly,  the  pulmonary  localization  is  yet  more  marked  or  extensive  in  some  cases. 
The  temperature  reaches  104°  F.,  the  cough  is  painful,  and  the  dyspnoea  acute.  Per- 
cussion reveals  dullness,  which  shows  the  extent  of  the  lesion.  We  might  be  tempted 
to  call  the  disease  pneumonia,  and  yet  analysis  of  the  signs  and  the  symptoms  proves 
that  it  is  not  a  true  case.     The  rale  is  neither  so  fine  nor  so  dry  as  in  pneumonia ;  the 


DISEASES  OF  THE  LUNG  121 

tubular  breathing  is  not  so  intense  ;  the  bronchophony  is  not  so  marked  ;  the  sputum, 
instead  of  being  rusty,  is  rather  streaked  with  blood.  Bronchitic  rales  or  friction 
sounds  are  scattered  through  the  chest ;  defervescence  is  not  sudden  ;  and,  although 
the  inflammation  may  reach  its  maximum  and  be  in  excess  of  the  hyperjemia,  still, 
the  disease  is  not  true  pneumonia. 

However,  I  must  say  that  these  forms  are  on  the  road  to  become  lobar 
pneumonia.  Pneumonia  does  not  always  present  the  classical  type  given 
for  purposes  of  description.  It  often  conforms  to  inflammation  of  the 
chest,  and  the  barrier  between  the  two  is  not  insurmountable.  Grasset 
regards  inflammation  of  the  chest  as  an  attenuated  pneumococcal  in- 
fection. 

The  prognosis  varies  according  to  the  variety  and  intensity  of  the  disease. 
Its  aetio  logical  conditions  are  diverse.  In  some  cases  it  forms  the  whole 
disease,  and  follows  upon  a  chill  (Woillez,  Bourgeois)  ;  in  others  it  is 
secondary  to  some  general  condition,  such  as  influenza  and  catarrhal  fever. 

Revulsives  (dry-cupping,  blisters),  local  bleeding  (leeches,  wet-cupping), 
emetics,  quinme,  and  alcoholic  drinks,  should  be  employed,  according  to 
the  nature  and  the  severity  of  the  malady. 

IV.  ACUTE  LOBAR  OR  FIBRINOUS  PNEUMONIA— PNEUMOCOCCIC 
INFECTION— PNEUMOCOCCIA. 

Pneumonia  is  called  lobar,  when  it  invades  a  lobe,  or  part  of  a  lobe, 
without  healthy  tissue  intervening,  in  contradistinction  to  lobular  pneu- 
monia, which  causes  isolated  or  confluent  nodules.  It  merits  the  name 
fibrinous  because,  of  all  the  inflammations  of  the  lung,  it  Is  the  richest  in 
fibrin  ;  the  fibrinous  exudate  fills  both  the  alveoli  and  the  bronchioles. 
The  alveolar  walls  and  the  connective  tissue  are  almost  completely  unaffected 
by  the  process,  and  the  parenchyma  of  the  lung  completely  recovers  its 
integrity  after  pneumonia. 

I  shall  first  describe  the  disease  as  localized  in  the  lung — that  is,  pneu- 
monia proper — and  then  leview  its  extra-pneumonic  localizations,  such  as 
pleurisy,  pericarditis,  endocarditis,  peritonitis,  arthritis,  gastritis,  menin- 
gitis, nephritis,  otitis,  etc.,  finally  discussing  the  different  clinical  types 
which  the  pneumonic  infection  may  assume. 

Pathological  Anatomy. — It  Is  customary  to  describe  three  stages  in 
pneumonia  ;  engorgement,  red  and  grey  hepatization.  The  third  stage  is 
somewhat  rare. 

Engorgement  is  characterized  by  intense  congestion.  The  congested 
region,  which  is  violet-coloured  and  increased  in  volume,  crepitates  a  little, 
and  pits  on  pressure  ;  it  Is  oedematous  and  infiltrated  with  a  reddish  scrum, 
which  flows  out  on  section.  The  capillaries  are  distended  with  blood,  and 
allow  plasma,  red  corpuscles,  and  leucocytes  to  pass  out.     The  cells  of  the 


122  TEXT-BOOK  OF  MEDICINE 

pulmonary  epithelium  become  vesicular  ;  some  fall  into  the  interior  of  the 
alveolus,  where  they  are  enclosed  by  a  fine  network  of  fibrin.  The  stage 
of  engorgement  lasts  from  twenty-four  to  forty-eight  hours. 

In  the  second  stage,  called  red  hepatization,*  the  lung  is  converted 
into  a  kind  of  solid  block,  which  is  red,  mottled,  and  homogeneous  through- 
out the  whole  extent  of  the  lesion.  The  hepatized  lung  is  heavy,  and  sinks 
in  water ;  it  has  become  friable,  and  is  easily  torn  or  crushed  by  the  finger. 
The  cut  section  is  practically  dry,  and  studded  with  granulations.  These 
granulations  are  about  1  millimetre  in  size,  and  are  due  to  the  fact  that  the 
infundibula  are  distended  and  moulded  by  the  coagulated  fibrin.  The 
diseased  lung  is  larger  and  heavier  than  the  healthy  one  ;  it  may  weigh  as 
much  as  tlirice  its  normal  weight.  The  hepatized  tissue,  after  washing, 
becomes  of  a  yellowish-grey  colour,  from  the  dissolution  of  the  red  corpuscles. 
Under  the  microscope  the  vessels  are  dilated  and  engorged  with  blood ; 
the  alveoli  are  filled  with  a  fibrinous  network,  which  enmeshes  epithelial 
cells  and  red  and  white  corpuscles,  f  The  alveolar  arches  and  the  epithelium 
are  unaffected.  Cells  and  fibrin  are  found  in  the  small  and  sometimes  in 
the  large  bronchi  (fibrinous  bronchitis).  The  pneumococcus  is  found  in 
the  granular  cells  and  the  fibrinous  reticulum.  After  three  to  five  days,  the 
red  hepatization  gives  place  to  resolution  :  the  fibrin  in  the  alveoli  becomes 
granular,  the  pus  cells  grow  large,  and  the  liquefied  and  altered  elements 
are  reabsorbed  in  situ  by  the  veins  and  lymphatics,  or  expelled  in  the 
sputum.     In  this  way  recovery  results. 

When,  however,  pneumonia,  instead  of  terminating  by  resolution,  goes 
on  to  grey  hepatization,  the  lung  takes  a  greyish  tint.  Its  cut  section  is 
granular  ;  the  fluid  which  exudes  is  purulent ;  the  tissue  becomes  very 
friable,  and  finger-pressure  produces  a  tear  filled  with  pus.  Under  the 
microscope  the  alveoli  appear  full  of  pus  corpuscles.  Microscopic  abscesses 
are  frequently  met  with.  The  parenchyma,  however,  is  seldom  destroyed, 
and  the  pus  is  not,  as  a  rule,  collected  so  as  to  form  an  abscess.  J 

Grey  hepatization  is  not  always  a  sign  of  pus  (Rindfleisch).  The  grey 
colour  of  the  lung  tissue  may  indicate  ordmary  resolution.  In  this  case 
the  colour  is  brownish  or  yellowish-grey,  and  the  tissue  is  fairly  firm  and 
granular,  like  that  of  red  hepatization.  The  grey  appearance  is  due  to  the 
small  number  of  red  corpuscles,  the  disappearance  of  the  haemoglobin,  and 
the  abundance  of  migratory  cells,  which  absorb  the  exudate. 

*  TKis  stage  was  called  red  softening  by  Andral. 

•f  This  exudate  is  very  rich  in  granules  of  glycogen  (Loeper,  Arch.  de.  Med.  Ex- 
'perimentale,  tSeptember,  1902). 

t  The  formation  of  abscesses  is  a  very  rare  termination  in  pneumonia.  In  thirty- 
six  cases  collected  by  Grisolles  ("  Traite  de  la  Pneumonic  "),  the  abscess  was  situated 
twelve  times  in  tlie  ujjper  lobe,  nine  times  in  the  lower  one,  twice  in  the  middle,  and 
four  times  in  several  lobes  at  once. 


DISEASES  OF  THE  LUNG  123 

Pneumonia  always  induces  lymphangitis.  The  lymphatic  vessels  of  the 
inflamed  region,  like  the  pulmonary  alveoli,  contain  fibrin,  endothelial 
cells,  and  red  and  white  corpuscles.*  The  corresponding  lymphatic  glands 
also  participate  in  the  process.  Lobar  pneumonia  is  found  more  often  on 
the  right  than  on  the  left  side,  in  the  proportion  of  3  to  2  (Lebert).  It  is 
unilateral,  or  double,  in  the  ratio  of  8  to  1  (Grisolle)  ;  it  affects  the  lower 
much  more  frequently  than  the  other  lobes.  The  blood  is  very  rich  in 
fibrin,!  and  contains  two  or  three  times  the  normal  amount. 

Bacteriology. — Pneumonic  infection  is  due  to  the  pneumococcus.  This 
organism  was  first  isolated  from  the  lung  by  Talamon  (1883),  and  was 
thoroughly  studied  by  Fraenkel.  Netter  has  demonstrated  its  intervention 
in  the  complications  of  pneumonia.  In  health  it  is  found  m  the  saliva,  where 
it  was  discovered  by  Pasteur ;  and  where  Netter  has  found  it  to  be  patho- 
genic in  one-fifth  of  normal  persons,  and  Bezancon  and  Griffon  have  shown 
that  it  exists  as  a  constant  saprophyte  on  the  surface  of  the  tonsils. 

The  pneumococcus  resembles  a  candle-flame  in  shape.  The  organisms 
usually  face  each  other  by  their  tapering  extremities,  sometimes,  however, 
by  their  other  ends. 

In  the  hepatized  lung  the  pneumococcus  is  present  in  pairs — i.e.,  as 
diplococci.  In  grey  hepatization  and  in  the  pus  from  the  complications  it 
often  forms  short  chains  (Griffon). 

The  pneumococcus  stams  readily  with  the  aniline  dyes  ;  the  microbe 
stains  by  Gram's  method.  Staining  with  carbolic  methylene  blue  shows  a 
capsule  which  surrounds  the  elements.  This  microbe  develops  between 
75°  and  108°,  but  preferably  at  98-5°  F.  On  agar  or  on  gelatinized  serum 
it  forms  transparent  colonies,  like  little  drops  of  dew.  The  best  culture 
medium  is  coagulated  rabbit  serum,  and  the  best  preservative  medium  is 
blood  rendered  uncoagulable,  or  blood  -  agar,  in  which  the  pneumococcus 
retains  its  vitality  for  several  months  (Bezancon  and  Griffon). 

The  pneumococcus  causes  pathological  results  which  differ  according  to 
its  virulence  and  to  the  species  inoculated.  In  the  mouse  little  reaction  is 
seen  at  the  point  of  inoculation,  but  generalized  infection  occurs.  In  the 
rabbit  the  lesions  differ  according  to  the  virulence  of  the  injection — local  and 
fibrinous  if  it  is  attenuated,  general  and  haemorrhagic  if  it  is  virulent 
(Bezancon  and  Griffon,  Fournier  and  Carnot).  In  the  slieep  and  the  dog, 
which  are  more  refractory,  the  local  reaction  is  very  intense,  and  inocuhitiou 
of  the  lung  produces  hepatization.     The  blood  contains  a  few  microbes. 

*  "  It  is  impossible  to  aflfirm  that  a  vaciiDlo  filled  with  pneumonic  exudalo  is  a 
transverse  section  of  a  lymphatic  canal  or  of  an  alveolus  "  (Cornil  and  Ranvier,  h>c.  cil., 
p.  G'JG). 

f  This  hyperinosis  of  the  blond  is  explained  by  (he  fact  thai  the  blood  is  charged 
with  fibrinogcaious  mattMial  from  the  iuHamed  organ. 


124  TEXT-BOOK  OF  MEDICINE 

In  man  the  germ  is  found  in  all  the  pneumonic  products  :  pneumonic 
secretion ;  hepatized  lung  tissue ;  fibrinous  exudate  in  the  bronchi ;  glands  of 
the  hilum ;  fibrinous  inflammations  of  the  pleura,  the  pericardium  and  the 
meninges ;  vegetations  of  the  endocardium,  kidney,  joints,  and  parotid  glands. 

The  pneumococcus  may  be  obtained  during  the  course  of  the  affection 
by  withdrawing  from  the  lung  a  drop  of  exudate  by  means  of  aseptic 
puncture,  or  by  isolating  it  from  the  sputum,  or  from  the  mucus  in  the 
throat. 

The  pneumococcus  may  be  found  m  the  blood-stream  ;  but  this  infection 
of  the  blood  does  not  imply  a  fatal  ending,  though  it  almost  always  coincides 
with  grave  pneumonia. 

To  discover  the  pneumococcus  in  the  rusty  sputum  or  in  the  saliva, 
examination  of  stained  films  is  not  trustworthy,  unless  the  prepara- 
tion literally  swarms  with  encapsuled  diplococci.  Inoculation  of  mice  is 
the  best  and  most  convenient  method.  These  animals  are  so  susceptible 
to  the  virus  that  death  supervenes  from  general  infection  twenty-four  to 
forty-eight  hours  after  inoculation  with  the  sputum,  and  post-mortem  the 
pneumococcus  is  found  in  the  blood  and  the  organs. 

The  toxine  secreted  by  the  pneumococcus  has  been  studied  by  Klemperer, 
and  quite  recently  by  Fournier  and  Carnot. 

Agglutinative  Reaction. — Pneumococcal  infection  causes  an  agglu- 
tinative reaction  which  is  as  follows  : 

A  little  serum  is  obtained  from  the  blood  of  a  healthy  individual  or  from 
a  person  suffering  from  some  other  disease  (rheumatism,  typhoid  fever, 
tuberculosis,  etc.).  This  serum  is  inoculated  with  a  minute  quantity  of  a 
culture  of  pneumococcus,  and  placed  in  the  oven  at  98°  F.  Next  day  this 
culture  is  as  clean  as  though  the  serum  had  not  been  inoculated.  Neither 
dust  nor  dots  are  visible,  and  if  the  tube  is  well  shaken,  the  culture  remains 
quite  limpid. 

On  the  other  hand,  if  a  culture  of  pneumococcus  is  sown  in  the  serum 
of  patients  suffering  from  pneumonic  infection  (pneumonia,  pleurisy,  peri- 
tonitis of  pneumococcal  origin,  etc.),  the  culture,  placed  in  the  oven  at 
98°  F.,  presents  a  characteristic  appearance  by  the  next  day.  Sometimes  a 
dome-like  false  membrane  is  present  at  the  bottom  of  the  tube  ;  at  other 
times  we  perceive  several  pseudo-membranous  fragments.  The  culture  in 
other  cases  contains  dots  resembling  a  coarse  dust,  which,  on  shaking,  make 
the  liquid  turbid  and  then  fall  to  the  bottom  of  the  tube.  Without  the  aid 
of  the  microscope,  by  the  comparative  study  of  tube  cultures,  we  can  say 
whether  pneumococcal  infection  is  present  or  not. 

Under  the  microscope,  if  we  examine  a  culture  of  pneumococci  on 
healthy  serum,  or  on  serum  from  those  with  some  other  malady  (rheumatism, 
tuberculosis,  typhoid  fever),  we  see  that  the  pneumococci  are  isolated,  and 


DISEASES  OF  THE  LUNG  125 

remain  so,  without  any  tendency  to  form  chains  or  groups.     No  agglutina- 
tion occurs. 

On  the  contrary,  if  a  culture  of  pneumococci  on  serum  from  patients 
with  pneumococcal  infection  is  placed  under  the  microscope,  we  see  that  the 
microbes  unite  in  long  wavy  chains,  circumscribing  clear  spaces,  in  which, 
as  a  rule,  free  pneumococci  are  not  present,  and  we  can  no  longer  distmguish 
the  capsules  of  the  pneumococcus. 

In  some  cases,  especially  in  the  experimental  infection  of  the  rabbit,  the 
collections  of  pneumococci  form  masses. 

In  human  infection  the  formation  of  a  true  mass  is  exceptional  at  the 
outset  of  pneumonia,  and  wavy  chains,  separated  by  empty  spaces,  are 
more  commonly  seen.  The  chain  therefore  appears  to  be  the  first  degree 
of  agglutination,  which  later  produces  massing  of  the  elements.  Towards 
the  end  of  the  second  stage  the  reaction  becomes  more  intense.  The  pneu- 
mococcal sero-reaction  gives  equally  positive  results  iia  the  primary  extra- 
pulmonary localizations  of  the  pneumococcus. 

Description. — In  25  per  cent,  of  the  cases  lobar  pneumonia  is  preceded 
by  prodromata,  which  include  lassitude,  pains  in  the  limbs,  headache, 
epistaxLs,  tracheitis,  insomnia,  and  fever  ;  thoy  last  possibly  one  or  two 
days.  More  often  pneumonia  begins  suddenly  with  a  single  rigor,  which  is 
as  prolonged  as  that  of  an  intermittent  fever,  and  is  accompanied  by  a  rise 
of  temperature  in  the  axilla  to  103°  F,  This  invasion  is  sometimes  accom- 
panied by  vomiting. 

By  the  end  of  the  first  day,  or  at  the  commencement  of  the  second, 
dyspnoea,  cough,  and  pain  appear.  The  patient  complains  of  a  pain  in  the 
side,  at  the  level  of  the  nipple.  This  pain  is  increased  by  the  res[)Lratory 
movements  and  fits  of  coughing.  In  some  cases  the  pain  is  abdominal,  or 
supraspinous,  or  may  even  be  found  on  the  healthy  side.  Distress  appears 
from  the  first.  The  jerky  and  painful  CO  ugh  is  at  first  dry,  but  by  the 
second  day,  or  in  the  course  of  the  third,  the  patient  brings  up  sputum, 
which  is  tinged  with  blood,  amber-coloured  or  rusty,  aerated,  and  viscid. 
It  sticks  to  the  sputum-cup,  and  is  pathognoTuouic  of  acute  lobar  pneumonia. 
The  sputum,  which  is  at  first  amber-coloured,  like  barley-sugar  or  apricot 
marmalade,  and  then  rusty,  may  on  the  following  days  become  of  a  brick- 
red  colour.  It  represents  the  pneumonic  exudate,  which  comprises  white 
and  red  corpuscles,  epithelial  cells,  surrounded  by  fibrin  and  some  fibrinous 
filaments  from  the  small  bronchi.  Pneumonic  sputum  is  rich  in  mucus  and 
chlorides.  Th(;  mucus  renders  it  transparent  and  gelatinous.  Tiie  pneu- 
mococcus is  found  in  abundance. 

Pneumonia  does  not  cause  anaemia,  and  the  red  blood-corpuscles  an;  little 
diminished  in  number.  The  blood-count  shows  a  leucocytosis  varyiu^f  from 
20,000  to  25,000,  with  considerable  increase  (85  per  cent.)  iji  the  poly- 


126  TEXT-BOOK  OF  MEDICINE 

nuclear  cells.     Insufficiency,  as  well  as  excess  of  leucocytosis,  may  mean  a 
bad  prognosis. 

Percussion  of  the  invaded  area  sometimes  yields  dullness  ;  at  other  times, 
according  to  Jaccoud,  a  transient  tympanitic  sound  ;  and  auscultation 
reveals  the  driest  and  finest  of  all  rales — i.e.,  the  crepitant  rale — which 
occurs  in  puffs  towards  the  end  of  inspiration.  It  is  not  heard  during 
expiration,  and  is  often  perceptible  only  after  making  the  patient  cough. 
The  crepitant  rale  must  at  times  be  looked  for  in  the  axillary  region. 

Durmg  the  following  days  (red  hepatization)  the  functional  symptoms 
increase,  and  though  the  pain  in  the  side  improves,  the  dyspnoea  reaches 
such  a  degree  that  the  respiration  rate  may  rise  to  40.  The  pulse,  which  is 
full,  varies  between  100  and  110  beats,  and  the  temperature  from  102°  to 
104°  F.,  with  a  slight  morning  remission.  At  this  time  the  aspect  of  the 
patient  is  characteristic — cheeks  burning,  face  injected,  eyes  bright,  tongue 
dry  and  coated,  and  voice  short.  The  hurried  working  of  the  nostrils  indi- 
cates the  acuteness  of  the  dyspnoea.  The  urine  is  scanty  and  high-coloured  ; 
it  is  rich  in  urea  and  uric  acid,  but  very  poor  in  chlorides,  which  appear  to 
be  absorbed  for  the  benefit  of  the  exudate.  Delirium,  which  sometimes 
appears  at  this  stage,  is  quiet,  but  may  be  violent  in  drunkards. 

In  the  hepatized  region  the  dullness  is  complete,  and  the  vocal  fremitus 
is  increased,  and,  as  the  voice  and  the  respiration  are  so  well  conducted  by 
the  solidified  tissues,  the  voice  is  loud,  but  not  articulate  to  the  listener's 
ear.  This  condition  is  called  bronchophony,  and  the  breathing  takes  on 
the  rough,  blowing  tone  known  as  tubular.  Further,  as  all  the  inflamed 
parts  do  not  undergo  their  different  changes  at  the  same  time,  we  may 
find  tubular  breathing  and  crepitations  close  together,  just  as  later  we 
notice  redux  crepitation  and  tubular  breathing  at  the  same  time. 

The  second  stage  lasts  three  or  four  days,  or  sometimes  longer,  after 
which  recovery  usually  commences.  The  situation  may,  however,  become 
worse.  When  pneumonia  ends  in  recovery,  the  fever  falls  very  rapidly 
with  symptoms  of  crisis  ;  the  wastmg  ceases,  and  the  patient  enters  on 
convalescence.  This  condition  coincides  with  the  liquefaction  of  the 
exudate ;  the  sputum  becomes  opaque  and  rich  in  fatty  elements,  the  dullness 
disappears,  and  the  tubular  breathing  gives  place  to  a  rale  that  is  larger 
and  more  moist  than  the  crepitation.  This  rale  is  the  redux  crepitation, 
which  would  better  be  called  a  subcrepitant  rale.  It  is  audible  both  during 
inspiration  and  expiration. 

If  pneumonia  passes  into  the  third  stage  (grey  hepatization),  the  sputum 
assumes  a  greyish  or  prune- juice  tmt,  the  fever  becomes  adynamic  m  type, 
the  pulse  is  small  and  irregular,  the  abdomen  is  distended,  diarrhoea  appears, 
clammy  sweat  covers  the  patient,  and  delirium  is  present  at  the  end,  which 
is  almost  always  fatal. 


DISEASES  OF  THE  LUNG  127 

Extrapulmonary  Localizations. 

The  infection  does  not  always  spend  all  its  force  on  the  lung.  In  many- 
cases,  even  in  frank  pneumonia,  but  especially  in  epidemic  pneumonia  of  a 
well-marked  infectious  type,  the  pneumococcus  invades  the  pleura,  peri- 
cardium, endocardium,  meninges,  stomach,  peritoneum,  joints,  ear,  etc. 
The  invasion  of  these  organs  may  be  consecutive,  parallel,  or  anterior  to 
that  of  the  lung ;  it  may,  indeed,  be  independent  of  the  pulmonary  invasion. 
Let  us  study  these  forms. 

1.  Pneumococcal  Pleurisy. — The  pleura  is  almost  always  affected  in 
pneumonia.  The  pleurisy  is  frequently  dry,  and  limited  to  the  production 
of  false  membranes,  which  vary  in  thickness,  and  cover  the  pleura  to  a 
variable  extent,  especially  at  the  mterlobar  fissures. 

In  other  cases  we  find  pleurisy,  with  sero-fibrinous  or  purulent  effusion. 
The  pleural  inflammation  sometimes  develops  as  a  contact  lesion  from 
the  pneumonic  focus ;  at  other  times  it  arises  at  a  distance  from  the  focus, 
the  pneumococcus  invading  the  pleura  on  its  own  account. 

Pleurisies  with  effusion  often  supervene  in  the  decline  of  pneumonia  or 
in  full  convalescence.  They  have,  therefore,  received  the  name  of  meta- 
or  post-pneumonic.  As  a  rule,  they  are  not  sero-fibrinous,  but  suppurative. 
Suppuration  may  be  caused  by  the  pneumococcus,  without  the  aid  of  the 
usual  pyogenic  organisms  (streptococcus  and  staphylococcus) ;  and  when 
these  organisms  are  present,  the  infection  is  secondary.  Meta-pneumonic 
pleurisy  may  invade  the  general  cavity  of  the  pleura,  or  else  be  encysted, 
i^iterlobar,  diaphragmatic,  or  mediastinal  (see  Chapter  V.),  These  forms 
may  arise  without  pain,  the  fever  may  or  may  not  return,  and  after 
three  to  six  weeks  they  often  end  by  vomica.  Some  eventually  open  in  an 
intercostal  space  ;  others,  especially  in  children,  termmate  in  absorption. 
The  prognosis  of  these  pleurisies  Is,  as  a  rule,  not  grave.  Those  which 
occupy  the  general  cavity  may  exceptionally  yield  to  thoracentesis,  but 
in  most  cases  operation  for  empyema  is  necessary. 

We  also  find  early  pleurisies  in  which  the  effusion  occurs  at  the  same  time 
as  pneumonia.     Lemoine  has  given  them  the  name  of  para-pneumonic. 

We  must  not  forget  that  aseptic  puriform  effusions  may  also  exist  in 
pneumonia  ;  they  must  not  be  confused  with  septic  purulent  pleurisy.* 

2.  Pneumococcal  Endocarditis. — Endocarditis  is  a  fairly  frequent 
complication  of  pneumonia.  It  aj)pears  during  the  course  of  this  affection 
(para-pneumonio),  but  most  often  during  convalescence  (meta-pneumonic). 
The  pneumococcus  itself  is  the  cause  (Netter),  and  is  rarely  found  in  associa- 
tion with  other  microbes,  such  as  streptococci  (Wcichsclbaum),  or  special 
bacilli  (Lion).  In  exceptional  cases  endocarditis  consecutive  to  pneu- 
monia is  the  result  of  the  streptococcus  alone  (Jaccoud),  und  the  uifection 

♦   Vide  Chapter  V.,  Section  6. 


128  TEXT-BOOK  OF  MEDICINE 

is  secondary.  Endocarditis  is  more  frequent  in  certain  epidemics  of  pneu- 
monia, in  cases  associated  with  influenza,  and  in  the  course  of  pregnancy. 
It  is  in  general  accompanied  by  other  extrapulmonary  infections  due  to 
the  pneumococcus,  such  as  purulent  pleurisy,  pericarditis,  arthritis,  etc. 
Suppurative  meningitis  iii  particular  is  frequently  associated  with  it.  The 
invasion  of  the  endocardium  by  the  pneumococcus  may  be  independent 
of  pneumonia,  and  show  itself  in  the  course  of  certain  affections  caused 
likewise  by  the  pneumococcus — viz.,  broncho-pneumonia,  cerebro -spinal 
meningitis,  inflammation  of  the  great  serous  membranes,  etc.  Endo- 
carditis may  develop  in  subjects  who  have  no  cardiac  lesion,  but  previous 
valvular  disease  is  singularly  favourable  to  its  appearance. 

Pneumococcal  endocarditis  usually  attacks  the  left  heart,  and  is  found 
at  the  aortic  more  often  than  at  the  mitral  orifice,  in  the  proportion  of 
3  to  2  (Netter).  Though  it  more  rarely  affects  the  right  heart  (one-seventh 
of  the  cases),  it  is,  nevertheless,  more  frequent  there  than  in  endocarditis 
due  to  other  microbes.  Pneumococcal  endocarditis  causes  vegetations 
rather  than  ulcerations.  The  vegetations  are  rounded,  with  a  regular  sur- 
face ;  the  largest  are  sessile,  with  a  broad  base,  and  very  adherent.  They 
are  only  detached  in  exceptional  cases.  Embolism  is  rare,  and  septic 
capillary  emboli  are  not  often  seen.  It  is,  therefore,  exceptional  to  find 
emboli  of  the  spleen,  kidneys,  etc.,  contrary  to  what  is  seen  in  streptococcal 
or  in  staphylococcal  endocarditis,  where  the  loosely  attached  vegeta- 
tions often  give  rise  to  these  accidents.  Destructive  lesions  may  be  seen — 
viz.,  little  ulcers  of  the  endocardium,  tiny  abscesses  m  the  myocardium, 
followed  by  the  production  of  valvular  aneurysms.  The  virulent  pneumo- 
coccus is  found  in  the  deep  parts  of  the  vegetations,  just  as  in  the  blood. 
Pneumococcal  endocarditis  has  been  caused  experimentally  in  the  rabbit 
after  previous  injury  to  the  valves,  and  even  without  traumatism. 

As  a  rule,  endocarditis  is  silent  when  it  develops  at  the  same  time  as 
pneumonia,  and  passes  unnoticed  if  the  heart  is  not  examined  daily.  Meta- 
pneumonic endocarditis,  which  supervenes  some  weeks  after  the  onset  of 
pneumonia,  and  often  after  a  more  or  less  complete  period  of  apyrexia, 
may  commence  with  a  rigor  and  rapid  rise  of  temperature.  It  commonly 
assumes  the  typhoid  form  of  malignant  endocarditis,  with  fever  and  grave 
adynamia.  Auscultation  may  reveal  blowing  murmurs,  variable  in  in- 
tensity and  position  at  the  different  orifices.  In  some  cases  the  symptoms 
of  concomitant  meningitis  are  the  chief  feature  (Osier).  The  usual  ter- 
mination is  death,  which  occurs  after  a  very  variable  period.  Exceptional 
cases,  followed  by  recovery  (Traube,  Lion),  with  or  without  persistence  of 
the  valvular  lesions,  are,  however,  recorded. 

3.  Pneumococcal  Pericarditis. — This  is  another  insidious  manifesta- 
tion, only  discovered  by  daily  auscultation.     This  pericarditis,  which  is 


DISEASES  OF  THE  LUNG  129 

almost  always  accompanied  by  pleurisy,  rarely  begins  before  the  fifth  day 
of  the  pneumonia.  Its  frequency  is  variable,  according  to  the  epidemic. 
Abundance  of  fibrin  is  present,  and  the  effusion  is  usually  purulent. 

4.  Pneumococcal  Meningitis. — Meningitis  may  supervene  during 
pneumonia,  or,  later,  during  convalescence.  In  the  former  event  it  often 
passes  unnoticed,  the  excitement  and  delirium  being  put  down  to  fever  or 
alcoholism.  This  is  a  common  error.  In  the  latter  form  the  symptoms 
comprise  fever,  headache,  quiet  or  violent  delirium,  pain  in  the  nape  of  the 
neck,  muscular  rigidity,  squint,  contraction  of  the  jaws,  inequality  of  the 
pulse,  Cheyne  Stokes  breathing,  and  coma. 

Post  mortem  the  pia  mater  is  infiltrated  with  greenish-yellow  exudate, 
and  the  dura  mater  is  converted  into  a  thick  cap.  Bulbar  and  spinal  menin- 
gitis are  frequently  met  with.  In  some  cases  epidemic  cerebro-spinal 
meningitis,  due  to  the  pneumococcus,  has  been  observed. 

5.  Pneumococcal  Nephritis. — The  urinary  troubles  are  various.  Albu- 
muiuria,  hsematuria,  and  anuria,  have  been  noted.  True  nephritis,  with 
ursemic  symptoms,  may  occur. 

The  renal  changes  have  been  minutely  studied  by  Caussade.  The 
kidney  is  large  and  ecchymotic.  The  nephritis  is  almost  always  haematuric. 
It  may  be  caused  by  the  pneumonic  infection,  for  the  pneumococcus  has 
been  found  in  the  kidney  or  may  be  grafted  upon  existing  lesions. 

G.  Pneumococcal  Gastritis. — The  stomach,  like  other  organs,  may  be 
infected  Ijy  the  pneumococcus.  I  have  quite  recently  seen  this  gastric 
infection  in  two  patients  suffering  from  pneumonia  with  generalized  infec- 
tion— viz.,  peritonitis,  pericarditis,  endocarditis,  meningitis,  and  arthritis.* 
These  patients  presented  gastric  symptoms  of  ])a,u\,  nausea,  vomiting,  and 
abundant  hsematemesis.  Post  mortem,  the  mucosa  was  studded  with 
haemorrhagic  erosions,  due  to  acute  necrobiosis.  In  one  case  pneumococci 
were  swarming  in  the  erosions.  This  form  of  gastritis  is  described  in  detail 
under  Ulcers  of  the  Stomach. 

7.  Pneumococcal  Peritonitis.— I  do  not  allude  here  to  the  primary 
form, I  which  will  be  described  later.  I  am  at  present  concerned  with 
peritonitis  which  arises  as  a  secondary  condition  in  the  course  of  pneumonia. 
Secondary  peritonitis  is  rarer  than  the  primary  form.  The  symptoms  aro 
abdomuial  pain,  tympanites,  nausea,  vomitiiig,  and  diarrhiea.  This 
secondary  peritonitis  is  not,  in  my  opinion,  as  serious  as  the  primary  form. 
It  was  on  the  road  to  recovery  in  the  two  cases  described.  J 

*  Diculafoy,  "  Gastrite  ulcereuso  pncumococciquo  "  {Clinique  Medicale  dc  VILUd- 
Difii,  1S99,  U""  le<,-on,  p.  219). 

•j-  Ditnilafoy,  "  rcritnnito  primitive  a  I'ncumocoquca  "  {Clinique  Medicale  dc  r/L'td- 
DIeu,  1S9G,  1S""=  kvon,  p.  .390). 

J    Vide  "  Ulcerative  Gastritis." 

9 


130  TEXT-BOOK  OF  MEDICINE 

8.  Pneumococcal  Arthritis. — Arthritis  and  synovitis  may  supervene 
during  the  course  or  the  decline  of  pneumonia.  In  exceptional  cases  they 
may  precede  it,  and,  indeed,  we  see  primary  arthritis  without  pneumonia. 
It  usually  presents  the  same  clinical  aspect.  The  affected  jomts  are  the 
seat  of  very  acute  pam,  which  is  soon  followed  by  swelling,  oedema,  and 
redness.  It  might  almost  be  called  a  blennorrhagic  arthritis,  for  the  peri- 
articular synovial  sheaths  often  participate  in  the  process.  Movement  is  very 
difficult,  pressure  is  very  painful,  the  temperature  is  raised,  and  the  tongue 
dry,  while  the  patient  is  prostrated  and  shows  the  signs  of  grave  infection. 

The  course  varies  somewhat  in  different  cases.  Sometimes  it  is  rapid, 
and  pus  forms  m  a  few  days,  but  at  other  times  its  progress  is  slower.  The 
prognosis  of  these  joint  lesions  is  usually  grave  not  from  the  arthritis,  but 
from  the  more  or  less  general  infection.  The  gravity  of  the  prognosis  can- 
not be  based  on  the  degree  of  virulence  of  the  pneumococcus,  for  in  a  case 
ending  favourably  the  pneumococcus  was  very  virulent,  while  in  one  ending 
fatally  its  virulence  was  low.  However  this  may  be,  the  therapeutic 
indication  is  to  let  out  the  purulent  fluid. 

Previous  lesions  (rheumatism.,  trauma)  may  favour  articular  infection 
by  the  pneumococcus.  Experiments  have  given  similar,  but  not  constant, 
results. 

The  lesions  vary,  accordhig  to  the  intensity  and  the  duration  of  the 
mfection.  We  may  find  serous  or  purulent  effusion,  thickenmg  of  the 
synovial  membrane,  and  destruction  of  the  articular  cartilages  and  the 
ends  of  the  bones.  In  one  of  my  patients  suffering  from  arthritis  of  the 
wrkt,  the  joints  contained  |  ounce  of  pus,  rich  in  pneumococci ;  the  articular 
surface  was  rough,  and  in  places  the  cartilage  had  completely  disappeared. 

9.  Pneumococcal  Otitis. — Otitis  is  a  fairly  frequent  complication  of 
pneumonia.  The  disease  has  an  acute  course,  and  usually  ends  in  recovery. 
Nevertheless,  it  may  give  rise  to  cerebral  or  cerebro -spinal  meningitis,  sinus 
plilebitls,  or  abscess  of  the  brain  and  of  the  cerebellum. 

The  enumeration  of  the  complications  of  pneumonia,  which  include 
pleurisy,  menmgitls,  parotiditis,  peritonitis,  otitis,  and  suppurative  arthritis, 
shows  that  suppuration  plays  a  great  part.  The  pneumococcus  alone  can 
cause  suppuration,  and  the  pus  in  such  a  case  has  special  characters.  It  is 
viscid,  rich  m  cellular  elements,  and  of  a  greenish  colour,  like  laudable  J3us ; 
the  serum  does  not  separate  out.  In  other  cases,  however,  the  usual 
organisms  of  suppuration — i.e,  streptococci  and  staphylococci — cause 
secondary  infection  and  suppuration. 

Varieties.— Pneumonia  does  not  always  show  the  same  characters,  but 
assumes  somewhat  different  forms,  accordmg  to  the  age  of  the  patient  (old 
age),  to  the  previous  condition  of  health  (want,  alcoholism,  pregnancy), 
to   the   numerous   extra-pulmonary   localizations,    to   the   seasons   of  the 


DISEASES  OF  THE  LUNG  131 

particular  year,  or  to  other  causes  which  are  still  imperfectly  known  (epidemic, 
or  influenzal  pneumonia)  ;  and,  as  Peter  says,  pneumonic  conditions  exist 
besides  pneumonia ;  in  other  words,  there  is  a  clinical  as  well  as  a  patho- 
logical aspect. 

Varieties  in  Situation. 

Central  Pneumonia. — Pneumonia  sometimes  remams  localized  hi  the 
deep  tissue  of  a  lobe,  and  though  the  symptoms — i.e.,  rigor,  high  tempera- 
ture, dyspnoea,  cough,  and  rusty  sputum — point  to  pneumonia,  yet  the 
physical  signs  are  wantmg ;  dullness,  rales,  and  tubular  breathuig  are 
absent,  until  the  inflammation  extends  and  yields  the  usual  signs. 

Double  Pneumonia. — A  second  attack  of  pneumonia  may  arise  durhig 
the  course  of  the  first.  This  second  attack. shows  itself  from  the  sixth  to 
the  eighth  day.  "  Pneumonia  is  never  double  from  the  fn-st  "  (Grisolle). 
As  regards  site,  every  variety  is  possible,  but  most  often  the  corresponding 
lobe  of  the  opposite  side  Is  affected.  The  second  pneumonia  ls  generally 
less  extensive  than  the  first,  and  the  inflammation  is  less  severe.  It  does 
not  begin  with  a  fresh  chill  or  pain  in  the  side,  and  the  appearance  of  the 
sputum  is  scarcely  altered.  Percussion  and  auscultation  reveal  the  fresh 
focus  which  the  symptoms  had  not  almounced.  The  dyspncea,  however,  is 
more  acute  at  the  time  of  the  fresh  mvasion,  and  the  temperature  in  the 
axilla  affords  valuable  help.  In  unilateral  j^neumonia  the  axillary  tempera- 
ture is  higher  by  some  tenths  on  the  affected  side  ;  in  double  pneumonia  the 
temperature  is  the  same  on  both  sides  (Landrieux). 

Apical  Pneumonia.— This  form  is  justly  regarded  as  very  grave,  and  is 
often  accompanied  by  collapse,  adynamia,  and  a  typhoid  state.  Suppura- 
tion is  prone  to  occur,  and  delirium  and  jaundice  may  appear,  while  the 
usual  signs  of  pneumonia — i.e.,  pain  in  the  side,  cough,  and  expectoration — 
are  less  marked.  Apical  pneumonia  is  a  serious  disease — first,  because  it  ia 
more  frequent  m  old  age,*  and  also  because  alcoholism  and  general  ill-health 
favour  apical  pneumonia.  The  reasons  for  this  predilection  are  well  dis- 
cussed by  Peter,  who  regards  the  upper  lobes  of  the  lung  as  endowed  with 
less  vitality,  and  as  "  auxiliary  and  additional." 

Apical  pneumonia  is  more  frequent  on  the  right  side,  and  when  the  signs 
cannot  be  found  m  the  clavicular  region  or  in  the  supraspinal  fossa,  they 
miLst  be  looked  for  in  the  axilla.  The  situation  of  this  variety  might 
lead  us  to  take  it  for  a  tubercular  lesion.  This  error  m  diagnosis  must  be 
avoided. 

Massive  Pneumonia.  -In  this  form  of  pneumonia  ((Jrancluu)  the 
fibrmous  coagulation  extends  throughout  the  whole  bronciiial  network  of 

*  VV<5  .SCO  ill  tlic  statist ics  uf  iJiiiund  Fiuilcl  lliat  in  lliirty  cjuscs  of  fatal  pnouuionia 
thu  apiucs  wore  aifuctud  cigLtcun  times  ("  Tiaitc  ties  Maladies  dcs  V'ioillurds,"  p.  4G0). 

y— 2 


132  TEXT-BOOK  OF  MEDICINE 

the  invaded  territory,  and  reaches  even  the  large  bronchi.  The  air,  there- 
fore, cannot  enter  the  bronchial  tubes,  and  most  of  the  stethoscopic  signs  of 
pneumonia  are  wanting.  Neither  tubular  breathing  nor  rales  are  heard ; 
expectoration  is  almost  absent.  It  is  therefore  evident  how  difficult  it 
may  be  to  distinguish  between  pleuritic  effusion  and  massive  pneumonia. 
However,  certam  signs  are  of  value  in  diagnosis.  The  dullness  of  pleural 
effusion  is  more  complete  and  more  fluid  than  that  of  pneumonia.  Further, 
the  displacement  of  organs  (notably  of  the  heart),  which  is  absent  in  the 
case  of  pneumonia,  is  more  or  less  marked  in  the  case  of  effusion. 

Varieties  of  Pneumonia,  according  to  Age. 

1.  Children  are  more  subject  to  lobular  than  to  lobar  pneumonia  ;  still, 
lobar  pneumonia  is  often  seen,  even  as  early  as  the  first  year.  In  young 
children  the  onset  is  often  accompanied  by  convulsions,  vomiting,  and 
erythematous  eruptions.  The  respiration  is  panting,  and  the  pulse-rate 
may  exceed  140.  About  the  age  of  five  years  the  dry,  crepitant  rale  is 
heard ;  below  this  age  we  find  rather  the  subcrepitant  rale.  The  other 
signs  closely  resemble  those  of  pneumonia  in  the  adult,  but  the  child  does 
not  expectorate,  and  hence  the  absence  of  rusty  sputum,  which,  however, 
is  sometimes  seen  'm.  four-  to  five-year-old  children.  Under  two  years  of 
age  the  cyclical  course  of  the  fever  is  really  the  only  differential  sign  between 
lobar  and  lobular  broncho-pneumonia.  The  prognosis  is  grave  only  in 
the  very  young  ;  a  little  later  the  disease  is  relatively  benign. 

2.  In  the  aged,  in  whom  there  is  little  organic  reaction,  pneumonia  is 
insidious  ;  the  rigor  is  insignificant,  and  the  pain  in  the  side  may  escape 
notice.  The  colour  of  the  face  and  the  dryness  of  the  tongue  are  sometimes 
the  only  signs.  We  wait  m  vain  for  rusty  sputum,  which  does  not  appear. 
The  crepitant  rale  is  coarser  than  in  the  adult — in  a  word,  pneumonia  is 
altered  by  the  age  of  the  individual.  At  the  Salpetriere  ambulatory  pneu- 
monia is  sometimes  seen  ui  old  women,  who  contmue  to  eat  and  to  attend 
to  their  occupations.  They  die  almost  suddenly,  and  suppurative  pneu- 
monia is  found  post  mortem. 

Clinical  Varieties  of  Pneumonia. 

At  the  beginning  of  this  article  I  described  the  ordinary  form  of  lobar 
pneumonia,  but  it  is  clear  that  the  extrapulmonary  localizations  in  the 
pleuja,  heart,  meninges,  and  kidneys  give  a  special  aspect  to  pneumonia. 
On  the  one  hand,  some  clinical  varieties  depend  upon  the  predominance  of 
the  lesions  in  a  certain  organ,  while  in  other  cases  the  varieties  depend  on 
the  general  appearance  of  the  morbid  complex,  and  the  disease  assumes 
special  features. 

1.  In  the  so-called  inflammatory  or  sthenic  form,  often  described  by 


DISEASES  OF  THE  LUNG  133 

old  writers,  and  frequent  in  the  country,  the  chief  characters  are  as  follows  : 
Redness  of  the  face,  epistaxis,  violent  headache,  restlessness,  severe 
inflammation  of  the  lung,  sputum  which  is  sometimes  bloody,  speedy 
hepatization,  rapid  and  quivering  pulse. 

2.  The  asthenic  form  is  characterized  by  the  following  symptoms : 
Insidious  onset,  lassitude,  early  delirium,  subsultus  tendinum,  prostration, 
stupor,  soft  and  imequal  pulse,  tendency  to  adynamia,  and  collapse. 

3.  The  nervous  forms  show  several  varieties.  Delirium  is  common, 
especially  in  drunkards.  It  may  not  be  associated  with  cerebral  lesions, 
while  in  other  cases  delirium  Ls  caased  by  cerebral  or  cerebro-spmal  menin- 
gitis, due  to  the  local  action  of  the  pneumococcus. 

The  paralyses  consecutive  to  pneumonia  show  different  forms.  In  the 
acute  phase  of  pneumonia  they  nearly  always  affect  the  hemiplegic  type, 
with  or  without  aphasia,  and  with  or  without  apoplexy.  These  pjiral3''ses, 
which  are  curable  in  the  adult,  but  fatal  in  the  elderly,  are  due  to  lesions  of 
the  cerebral  vessels  (Lepine). 

The  paralyses  which  supervene  during  convalescence  affect  the  para- 
plegic type,  or  the  type  of  isolated  paralyses,  with  or  without  muscular 
atrophy.  These  paralyses  are  in  some  cases  due  to  meningo-spinal  changes, 
in  others  to  peripheral  neuritis  of  'toxic  origin,  like  the  palsies  of  diph- 
theria. 

4.  Biliary  pneumonia  comprises  two  very  distinct  forms.  In  the  one 
there  is  pneumonia  with  jaundice,  which  is  consecutive  to  catarrhal  inflam- 
mation of  the  bile-ducts,  or  to  perihepatitis  produced  by  right  basal 
pneumonia.  These  lesions  are  then  purely  local.  In  the  other  there  is 
pneumonia  with  a  biliary  condition,  which  depends  on  a  general  morbid 
state.  This  condition  is  characterized  by  a  subicteric  tint,  with  al)sence  of 
active  reaction,  soft  pulse,  headache,  foul  tongue,  vomiting,  and  diarrhoea. 
The  biliary  condition  accompanies  the  grave  forms  (apical  pneumonia, 
alcoiiolism).  It  is  connected  with  "the  medical  constitution  of  the  season 
of  the  year."  It  forms  part  of  what  was  called  peripneumonic  biliary  fever, 
and  explains  tlie  epidemics  of  biliary  pneumonia.  In  some  exceptional 
cases  pneumonia  is  connected  with  a  diffuse  hepatitis,  a  variety  of  icterus 
gravis. 

5.  Malignant  and  Epidemic  Pneumonia.— Every  pneumonia,  whether 
benign  or  malignant,  is  an  infective  dis(!ase,  but  clinically  it  is  customary  to 
reserve  the  epithets  "  infective  "  and  "malignant "  for  the  grave  and  abnormal 
forms.  There  is,  first  of  all,  the  infectious  pneumonia  which  has  at  different 
times  appeared  in  epidemic  form  during  epidemics  of  malaria,  scurvy,  and 
typhoid  fever.  Next,  there  is  secoiidary  pneumonia,  supervening  in  tlio 
course  of  some  general  disease,  and  deriving  its  character  and  gravity  from 
the  surroundings  in  wliieh  it  develops. 


134  TEXT-BOOK  OF  MEDICINE 

In  many  cases,  however,  pneumonia  develops  on  its  own  account — ■ 
sometimes  in  an  isolated  form,  but  more  often  in  the  form  of  more  or  less 
circumscribed  epidemics,  which  may  be  associated  with  those  of  influenza. 
It  is  accompanied  by  all  the  features  of  an  infectious  malady. 

The  contagion  is  quite  proved.  The  epidemic  breaks  out  in  a  prison,  in 
barracks,  or  in  a  small  area,  or  confines  itself  to  a  house  or  to  a  family, 
tliree  or  four  members  being  affected  simultaneously  or  successively. 

In  some  cases  this  epidemic  pneumonia  differs  but  little  from  genuine 
pneumonia.  As  a  rule,  it  presents  special  features,  which  have  earned  for 
it  the  names  "  typhoid,"  "  asthenic,"  "  adynamic,"  etc.  Hepatization 
sometimes  occurs  at  several  foci.  The  sputum  is  bloody  rather  than  rusty, 
and  the  disease  is  accompanied  by  swelling  of  the  spleen,  diarrhoea,  albu- 
minuria, jaundice,  pleurisy,  pericarditis,  vegetative  endocarditis,  menin- 
gitis, parotiditis,  precordial  distress,  and  prostration.  The  fever-chart 
does  not  resemble  that  of  frank  pneumonia.  The  histological  lesions  are 
somewhat  special.  The  prognosis  is  not  absolutely  bad.  The  disease  is 
benign  m  one  epidemic,  malignant  in  another.  The  prognosis,  like  the 
clinical  picture,  comprises  every  intermediate  form. 

6.  Pregnancy  and  Pneumonia. — Grisolle  maintained  that  lobar  pneu- 
monia is  formidable  in  pregnant  women.  At  the  present  day  the  opposite 
opinion  holds  good.  Many  cases  of  pneumonia  occurring  at  different 
stages  of  pregnancy  have  been  published.  The  ,  disease  was  relatively 
benign  for  mother  and  child.  Last  year  I  saw  tliree  cases  of  pneumonia 
during  pregnancy,  one  at  a  very  late  stage.  The  women  recovered,  and 
delivery  took  place  without  mishap.  The  transmission  of  pneumonia  to 
the  foetus  is  an  established  fact.  In  the  published  cases  the  child  has 
succumbed  a  few  days  after  delivery.  The  infant  may  succumb  without 
showing  any  lesions  in  the  lung.  Post  mortem  we  fbid  lesions  in  the  liver 
and  the  spleen,  due  to  toxines  which  have  traversed  the  placenta. 

Pneumonia  in  a  nursing  woman  diminishes  or  suppresses  the  secretion 
of  milk.  As  the  pneumococcus  can  be  transmitted  by  suckling,  the  mother 
should  not  continue  to  suckle  her  child. 

etiology. — Lobar  pneumonia  is  a  disease  of  adults.  In  the  aged  it 
assumes  special  features,  and  the  child,  though  more  subject  to  the  lobular 
form,  may  contract  the  lobar  variety.  Changes  of  season — -as  in  November, 
March,  and  April— appear  favourable  to  its  development.  Previous 
debility  is  not  necessary  as  a  predisposing  cause,  for  pneumonia  frequently 
attacks  people  in  perfect  health.  Some  persons  have  a  special  pre- 
disposition to  recurrences  and  contract  several  attacks.  Probably  the 
pneumococcus  is  always  present,  awaiting  a  favourable  opportunity  for 
development. 

I   have    previously   discussed   epidemicity.     Epidemics   of   pneumonia 


DISEASES  OF  THE  LUNG  135- 

may  be  limited  to  a  locality,  or  spread  thsough  a  town,  province,  or  country. 
They  often  coincide  with  influenza,  and  are  due  to  unknown  atmospheric 
or  climatic  causes,  which  increase  the  virulence  of  the  microbe. 

The  question  of  contagion  demands  notice.  Pneumonia  is  contagious, 
and  the  sputum  most  often  spreads  contagion,  which  may  be  active  long 
after  recovery.  The  foetus  may  be  infected  by  its  mother,  and  may  itself 
show  the  pulmonary  and  extrapulmonary  lesions  of  the  infection. 

The  nature  of  lobar  pneumonia  has  been  interpreted  in  various  ways, 
and  till  recently  two  chief  theories  were  in  evidence.  One — the  Hippo- 
cratic  doctrine,  upheld  and  defended  by  the  Montpellier  school — regarded 
the  lesion  of  the  lung  as  the  local  and  secondary  expression  of  a  general 
state,  called  pneumonic  fever.  Pneumonia — that  is  to  say,  the  lesion — 
would  then  be  the  result  of  pneumonic  fever,  which  is  the  disease.  The 
anatomo-pathological  school  of  Paris  has  brought  forward  quite  an  opposite 
theory :  The  lesion  in  the  lung  represents  the  whole  disease,  and  the  local 
lesion  Is  the  cause  both  of  the  fever  and  of  the  general  symptoms. 

Between  these  extremes  an  intermediate  opinion  has  found  a  place.  It 
Is  generally  admitted  that  a  chill  is  perhaps  the  commonest  cause  of  pneu- 
monia ;  for  effective  action,  cold,  or  any  other  provoking  cause,  must  find 
the  system  in  a  favourable  condition  of  receptivity. 

Firstly,  is  it  true  that  cold  plays  such  a  large  part  in  the  development 
of  pneumonia  ?  According  to  some  statistics,  cold  Is  said  to  act  as  a  pro- 
voking agent  in  only  a  half  or  a  third  of  the  cases.  The  cause  of  lobar 
pneumonia  resides  in  the  existence  of  an  infectious  organism — the  pneumo- 
coccus — but  the  chill  is  tlie  chief  provokmg  agent. 

The  pneumococciLS  being  the  cause  of  pneumonia,  how  are  we  to  admit 
that  its  entrance  into  the  lung  may  be  followed,  after  such  short  delay,  by 
the  symptoms  of  acute  pneumonia  ?  In  answer  to  this  objection,  Jaccoud 
admits,  with  good  reason,  the  possibility  of  auto -infection.  "  The  human 
organism  constantly  lodges  various  microbes  in  large  numbers.  As  long 
as  its  functions  are  normal,  it  Is  a  hostile  medium,  which  wards  off  their 
noxious  effects.  However,  let  disturbance  arise  and  alter  the  physiological 
functions,  the  hostile  medium  becomes  friendly,  and  the  affected  organism 
is  deprived  of  effective  resistance  against  the  very  microbes  which  it 
but  lately  tolerated  without  being  affected."  The  pneumococcus  exists 
normally  in  the  mouth  (Pasteur),  in  the  pharynx,  and  in  the  bronchi  (Netter). 
Sliould  it  enter  the  lung  in  those  who  are  not  in  a  state  of  receptivity,  its 
j)athogoiuc  iiiHuonce  is  annihilated  by  the  activity  of  the  ])liagocytes.  In 
the  ojiposite  condition  pneumonia  dcf^lares  itself. 

The  dissemination  of  the  pneumococcus  produces  the  extrapulmonary 
localizations  above  described. 

In  opposition  to  the  primary  form   just  described,   wc  ^oo  secondary 


'  136  TEXT-BOOK  OF  MEDICINE 

infections  which  are  less  frank  in  evolution,  and  supervene  in  other  diseases 
(diabetes,  cachexias,  gout,  eruptive  fevers,  etc.).  This  variety  of  lobar 
pneumonia  is  somewhat  rare,  for  the  secondary  form  chiefly  devolves  upon 
lobular  pneumonia. 

Course — Duration — Termination. — Lobar  pneumonia  has  a  mean 
duration  of  five  to  ten  days.  The  period  during  which  the  temperature 
rises  is  short  and  rapid.  By  the  second  day  it  reaches  its  maximum  (104°  to 
106°  F.),  remains  stationary  for  some  days,  with  a  morning  remission  of  J°  to 
1°,  and  in  most  cases  defervescence  is  sudden  and  complete  in  twenty- 
four  hours.  This  defervescence,  which  usually  occurs  between  the  fifth 
and  the  seventh  days,  is  often  accompanied  by  symptoms  of  crisis — viz., 
sweating,  epistaxis,  diarrhoea,  and  profuse  secretion  of  urine  contaming 
albumin  and  excess  of  chlorides.*  This  increase  varies  in  proportion  to 
the  retention  of  chlorides  m  the  tissues  during  the  illness.  It  is  remark- 
able that  the  defervescence  is  sometimes  preceded  by  transient  aggravation 
of  the  disease.  This  has  been  called  the  precritical  phase.  Labial  herpes 
cannot  be  considered  as  a  symptom  of  crisis,  for  it  often  appears  at  the  onset 
of  pneumonia. 

Suppuration  in  the  lung  is  a  frequent  cause  of  death,  which,  however, 
may  occur  before  the  appearance  of  grey  hepatization.  Some  patients  are 
struck  down  by  adynamia  and  fatal  collapse  during  the  stage  of  red  hepati- 
zation, while  others  succumb  through  the  extensive  nature  of  the  lesion, 
which  invades  several  lobes,  narrows  the  field  of  haematosLs,  and  induces 
asphyxia  and  cardiac  paralysis.  In  some  well-proved  cases  suppurative 
pneumonia  has  caused  death  by  purulent  infection,  and  the  affected  tissue 
may  suppurate  as  a  result  of  the  pneumococcus  alone. 

Diagnosis — Prognosis. — Let  us  first  differentiate  between  lobar  pneu- 
monia and  other  inflammations  of  the  lung. 

1.  Lobar  pneumonia  is  nearly  always  primary.  It  invades  one  or 
several  lobes,  remains  confined  to  a  definite  area,  and  spares  the  rest  of  the 
organ.  Onset,  course,  and  termination  are  clearly  marked  :  the  crepitant 
rale,  the  tubular  breathing,  and  the  rusty  sputum  scarcely  permit  confusion  ; 
suppuration  is  exceptional,  and  recovery  is  tlie  usual  termination  when  the 
infection  does  not  involve  other  organs.  These  characters  are  distorted 
when  the  pneumonia  is  secondary,  takes  on  an  epidemic  form,  or  develops 
in  the  aged. 

I  would  add,  too,  that  even  in  its  frank  forms  lobar  pneumonia  does  not 
always  present  the  complete  picture  sketched  in  this  chapter.  It  has  been 
my  lot  to  see  cases  of  lobar  pneumonia  which  differ  from  the  classical  type. 
Many  so-called  lobar  pneumoniae  border  on  inflammation  of  the  chest, 

*  Up  to  defervescence  the  urine  was  scanty,  dark,  and  in  twenty-four  hours  con- 
tained 35  to  50  grammes  of  urea,  instead  of  the  normal  quantity  of  28  to  30  grammes. 


DISEASES  OF  THE  LUNG  137 

and  are  the  intermediary  forms  which  unite  clinically  the  various  inflamma- 
tions of  the  respiratory  passages. 

2.  Lobular  or  broncho-pneumonia  is  especially  frequent  in  children, 
and  is  often  consecutive  to  some  other  malady  (measles,  diphtheria,  whoop- 
ing-cough, influenza,  tuberculosis,  etc.).  It  deserves  the  name  of  "  fibrinous  " 
less  than  the  preceding  form.  It  Ls  lobular — that  is  to  say,  it  spreads  by 
centres  which  are  scattered  tlirough  both  lungs,  and  may  be  isolated  or 
confluent.  The  disease  does  not  exhaust  all  its  action  on  the  inflamed 
centres.  It  progresses  by  successive  outbursts.;  its  lesions  and  its  course 
are  irregular,  and  its  description  differs  notably  from  that  of  lobar  pneumonia. 

3.  Inflammation  of  the  chest  is  not  pneumonia,  and,  on  the  other 
hand,  differs  from  simple  congestion.  It  is  a  morbid  condition  in  wliich 
the  hyperaernic  and  inflammatory  elements  are  differently  combined. 
The  inflammation  affects  one  or  several  lobes,  and  does  not  spare  the  other 
parts  of  the  respiratory  system.  The  bronchi,  the  pleura,  and  the  muscles 
of  the  thorax — in  fact,  all  the  superposed  layers  of  the  chest — may  be 
affected  in  different  degrees. 

4.  Spleno-pneumonia  (Grancher)  is  thus  defined  by  this  author : 
"  Between  pulmonary  congestion  and  lobar  pneumonia,  and  side  by  side 
with  broncho-pneumonia,  there  exists  a  morbid  condition  of  the  lung — a 
kind  of  subacute  pneumonia,  which  simulates  pleurisy  with  moderate 
effusion,  and  deserves  its  own  description  and  denomination."  Potain 
has  described  a  variety  of  pneumonia  which  he  has  named  congestive,  and 
to  which  he  says  spleno-pneumonia  may  be  likened. 

5.  Hypostatic  pneumonia  has  not  the  anatomical  attributes  of  a  true 
pneumonia.  It  is  a  mixed  condition,  in  which  passive  congestion  and 
oedema  play  the  chief  part,  and  are  accompanied  by  slight  transudation 
of  fibrin,  and  sometimes  by  hsemorrhage.  This  morbid  condition,  con- 
secutive to  heart  disease,  hypostasis,  and  prolonged  decubities,  chiefly 
involves  the  posterior  and  lower  parts  of  the  lungs. 

0.  Pleurisy  at  first  presents  numerous  analogies  with  pneumonia.  In 
pleurisy,  however,  the  chill  is  less  violent,  the  initial  temperature  is  not  so 
high,  the  pain  in  the  side  is  often  more  acute,  expectoration  is  absent,  and 
the  friction  soinid  is  more  moist  and  diffuse  tlian  the  dry,  crepitant,  and 
clearly  localized  rule  of  pneumonia. 

It  is  not  sufficient  to  diagnose  pneumonia  :  wc  must  also  know  whether 
it  is  inflammatory,  biliary,  or  adynamic  ;  whether  it  is  or  is  not  complicated 
by  pleurisy,  endocarditis,  ])ericarditis,  meningitis,  or  otitis  ;  whether  it  is 
primary  or  secondary  ;  whether  it  is  arc'f)in[)anied  by  alcoholism  ;  whether 
it  is  the  first  act  in  commencing  typhoid  fever  ;  whether  it  has  developed 
in  a  diabetic  or  in  a  tubercular  subject.  Each  of  the.se  points  affects  the 
prognosis  and  the  treatment  as  mucli  as  the  diagnosis. 


138  TEXT-BOOK  OF  MEDICINE 

Treatment. — The  treatment  of  pneumonia  should  be  especially  directed 
to  the  general  condition.  When  pneumonia  is  regular  and  benign,  we  should 
be  content  with  watchful  expectancy,  ordering  acid  drinks,  laxatives,  broths, 
and  wine  diluted  with  water.  In  the  contrary  case  the  indications  must  be 
acted  on.     Blisters  are  more  harmful  than  useful  in  my  opinion. 

Pain  in  the  side  may  be  relieved  by  leeches,  antipyrin,  injections  of 
morphia,  or  by  an  ointment  of  vaseline  10  parts,  methyl-salicylate  1  part. 

In  sthenic  pneumonia  antiphlogistic  treatment  should  be  employed — 
i.e.,  blood-letting,  cupping,  leeches,  and  tartarate  of  antimony,  or,  better 
still,  kermes,  administered  to  Trousseau's  prescription  :. 

Kermes        . .  . .  . .  . .  . .  . .      gr.  xxx. 

Extract  of  digitalis . .  . .  . .  . .         . .      gr.  iii. 

Medicinal  soap        . .         . .         . .         . .         . .      q.s. 

For  20  pills. 

Ten  to  fifteen  pills  are  given  in  the  twenty-four  hours,  and  if  vomiting  or 
diarrhoea  supervene,  1  drop  of  Sydenham's  laudanum  is  given  with  each  pill. 

Good  results  are  also  obtamed  by  infusion  of  digitalis,  given  at  mtervals 
in  the  twenty-four  hours  (Hirtz)  ;  but  I  have  never  tried  this  remedy. 
Biliary  pneumonia  may  be  cut  short  by  emetics,  and  especially  by  ipecacu- 
anha. Adynamic  pneumonia  should  be  treated  with  tonics  and  stimulants, 
such  as  quinine,  tincture  of  coca,  wine,  or  brandy.  If  the  fever  is  severe, 
sulphate  of  quinine  and  antipyrin  may  be  given. 

When  pneumonia  takes  the  ataxic  form,  with  delirium,  restlessness,  and 
high  fever,  the  following  draught,  in  tablespoonfuls  every  hour,  may  be 
given  with  advantage  : 

Orange-flower  water  . .  . .  . .  . .  . .  gilL 

Cherry-laurel  water  . .  . .  . .  . ,  . .  Siii- 

Syrup  of  ether . .  . .  . .  . .  . .  . .  3x. 

Bromide  of  potash  . .  . .  . .  . .  . .  3ss. 

Cold  baths  have  been  extolled  in  the  ataxic  and  hyperthermic  forms  of 
pneumonia.  I  have  used  this  treatment'  several  times  with  success.  I 
would  advise  giving  the  baths  just  as  in  typhoid  fever. 

If  pneumonia  is  accompanied  by  irregular  pulse,  feeble  heart-action,  and 
a  tendency  to  syncope,  subcutaneous  injections  of  the  following  solution  of 
caffein  should  be  given  : 

Distilled  water  . .  . .         . .  . .  . .     3ii. 

Benzoate  of  soda         . .  . .  . .  . .         . .     3ss. 

Benzoate  of  caffeine   . .  . .  . .  . .  . .     3ss. 

I  would  also  advise  in  such  a  case  injections  of  serum  (8  to  16  ounces  or 
more  daily).     For  further  details,  see  chapter  on  Therapeutics. 

The  patient  should  drink  plenty  of  milk,  fresh  water,  and  tisanes,  with 


DISEASES  OF  THE  LUNG  139 

or  without  lactose,  for  it  is  essential  to  promote  urinary  secretion.  Milk 
lias  the  further  advantage  of  protecting  the  kidney — a  fact  not  to  be 
despised,  especially  as  pneumococcal  nephritis  is  now  well  recognized. 

Lastly,  I  must  say  a  few  words  about  the  treatment  of  pneumonia  by 
subcutaneous  injections  of  essence  of  terebinth. 

Fochier  (of  Lyons)  observed  that  in  certain  cases  of  puerperal  infection, 
when  no  important  lesion  can  be  found,  sudden  improvement  may  coincide 
with  the  appearance  of  pus  in  the  iliac  fossa,  the  breast,  a  joint,  or  else- 
where. The  appearance  of  a  local  abscess  or  cellulitis  seemed  to  have  a 
curative  action.  Fochier  gave  it  the  name  of  abscess  of  fixation.  The 
question  was  then  asked  whether  analogous  abscesses  could  not  be  produced 
therapeutically.  In  women  whose  condition  appeared  desperate  recovery 
was  induced  by  subcutaneous  injections  of  essence  of  terebinth. 

As  Lepine  had  been  successful  in  a  case  of  pneumonia,  I  applied  the 
treatment  to  two  women  suffering  from  severe  pneumonia  which  was 
probably  on  the  point  of  suppuration.  Both  patients  recovered.  The 
treatment  is  as  follows  :  An  injection  of  L5  minims  of  essence  of  terebinth 
— i.e.,  60  minims  for  the  four  injections — is  given  by  means  of  a  sterilized 
syringe,  in  the  subcutaneous  tissue  of  the  outer  surface  of  each  thigh  and 
of  the  deltoid  region  of  each  arm.  These  injections  produce  extremely 
acute  pain,  lasting  about  two  hours.  The  next  day  the  injected  regions 
present  an  oedematous,  whitish,  and  diffuse  thickening.  The  abscess  which 
forms  IS  opened,  and  the  pus  in  my  two  cases  was  amicrobic. 

Whether  these  phlegmons  be  called  abscesses  of  fixation  or  abscesses 
of  derivation  matters  little.  What  does  matter  is  the  therapeutical  result. 
It  deserves,  I  think,  to  be  taken  into  serious  consideration.  This  treatment, 
in  my  opinion,  should  be  reserved  for  patients  who  are  suffering  from  grave 
])neumonia  in  which  grey  hepatization  is  imminent. 

Collargol  has  sometimes  given  good  results  (Netter).  An  ointment  con- 
taining 13  per  cent,  of  collargol  is  employed,  and  a  piece  about  the  size 
of  a  nut  is  daily  rubbed  into  the  skin.  It  is  better  to  use  intravenous  injec- 
tion of  ].")  to  .'}()  grains  of  collargol. 

The  prophylactic  treatment  of  pneumonia  should  not  be  neglected.  It 
must  not  be  forgotten  that,  as  pneumonia  is  contagious,  proper  precautions 
must  be  taken  to  isolate  the  sick,  and  to  disinfect  the  sputum  and  articles 
of  bedding  or  clothing  used  by  the  patient. 

V.  CHRONIC  PNEUMONIA— FIBROSIS  OF  THE  LUNG. 

Chronic  inflammation  of  the  limg  may  affect  the  pareiu-hyina  and  liie 
con?u'ctive  tissue.  These  lesions  give  rise  to  the  varieties  of  chronic  pneu- 
monia known  as  lobar,  lobular,  and  cortical. 


140  TEXT-BOOK  OF  MEDICINE 

The  chronic  pneumonia  called  caseous  is  really  tubercular,  and  will  be 
studied  later,  under  Phthisis. 

Chronic  Lobar  Pneumonia. — The  lobar  form  is  much  rarer  than  the 
lobular  one.  It  may  be  primary,  or  may  follow  acute  pneumonia.  Malaria 
appears  to  play  some  part  in  its  development. 

In  our  study  of  acute  pneumonia  we  have  seen  that  residual  inflammation 
may  still  remain  in  the  alveoli,  and  may  take  several  weeks  to  absorb 
(Andral).  This  process,  though  it  may  be  slow,  rarely  ends  in  chronic 
pneumonia,  because  the  parenchyma  of  the  lung  is  unaffected ;  and  if  it  do 
so  end,  it  is  because  the  parenchyma  is  affected  by  fresh  inflammation. 

Two  stages  are  described  in  chronic  pneumonia — viz.,  red  and  grey 
induration.  The  lung  tissue  affected  with  red  induration  is  firm  and 
increased  in  size  ;  the  cut  section  is  less  granular,  and  the  tissues  are  less 
friable  than  in  the  red  hepatization  of  acute  pneumonia.  The  indurated 
part  does  not  crepitate,  and  sinks  in  water.  The  walls  of  the  alveoli  and 
the  perilobular  connective  tissues  are  invaded  by  fibrous  tissue.  The 
alveolar  cavities  are  narrowed,  and  at  times  invaded  by  nodules  of  fibrous 
tissue  which  has  replaced  the  wall  of  the  alveolus. 

The  fibrosis  is  intra-  and  extra-lobular.  After  several  months  red  in- 
duration gives  place  to  grey  induration.  The  lung  tissue,  which  has  become 
impermeable,  retracts  and  diminishes  in  volume.  It  is  hard,  creaks  under 
the  knife,  and  has  all  the  attributes  of  fibrous  tissue  (Cruveilhier's  fibrous 
metamorphosis).  In  this  fibrous  tissue  excavations  (ulcers  of  the  lung)  are 
sometimes  met  with,  but  no  bronchiectasis  is  found,  contrary  to  what  is 
seen  in  chronic  broncho-pneumonia. 

This  chronic  pneumonia  extends  in  an  uniform  way  tlirough  a  whole 
lobe  or  a  part  of  the  lung.  It  is  more  common  at  the  base  than  at  the 
apex. 

Dullness,  deformity  of  the  chest,  muco-purulent  sputum,  tubular  breath- 
ing, rales,  and  gurgling,  are  the  signs  of  chronic  pneumonia  ;  and  if  we  add 
frequent  hsemoptysis  and  cachexia,  with  fever,  sweats,  and  wasting,  it  will 
be  admitted  that  the  diagnosis  from  phthisis  would  be  very  difficult  if  the 
existence  of  the  latter  were  not  confirmed  by  the  presence  of  bacilli  in  the 
sputum. 

Chronic  Broncho-Pneumonia. — Chronic  broncho-pneumonia  is  more 
frequent  than  the  preceding  form,  and  usually  follows  acute  or  subacute 
broncho -pneumonia.  It  is  most  common  in  early  life,  and  is  caused  by 
measles,  diphtheria,  whooping-cough,  influenza,  typhoid  fever,  and  syphilis. 

In  the  chronic,  as  in  the  acute,  form  the  lesions  affect  both  the  bronchus 
and  the  lobule.  In  a  vertical  section  of  the  lobule,  during  the  subacute 
phase  the  bronchus  is  dilated,  and  its  normal  elements  are  converted  into 
embryonic  tissue.     The  region  of  the  alveoli  which  surrounds  the  bronchus 


DISEASES  OF  THE  LUNG  141 

is  affected  by  hepatization ;  the  walls  of  the  alveoli  show  embryonic  infil- 
tration, and  the  alveolar  cavities  contain  exudate,  with  epithelial  cells  and 
leucocytes.  Around  the  hepatized  area  we  find  the  splenized  zone,  which 
is  the  seat  of  congestion  ;  the  epithelial  cells  desquamate  and  fall  into  the 
alveolar  cavity. 

As  the  lesion  becomes  chronic  the  intra-alveolar  elements  undergo 
granulo-fatty  degeneration,  and  the  embryonic  cells,  which  infiltrate  the 
parenchyma,  change  into  fibrous  tissue.  The  fibrosis  affects  the  peri- 
bronchial and  perilobular  connective  tissue  and  the  parenchyma  of  the 
lung  atrophies. 

Chronic  broncho-pneumonia  chiefly  afEects  the  lower  lobes  and  the 
posterior  part  of  the  upper  ones.  The  lung  tissue  is  violet-coloured,  dense, 
and  dry ;  the  cut  section  is  smooth,  without  granulations,  and  the  divisions 
between  the  lobules  are  still  perceptible  under  the  low  power.  These 
lesions  were  called  camification,  by  comparison  with  muscular  tissue.  In 
some  cases  the  lung  is  fibrous  and  atrophied,  and  dilatations  of  the  bronchi 
are  found.  They  are  due  to  changes  in  the  bronchial  walls,  and  as  they 
are  found  before  the  lung  atrophies  (Charcot),  it  is  hardly  probable  that 
they  are  consequent  on  the  pulmonary  fibrosis,  as  Corrigan  supposed. 

The  progress  of  chronic  broncho-pneumonia  is  very  slow,  and  the  disease 
passes  through  a  subacute  stage,  subject  to  periods  of  arrest.  Dullness, 
rales,  tubular  breathmg,  and  sometimes  gurgling,  arc  the  most  usual  signs. 
Fever  is  common,  the  expectoration  is  muco-purulent,  or  at  times  blood- 
stained, and  the  disease  usually  ends  in  hectic  fever. 

Chronic  Cortical  Pneumonia. — In  some  cases  of  pleurisy,  when  the 
absorption  of  fluid  is  very  slow,  the  pleura  becomes  thickened,  and  forms 
a  fibrous  shell  over  the  lung.  The  lobes  are  adherent  to  one  another,  and 
the  parietal  pleura  is  likewise  adherent  to  the  chest-wall.  This  fibro-plastic 
process  does  not  always  remain  limited  to  the  pleura,  but  reaches  the  lung 
probably  along  the  lymphatics.  The  connective  spaces  between  the  lobules 
are  transformed  into  fibrous  arches,  which  surround  the  lobules,  and  finally 
involve  the  alveoli  themselves. 

Pleuro-pulmonary  fibrosis  is  thus  brought  about.  These  cases  are 
somewhat  rare  (Brouardel,  Tapret).  I  have  seen  one  case  in  which  bronchi- 
ectasis was  also  present. 

Pulmonary  fibrosis  as  a  secondary  lesion  is  associated  with  diverse 
changes  in  the  lung.  It  accompanies  emphysema,  tuberculous  lesions, 
tumours,  hydatid  cysts,  pneumokoniosis,  etc.  It  is  fairly  common  in 
elderly  people.  The  fibroid  regions  arc  indurated  and  pigmented,  the  fibrous 
framework  of  the  lung  is  thickened,  the  walls  of  the  vessels  take  part  in  the 
change,  and  the  alveolar  cavities  are  atrophied  by  the  new  tissue.  Syphilitic 
fibrosis  of  the  lung  exists,  and  will  be  studied  under  Sypliilitic  Legions  of 


142  TEXT-BOOK  OF  MEDICINE 

the  Lung.  The  lesion  called  slaty  induration  of  the  apices,  and  frequent 
in  the  lungs  of  elderly  people,  is  nothmg  but  a  highly  pigmented  fibrous 
tissue.  This  tissue  bounds  the  alveoli,  which  are  atrojihied  in  some  parts, 
emphysematous  m  others,  and  often  contains  small  cysts  of  long  standing, 
transformed  into  caseous  or  chalky  material. 

VI.  OCCUPATION  PNEUMONIAS— PNEUMOKONIOSIS. 

The  dust  from  coal,  iron,  steel,  copper,  and  silicon,  gives  rise  to  chronic 
pneumonia,  which  we  shall  study  under  the  names  of  anthracosis,  siderosis, 
and  chalicosis. 

Anthracosis. — Antliracosis  may  be  physiological,  most  human  lungs 
being  normally  mottled  with  black.  When,  however,  the  infiltration  of 
carbon  becomes  excessive,  the  lesions  cause  special  symptoms.  Anthracosis 
occurs  chiefly  among  miners,  charcoal-burners,  and  moulders  in  copper, 
brass,  or  bronze,  who  use  carbon  dust  m  their  work. 

The  lesions  seen  are  :  at  first  emphysema,  then  a  black  coloration  of 
the  lung,  which  no  longer  crepitates,  creaks  under  the  knife,  and  sinks  m 
water.  On  crushing  the  lung  tissue,  the  fingers  are  coloured  black,  and  also 
the  water  allowed  to  flow  over  its  surface.  The  cut  section  may  be  mottled 
with  black  or  be  of  an  uniform  black  colour.  The  lung  tissue  is  divided  by 
large  bands  of  connective  tissue,  which  contam  particles  of  carbon,  heaped 
up  at  certam  spots  to  form  nodules.  Histologically,  we  see  fibrosis,  which 
affects  the  connective  tissue  surrounding  the  lobule  and  its  central  bronchus. 
A  fibrous  mass,  crammed  with  black  grams,  is  found  m  these  regions.  Bronchi- 
ectasis is  hardly  ever  seen ;  on  the  other  hand,  obliteration  of  the  bronchial 
arterioles  is  frequent,  and  hollow,  irregidar  ulcerations,  containmg  black, 
putrid  material,  are  the  result.  The  bronchial  walls  are  intact.  The  pleura 
is  adherent  and  thickened ;  the  glands  are  hard  and  black.  Lesions  of  the 
right  heart  are  sometimes  seen. 

Does  antliracosis  predispose  to  tuberculosis  ?  Authorities  are  not  in 
accord  on  this  pomt.  Oberthiir  says  positively  that  tuberculosis  is  rare  in 
coal-miners.  It  may  be  admitted  (Boulland)  that  if  the  damage  to  the 
lung  favour  the  growth  of  the  bacillus,  this  growth  is  arrested  by  the  fibrosis, 
which  isolates  the  foci  and  prevents  their  development.  The  symptoms 
display  three  periods  (Tardieu).  In  the  first  period  we  see  malaise,  with 
loss  of  appetite,  wastmg,  and  fits  of  coughmg,  which  are  followed  by  blackened 
expectoration.  On  auscultation,  the  vesicular  murnmr  is  feeble,  the  voice- 
sounds  are  exaggerated  and  sibilant  and  snoruig  rhonchi  are  sometimes 
audible .  In  the  second  jDcriod  the  symptoms  grow  worse.  Vomitmg  appears, 
the  distress  mcreases,  and  the  induration  of  the  lung  is  complete.  Muco-pus  is 
often  fomid  m  the  sputum,  and  at  times  a  little  blood  is  present.     The  third 


DISEASES  OF  THE  LUNG  143 

period  is  characterized  by  the  progress  of  the  ansemia  and  by  decline.  The 
lung  is  hollowed  out  by  cavities,  and  death  supervenes,  either  by  cachexia 
or  by  asystole.     The  duration  may  be  several  years. 

Chalicosis. — Infiltration  of  the  lung  by  the  dust  of  silica  (chalicosis)  is 
seen  among  stone-cutters  (quarrymen,  millstone  sharpeners,  flint-cutters, 
road  labourers),  needle  sharpeners,  glass,  china,  and  earthenware  workers, 
potters,  and  flax-combers  (Greenhow). 

Post  mortem  the  lungs  are  crammed  with  nodules,  which  are  very  hard 
and  blackish,  or  at  times  grey,  white,  or  yellowish.  Histologically,  we  find 
lobular  fibrosis,  with  narrowing  of  the  alveoli  and  small  crystalloid  granules, 
which  are  strongly  refractive  to  light,  and  composed  of  silica.  Cavities, 
surrounded  by  grains  of  silica,  may  exist.  The  glands  are  hard  and  of  a 
blackish-grey  colour.  Lesions  of  the  right  heart  are  common.  The  symp- 
toms, as  in  anthracosis,  may  present  three  periods.  The  sputum  appears 
more  abundant,  and  hsenioptysis  is  more  frequent.  The  disease  lasts  three 
or  four  years.  The  phthisis  of  earthenware-makers  (Porte)  shows  three 
forms — pneumonic,  emphysematous,  and  suffocating. 

Siderosis. — Up  to  the  present  twenty-one  cases  of  infiltration  of  the 
lung  by  particles  of  iron  have  been  collected  (Zencker  and  Merckel) ;  they 
have  been  seen  in  workmen  using  red  oxide  of  iron  (looking-glass -makers, 
gold-beaters,  and  muTor -polishers).  In  one  autopsy  (Zencker)  the  surface  of 
the  lung  was  of  an  intense  and  uniform  brick-red  colour,  streaked  with 
darker  lines,  corresponding  to  the  interlobular  spaces.  The  pleura  was 
covered  with  red  patches.  There  were  several  cavities  in  the  lung,  without 
a  trace  of  tubercles.  The  microscope  showed  fibrosis  of  the  lung,  with 
graimles  of  iron,  which,  on  chemical  exammation,  gave  its  special  reactions. 

The  physical  signs  resemble  those  of  anthracosis,  and  the  red  sputum  is 
characteristic. 

The  diagnosis  is  chiefly  ba^cd  on  the  characters  of  the  sputum,  which  is 
black  in  anthracosis,  red  in  siderosis,  and  without  objective  characters  in 
chalicosis.  Tlie  diagnosis  from  pulmonary  tuberculosis  and  from  latent 
cancer  of  tlie  stomach  is  most  puzzling.  In  the  first  case  inquiry  as  to  the 
patient's  profession,  and  examination  of  the  sputum  from  the  chemical  and 
bacillary  standpoint  will  be  the  chief  points.  In  the  case  of  latent  cancer 
of  the  stomacli,  where  confusion  is  possible  (Lctulle),  error  can  only  be 
avoided  by  careful  study  of  the  course  of  the  disease. 

Treatment  is,  in  the  first  place,  propliylactic.  Workrooms  must  be  freely 
veutiluted,  attempts  at  preventing  the  jjropagation  of  dust  nuist  be  inaih-,  and 
masks  used.  When  piieuniokoniosis  is  present,  change  of  profession  should 
be  advised.  1'liis  radi(-al  measure  often  arrests  the  disease.  Revulsives, 
balsams,  arsenic,  anil  iodide  of  potash  are  employed  for  the  fibrosis. 


144  TEXT-BOOK  OF  MEDICINE 


VII.  THROMBOSIS  AND  EMBOLISM  OF  THE  PULMONARY 

ARTERY. 

Thrombosis  of  the  pulmonary  artery  is  the  obliteration  of  the  vessel  by 
a  clot  of  blood  formed  during  life.  It  has  many  causes,  such  as  cachexia 
(tuberculosis,  atlirepsia,  malaria),  compression  of  the  artery  by  a  mass 
of  glands,  or  by  a  mediastinal  tumour.  Thrombosis  is  sometimes  consecutive 
to  extensive  pneumonia,  gangrene  of  the  lung,  and  pleurisy  (Vergely). 
Atheroma  and  fatty  changes  in  the  vessel  are  exceptional  causes. 

Embolism  is  the  sudden  obliteration  of  the  vessel  by  a  body  circulating 
in  the  blood;  This  body,  or  embolus,  often  arises  from  a  thrombus.  The 
results  of  embolism  and  the  lesions  to  which  it  gives  rise  vary  with  the 
si2;e  of  the  artery  obliterated,  and  also  with  the  nature  of  the  embolus. 
It  is  therefore  customary  to  study  embolisms  of  the  large,  medium,  and  small 
branches  of  the  pulmonary  artery.  To  this  last  category  belong  the  capillary 
embolisms  ;  to  the  two  first,  the  lobular  and  lobar  ones. 

The  large  embolus,  which  is  arrested  in  an  artery  of  large  or  of  medium 
size,  is  generally  caused  by  an  mert  body ;  the  embolism  is  then  called 
mechanical.  Capillary  embolism  may  also  be  mechanical,  but  is  more  often 
infective  and  microbic. 

Mechanical  Embolisms  of  the  Pulmonary  Artery. 

Pathogenesis. — The  tlu-ombus  may  break  up  and  give  rise  to  emboli, 
which,  however,  arc  much  more  rare  than  those  which  have  their  origin  in 
the  heart  or  in  the  great  vems. 

1.  Embolisms  of  cardiac  origin  are  chiefly  seen  in  mitral  lesions,  and  in 
mitral  stenosis  in  particular  (Duguet).  Aortic  affections,  on  the  contrary, 
rarely  give  rise  to  them.  Bucquoy  has  laid  ^ress  on  pulmonary  embolisms 
consecutive  to  arterio-sclerosis  ;  but  as  the  affection  is  often  accompanied  by 
chronic  myocarditis,  this  is,  without  doubt,  a  cause  of  embolism.  In  all 
these  cases  the  process  is  as  follows  :  On  the  walls  of  the  right  heart,  and 
especially  of  the  right  auricle,  masses  of  fibrin  are  deposited,  and  become 
interwoven  with  the  muscular  bmidles  which  project  into  the  cavity  of  the 
auricle.  The  slowing  of  the  stream  and  the  change  in  the  blood  cause 
coagulation.  The  clot  beaks  down  gradually,  and  its  fragments  escape  to 
form  embolisms  m  the  branches  of  the  pulmonary  artery.  Sometimes  the 
embolus  consists  of  the  debris  of  the  valves  and  chordae. 

2.  Phlebitis  is  a  very  frequent  cause  of  embolism,  especially  in  acute 
infectious  diseases  (typhoid  fever,  erysipelas,  diphtheria,  mfluenza,  variola, 
etc.),  because  the  clot  develops  rapidly,  and  its  adhesion  to  the  walls  of  the 
veins  is  very  slight.     A  separate  place  must  be  given  to  pulmonary  embolism. 


DISEASES  OF  THE  LUNG  145 

following  puerperal  phlegmasia.  This  accident  usually  appears  within  three 
weeks  of  the  confinement ;  beyond  the  fifth  week  puerperal  embolism  is 
exceptional. 

Phlebitis  in  chronic  infectious  maladies  (tuberculosis,  cancer)  and  cachexia 
(malaria,  diabetes,  gout,  etc.)  is  more  rarely  followed  by  pulmonary  em- 
bolism. 

Phlebitis  consecutive  to  varices,  fractures,  or  compression  by  tumour, 
may  also  give  rise  to  embolism,  especially  if  the  lesion  affect  a  vein  in  the 
lower  limbs.  In  some  cases  phlebitis  has  a  deep  origin,  as  in  phlebitis  of 
the  uterine  and  utero-ovarian  veins  (cancer  of  the  uterus,  uterine  fibroma, 
cysts  of  the  ovary,  renal  tumours,  etc.),  and  yet  in  these  different  diseases 
embolism  is  to  Ije  feared. 

Pathological  Anatomy. — In  order  to  understand  the  lesions  which  result 
from  pulmonary  emboHsm,  we  must  bear  in  mind  that  the  lungs  receive  two 
kinds  of  arterial  vessels — the  bronchial  arteries,  charged  with  the  nutrition 
of  the  organ,  and  the  branches  of  the  pulmonary  artery,  cliarged  with 
assuring  haematosis.  These  two  systems  remain  independent.  The 
branches  of  the  pulmonary  artery,  like  those  of  the  spleen  and  kidney,  are 
terminal  (Cohnheim) — that  is,  each  vessel  occupies  its  own  proper  area, 
and  does  not  ana.stomose  with  its  'neighbours.  The  result  is  a  complete 
independence  in  their  function  and  their  diseases.  In  the  case  of  throm- 
bosis there  is,  then,  no  reason  to  count  upon  the  collateral  circulation  to 
remedy  the  effects  of  obstruction  in  the  vessel. 

When  the  obstruction  affects  a  lobar  artery  or  the  trunk  of  the  pulmonary 
artery,  anaemia  is  seen,  or  in  case  of  sudden  death,  atelectasis  of  the  terri- 
tory that  is  no  longer  irrigated  is  found  post  mortem.  If,  on  the  other 
hand,  the  patient  has  survived  some  hours,  we  find  congestion,  oedema, 
or  perhaps  an  infarct,  which  may  occupy  nearly  a  whole  lobe. 

As  a  rule,  the  obliterated  vessel  is  much  smaller — m  most  cases  a  lobular 
artery.  The  obstruction  then  shows  itself  by  the  formation  of  an  infarct, 
which  is  called  hamoptoic  (Laennec),  These  infarcts  may  occur  all  over 
the  lung,  but  are  more  frequent  on  the  right  side  than  on  the  left,  and  usually 
occur  at  the  base,  the  posterior  surface,  and  the  edges  of  the  lungs.  They 
are  sometimes  single,  at  other  times  multiple,  when  their  number  may  be 
unlimited,  just  like  the  number  of  embolisms  which  give  rise  to  them.  They 
have  a  blackisli,  truffled  colour,  and  a  firm  consistency,  which  permits  their 
recognition  by  simple  pressure,  when  they  are  situated  deep  in  the  paren- 
chyma of  the  lung.  Their  cut  siu-f  ace  is  shining,  dry,  and  smooth,  or  granular 
if  the  blood  distends  the  alveoli.  Around  tlie  infarct  the  lung  tissue  is  bright 
red,  passing  to  yellow  as  the  distance  from  the  infarct  increases.  G?lderaa 
of  the  lung  and  pleurisy,  which  is  generally  quite  limited,  are  frequently 
found. 

10 


146  TEXT-BOOK  OF  MEDICINE 

Under  the  microscope  the  alveoli  are  filled  with  red  corpuscles,  which 
are  crowded  together,  and  more  or  less  deformed,  according  to  the  age  of 
the  infarct.  The  interalveolar  spaces  and  the  septa  are  packed  with  red 
corpuscles.  In  an  old  infarct  the  red  corpuscles  are  no  longer  recognizable, 
and  crystals  of  ha3matoidin  and  of  hsematin,  pigmentary  granules  infil- 
trating the  alveolar  walls,  and  fatty  granulations  predominate.  The  con- 
nective network  is  always  thickened.  This  thickening  is  sometimes  but 
slightly  marked,  and  as  the  arteriole  agam  becomes  permeable,  restitutio  ad 
integrum  is  favoured.  Sometimes,  on  the  other  hand,  fibrosis  predommates 
and  causes  a  fibrous  cicatrix,  which  is  retractile  and  prone  to  infiltration  with 
calcareous  salts  (Pitres). 

The  uifarct  may  be  uivaded  by  various  micro-organisms,  whence  the 
possible  coexistence  of  suppurative  or  gangrenous  centres.  In  other 
patients  the  embolus  (phlebitis  in  puerperal  women)  contains  the  micro- 
organisms of  suppuration  or  of  gangrene. 

The  chief  factor  in  the  production  of  infarcts  is  still  surrounded  by 
obscurity,  in  spite  of  experimental  researches.  Ranvier  and  Duguet  have 
shown  that  some  time  elapses  between  the  obliteration  of  the  artery  and 
the  formation  of  the  mfarct.  The  interval  between  these  accidents  is  some- 
times as  long  as  two  or  tlu"ee  days,  and  it  is  then  supposed  that  the  walls  of 
the  artery  become  mflamed  on  the  proximal  side  of  the  obliteration,  break 
down,  and  fuially  burst.  The  infarct  is  produced  at  this  moment.  This 
interpretation  is  to-day  more  generally  admitted  than  that  of  collateral 
congestion  (Virchow,  Rmdfleisch). 

When  the  capillary  embolisms  (non-infectmg)  are  few  in  number,  they 
are  not,  as  a  rule,  accompanied  by  any  change  in  the  lung  tissue,  because  the 
circulation  is  re-established  by  the  anastomoses  of  the  capillary  network.  If 
their  number  is  considerable,  they  may  give  rise  to  grave  results  from  the 
many  capillaries  obliterated.  Experimentally,  capillary  embolisms  are  easily 
caused  by  the  injection  of  finely-divided  substances  into  the  jugular  vein. 
As  these  substances  are  irritant  to  the  lung  tissue,  they  determme  pseudo- 
tuberculous granulations  at  the  point  where  they  are  arrested. 

Symptoms — Diagnosis. — The  large  embohsms  give  rise  to  very  dis- 
similar results.  The  patient  may  be  struck  down  by  syncope,  and  die 
suddenly ;  he  may  survive  some  minutes  or  hours.  Intense  dyspnoea, 
rapid  cyanosis,  and  cardiac  troubles  (angina  and  palpitations)  are  seen, 
though  examination  of  the  heart  and  of  the  lungs  reveals  no  lesion.  Lastly, 
in  some  cases  the  patient  is  seized  with  intense  pain  in  the  side,  severe 
dyspnoea,  and  perhaps  a  rigor.  Improvement  soon  occurs,  and  he  sub- 
sequently coughs  up  more  or  less  profuse  blood-stamed  sputum,  provmg  an 
infarct.  In  this  form  of  embolism  recovery  may  take  place,  but  the  patient 
often  succumbs  in  a  few  days,  after  several  attacks,  with  signs  of  acute  asystole. 


DISEASES  OF  THE  LUNG  147 

The  setiological  conditions  have  a  capital  importance  in  diagnosis.  The 
large  embolLsms  are  due  to  phlebitis,  while  the  medium  ones  usually  arise  in 
cardiac  lesions.  These  same  a?tiological  indications  will,  in  the  case  of  sudden 
death,  and  hi  the  absence  of  an  autopsy,  justify  the  diagnosis  of  puhnonary 
embolism,  and  not  that  of  angina  pectoris  due  to  aortic  disease.  Likewise 
the  asthmatic  attack,  the  sudden  suffocations  of  uraemia,  which  arise  under 
very  different  conditions,  will  hardly  give  rise  to  confusion.  EmboUsms  of 
moderate  size — that  is  to  say,  those  which  always  end  in  the  formation  of 
infarcts — have  a  more  clear  clinical  history  than  the  precedmg  variety. 

We  can  diagnose  an  infarct  in  a  cardiac  patient  whose  heart  begins  to 
fail  if  we  find  sudden  dyspnoea  and  intense  pahi  in  the  side,  followed,  some 
hours  later,  by  the  rejection  of  bloody  sputum.  The  patient  coughs  up 
brownish  or  blackish  viscid  sputum,  and  not  frothy  blood,  as  m  haemop- 
tysis. Auscultation,  which  is  negative  when  the  infarct  is  deep,  reveals, 
in  the  case  of  a  superficial  uifarct,  a  silent  or  tubular  area,  around  which 
subcrepitant  rales  are  heard.  Friction  sounds,  due  to  dry  pleurisy  or  to 
slight  effusion,  may  be  heard.  The  early  rales  sometimes  become  moister 
and  larger,  while  the  vesicular  murmur  reappears ;  sometimes  cavernous 
breathing  is  heard  when  the  infarct  has  been  emptied  tlu-ough  the  bronchi, 
leaving  a  cavity,  which  will  finally  be  filled  up.  Li  cases  where  some 
secondary  uifection  is  grafted  on  the  infarct,  so  as  to  produce  suppiu-ation 
or  gangrene,  fever  appears,  and  the  expectoration  takes  special  characters 
as  regards  appearance  and  odour. 

In  elderly  people  the  discovery  of  sudden  effusion,  which  is  preceded  by 
pain  in  the  side,  often  finds  its  explanation  ia  a  latent  uifarct  (Vulpian). 

The  repetition  of  complications  and  the  coexistence  of  progressive 
cardiac  weakness  govern  the  prognosis. 

We  have  already  shown  the  means  of  distinguishing  between  hsemoptysis 
and  the  bloody  expectoration  due  to  infarct ;  in  some  cases,  however,  the 
Uifarct  may  give  rise  to  true  haemoptysis.  The  rusty  sputum  of  pneu- 
monia is  more  viscid  and  aerated  than  that  of  pulmonary  embolism,  and 
again  the  clinical  picture  is  quite  different. 

Treatment. — To  prevent,  as  far  as  possible,  the  formation  of  emboli 
every  patient  suffering  from  phlebitis  should  be  kept  in  bed  four  or  live 
weeks.  When  embolism  occurs,  we  must  treat  symptoms :  cupping,  in- 
halations of  oxygen,  and  sinapisms,  (|uict  the  dyspnoea.  The  (juantity  of 
blood  brouglit  up  is  rarely  so  abundant  Jis  to  be  formidable.  The  means 
recommended  for  hastening  the  absorjition  of  an  infarct  are  practically 
futile.  It  is  important  to  watch  the  condition  of  the  heart,  and  to  restore 
its  tone  by  dijiitalis  and  caffeiu. 


10—2 


148  TEXT-BOOK  OF  MEDICINE 

Special  and  Infecting  Pulmonary  Embolisms. 

The  name  of  special  embolisms  is  given  to  the  capillary  obliterations 
due  to  inanimate  foreign  bodies,  as  opposed  to  microbic  infecting  em- 
bolisms. The  first  act  mechanically ;  the  second,  on  the  other  hand,  are 
endowed  with  vital  properties,  which  cause  suppuration,  sloughing,  and 
gangrene.  The  first  group  includes  the  debris  of  the  fibrinous  clot,  broken 
up  by  disaggregation,  as  in  old  foci  of  phlebitis,  fibrmous  cysts  in  vems 
(Verneuil),  and  accumulations  of  cellular  debris  at  a  given  spot  (burns, 
frost-bite,  certain  intoxications).  When  the  embolLsms  occur  at  many 
points  at  once,  they  may  end  in  death  by  suffocation,  miless  they  pass 
mmoticed. 

More  important  are  fatty  embolisms,  following  fractures  and  osteo- 
myelitis. Dejerine  thinks  that  the  increase  of  the  intramedullary  pressure 
consequent  upon  inflammation  causes  the  little  oil-drops  of  the  bony 
marrow  to  enter  the  capillaries.  These  embolisms  cause  sudden  and  ex- 
treme dyspnoea.  The  injured  man  has  air-hunger  ;  his  face  and  limbs  are 
cyanosed  ;  he  sometimes  brings  up  blood-stained  froth,  and  rapidly  succumbs, 
with  or  without  convulsions.  Innumerable  fatty  droplets  mixed  with  blood 
are  found  post  mortem  in  the  vessels  of  the  lung,  and  some  authors  there- 
fore refer  diabetic  coma  and  suffocation  in  eclampsia  to  fat  embolism. 

Gaseous  embolisms  belong  rather  to  the  domain  of  surgery,  and  usually 
follow  the  entrance  of  air  mto  the  cervical  veins.  This  accident  shows  itself 
by  a  characteristic  whistlmg  ;  severe  dyspnoea  develops  suddenly,  and  death 
usually  follows. 

The  infective  microbic  embolisms  are  daily  becoming  more  numerous 
as  the  life-history  of  micro-organisms  becomes  better  known.  Some  reach 
the  lungs  m  the  debris  of  clots  ;  others  make  up  the  embolus  alone.  The 
Streptococcus  pyogenes  is  the  most  common  ;  then  come  the  staphylococci, 
coli  bacillus,  and  a  host  of  other  aerobic  or  anaerobic  micro-organisms,  which 
reproduce  in  situ  most  of  their  original  processes.  Miliary  abscesses, 
suppurative  and  gangrenous  infarcts,  admit  no  other  cause.  This  variety 
of  embolism  will  be  studied  under  gangrene  of  the  lung.  Pulmonary  tuber- 
culosis and  certam  forms  of  pseudo-tuberculosis  (tuberculosis  due  to  Asper- 
gillus glaucus,  fumigatus,  etc.),  frequently  spread  by  the  circulatory  system, 
and  can  be  reproduced  experimentally  (Renon).*  The  secondary  cancerous 
nodules  develojDcd  in  the  lung  are  due  to  embolisms  of  cancerous  origin,  just 
as  the  white  pulmonary  infarcts  of  leucocytheemia  are  due  to  accumulation 
of  hypertrophied  leucocytes,  and  as  the  pigmentary  embolisms  of  malaria 
are  due  to  the  arrest  of  pigment  granules  in  the  capillaries  of  the  lung. 

*  See  the  chapter  on  Aspergillary  Pseudo-Tuberculosis. 


DISEASES  OF  THE  LUNG  149 


VIII.  GANGRENE  OF  THE  LUNG— GANGRENE  OF  EMBOLIC 
ORIGIN— GANGRENE  OF  AERIAL  ORIGIN. 

We  must  first  define  the  meaning  of  the  word  gangrene.  Gangrene  ia 
not  simply  the  death  of  a  tissue  (necrosis  or  necrobiosis) ;  it  is  death,  with 
which  putrefaction  or  fermentation  is  associated.  This  fermentation  is 
due  to  anaerobic  organisms  (Pasteur).  Gangrene,  therefore,  is  not  simply  the 
death  of  a  tissue  ;  it  is  the  death  of  a  tissue  accompanied  by  putrid  changes. 
"  Sometimes  gangrene  pervades  an  already  necrosed  area,  in  which  case 
it  is  secondary;  at  other  times  necrosis  and  putrefaction. of  living  tissues 
are  caused  by  the  same  process,  in  which  cases  the  gangrene  is  primary. 
Gaseous  gangrene,  symptomatic  anthrax,  noma,  and  some  cases  of  pul- 
monary gangrene  belong  to  the  category  of  primary  gangrenes." 

Two  great  processes  are  responsible  for  gangrene  of  the  lung — ^gangrene 
of  embolic  origin,  the  germs  reachmg  the  lung  m  the  form  of  emboli  by  the 
venous  channels  ;  and  gangrene  of  aerial  origin,  the  germs  reaching  the  lung 
by  the  respiratory  tract. 

1.  Pulmonary  Gangrene  of  Embolic  Origin. 

Pathology. — Whenever  a  purulent,  putrid,  or  gangrenous  centre  exists 
somewhere  in  the  economy  (otitis,  appendicitis,  suppurative  phlebitis, 
osteo-myelitis,  etc.),  this  centre  may  give  rise  to  specific  emboli  which  end 
in  the  lung.  Having  reached  the  lung,  the  embolus  provokes  a  like  infection. 
If  it  contains  germs  of  suppuration,  the  infarct  suppurates  ;  if  it  contains 
those  of  putrefaction,  the  infarct  becomes  putrid  ;  if  it  carries  the  germs  of 
gangrene,  both  these  changes  occur  at  the  same  time.  Furthermore,  puru- 
lent germs  may  sometimes  start  from  an  infected  centre ;  at  other  times, 
those  of  putrefaction  and  gangrene,  as  in  the  examples  quoted  l)elow. 

Let  us  take  otitis,  which  I  have  compared  to  appendicitis,  as  it  resembles 
the  latter  affection  closely,  in  that  the  infection  is  elaborated  hi  a  closed 
cavity  and  in  the  multiplicity  of  its  complications.  Whether  the  otitis  be 
acute  or  chronic  matters  little  ;  it  may  at  a  given  moment  give  rise  to  suppu- 
rative or  gangrenous  lesions.  The  former,  such  as  cervical  abscess,  menin- 
gitis, abscess  of  the  cerebellum,  or  of  the  cerebrum,  will  be  studied  later. 
Pulmonary  gangrene  consecutive  to  otitis  will  be  studied  here,  and  in 
order  to  judge  of  its  importance  I  give  a  resume  of  cases. 

Case  1. — A  young  woman,  who  had  excellent  health  in  spile  of  a  discharge  from 
I  lie  ear  for  five  years,  wa.s  seized  suddenly  with  sharp  pains  in  the  right  ear,  fever, 
headache,  and  vomiting.  A  week  later  she  came  into  hospital  :  prostration,  severe 
headache  on  the  right  side,  some  right  otorrhosa,  no  mastoid  pain  on  pressure,  tonguo 
dry,  and  breath  ftetid.  Some  days  later  intense  pain  under  li-ft  hreast,  suIk  lepitant 
rules,  high  fever,  acute  dyspna'a,  frequent  cough,  fa'tid  sputum,  albuniinuriu,  and 


150  TEXT-BOOK  OF  MEDICINE 

death.  Post  mortem  several  gangrenous  infarcts  in  right  Imig,  and  gangrenous  pleurisy, 
with  15  ounces  of  fluid.  The  tympanic  cavity,  which  was  the  starting-point  of  these 
troubles,  contained  a  small  quantity  of  foetid  pus. 

Case  2. — A  child,  who  for  three  years  had  discharge  from  the  left  ear,  was 
suddenly  taken  ill  with  fever,  mastoid  pain,  and  vomiting.  Brun  opened  the  mastoid, 
and  found  foetid  pus  in  the  antrum.  A  diffuse  gaseous  phlegmon  soon  developed  in  the 
cervico-dorsal  region  ;  breath  foetid ;  respiration  panting ;  death.  Post  mortem 
thrombo-phlebitis  of  left  lateral  sinus,  and  embolic  gangrene  of  lung,  both  consecutive 
to  otitis. 

Case  3. — Boy,  affected  for  three  years  with  apparently  benign  discharge  from  the 
right  ear.  High  fever,  with  intense  dyspnoea,  rigors,  and  pain  in  chest,  supervened. 
Auscultation  showed  mischief  at  right  base.  Pains  in  chest  became  most  acute  ;  breath 
was  foetid  ;  temperature  rose  to  104°  F.  ;  death.  Post  mortem  both  lungs  riddled  with 
gangrenous  centres  "of  various  sizes  and  miliary  abscesses  consecutive  to  otitis. 

Appendicitis,  like  otitis  (increased  virulence  of  micro-organisms  in  a 
closed  cavity),  may  also  give  rise  to  remote  suppuration  (liver,  pleura, 
meningitis,  etc.)  and  embolic  gangrene  of  the  lung.  I  shall  here  deal  with 
gangrene  of  the  lung. 

I  saw  the  following  case  at  the  Hotel-Dieu : 

Man  admitted  for  sharp  pain  at  the  right  base.  No  expectoration.  Signs  of 
pneumonia  found  at  the  painful  region.  Temperature  raised.  Patient  also  complained 
of  sharp  pains  below  the  right  ribs  in  the  flank  and  iliac  fossa.  Palpation  gave  a  feeling 
of  thickening  and  fluctuation.  We  therefore  thought  of  an  abdominal  abscess,  with 
consecutive  pneumonia.  Patient  transferred  to  siu"gical  ward  and  examined  under 
cliloroform,  but  the  abdominal  effusion  was  not  confiimed.  Death  two  days  later.  On 
opening  the  abdomen  we  found  a  collection  of  foetid  pus, 'with  false  membranes  and 
adhesions.  This  collection  was  due  to  apjiendicitis.  It  started  from  the  iliac  fossa 
and  tracked  up  below  the  liver,  where  a  subphrenic  pocket  was  found.  At  the  base  of 
the  right  lung  a  gangrenous  centre  as  large  as  an  orange.  This  centre  was  composed 
of  two  concentric  layers — the  outer  reddish,  the  inner  blackish,  excavated,  and  foul- 
smelling. 

The  examples  above  quoted  give  an  idea  of  embolic  gangrene  of  the  lung. 
I  have  chosen  my  examples  from  otitis  and  appendicitis,  but  many  other 
foci  (bone  lesions,  bed-sores,  puerperal  lesions,  endocarditis,  etc.)  may  end 
in  the  same  result. 

Pathological  Anatomy.— This  form  corresponds  to  Laennec's  circum- 
scribed gangrene,  with  the  nearly  constant  addition  of  gangrenous  pleurisy. 
The  gangrenous  centres  vary  from  the  size  of  a  cherry-stone  to  that  of  an 
egg ;  they  are  mostly  present  in  both  lungs,  and  are  multiple ;  some  are 
superficial  and  sub  pleural ;  others  are  deep-seated.  The  subpleural  centres 
have  the  conical  shape  of  infarcts  and  a  haemorrhagic  tint.  An  arteriole  is 
usually  seen  at  the  apex  of  the  cone.  The  deep  centres  have  the  shape 
of  blackish  nodes,  distinct  from  one  another.  Gangrenous  infarcts  show 
the  following  forms  :  "  Small,  firm  infarcts,  which  appear  to  be  quite 
recent,  show  on  section  a  yellowish  caseous  nodule,  purulent  and  ex- 
tremely foetid,  in  the  centre  of  a  brownish  or  greenish  tissue  engorged 


DISEASES  OF  THE  LUNG  151 

with  blood.  The  older  infarcts  have  in  their  centre  softened  inaterial 
of  a  chocolate-brown,  surrounded  by  a  scalloped  collarette.  Beneath  the 
pleura,  infarcts  with  a  liquefied  centre  are  found.  The  pleura  is  raised  by- 
gaseous,  foul-smelling  bullae,  forming  little  caverns,  which  do  not  appear  to 
communicate  with  the  bronchi.  At  its  entrance  into  the  infarct  the  arteriole 
is  filled  with  blood  and  with  bacteria  in  enormous  numbers.  At  the  centre  of 
the  infarct  it  has  necrosed,  and  its  wall  is  reduced  to  a  shred.  The  bronchiole 
which  accompanies  it  is  flattened  and  full  of  desquamated  cells  and  leuco- 
cytes (Guillemot). 

The  gangrenous  cavity  contains  a  greyish  pulp,  composed  of  the  following 
"elements  :  pus  corpuscles,  large  cells  infiltrated  with  fatty  granules,  masses 
composed  of  threads  of  connective  or  of  elastic  tissue  and  debris  of  capillaries, 
pigmentary  granules,  crystals  of  margarine,  leucin,  tyrosin,  and  various 
micro-organisms.     All  these  elements  are  found  in  the  sputum. 

The  cavity  is  surrounded  by  a  first  layer,  which  serves  as  a  wall  and 
limits  the  loss  of  substance.  This  layer  is  made  up  of  debris  of  lung  tissue, 
elastic  fibres,  and  obliterated  vessels,  which  are  continuous  with  the  next 
layer.  The  second  layer  is  formed  of  lung  tissue  in  the  condition  of  grey 
hepatization.  It  is  friable  and  sanious  ;  the  alveoli  are  filled  with  pus  and 
large  fatty  cells,  and  the  vessels  are  blocked  by  coagulated  fibrin.  The 
third  layer,  which  is  continuous  with  the  healthy  part  of  the  lung,  shows  the 
lesions  of  catarrhal  pneumonia. 

2.  Pulmonary  Gangrene  of  Aerial  Origin. 

Gangrene  of  aerial  origin  corresponds  to  the  difluse  form.  It  presents 
much  the  same  changes  as  the  circumscribed  form,  save  that  they  are 
diffused  and  very  extensive. 

In  certain  cases  the  well-marked  nodules  of  circumscribed  gangrene  and 
the  irregular  lesions  of  the  diffuse  form  are  found  together. 

Gangrene  of  the  lung  (circumscribed  or  diffuse)  Is,  as  a  rule,  accompanied 
by  pleurisy,  which  may  be  gangrenous,  purulent,  or  sero-fibrinous.  Pneumo- 
thorax Is  not  rare  ;  it  may  result  from  perforation  or  from  putrefaction. 
Lastly,  particles  of  sloughs  may  pass  through  the  pulmonary  vems  into  the 
left  heart  and  the  general  arterial  circulation,  and  set  up  lesions  due  to 
capillary  oinbolisms. 

Pathogenesis.— Pulmonary  gangrene  of  aerial  origin  may  depend  on 
various  mechanisms. 

Since  the  cavity  of  the  bronchi,  bronchioles,  and  alveoli  are,  as  it  were, 
the  prolongation  of  the  bucco-pharyngeal  cavity,  it  Is  clear  that  microbes 
inhabiting  this  latter  cavity  may  gradually  reach  and  develop  in  regions 
when^  Ihoy  do  not  normally  exist.  For  their  growth,  however,  the  soil 
must  be  prepared ;  the  individual  must  be  in  a  state  of  receptivity. 


152  TEXT-BOOK  OF  MEDICINE 

For  this  reason  this  gangrene  Ls  not  usually  seen  in  robust  people  ;  on 
the  other  hand,  it  is  frequent  in  alcoholics,  diabetics,  and  in  sufferers  from 
Bright's  disease,  malaria,  mental  disease,  or  chronic  cerebral  affections.  It 
is  sometimes  met  with  in  the  course  of  acute  infectious  diseases — measles, 
variola,  typhoid  fever,  etc. — or  in  subjects  exposed  to  intense  and  pro- 
longed chill  (Bucquoy). 

In  other  cases  it  may  supervene  as  a  complication  in  the  course  of  various 
lesions  of  the  respiratory  tract — cavities  of  phthisis,  cancer  and  sarcoma  of 
the  lung,  chronic  pneumonia,  hydatid  cysts,  foreign  bodies  in  the  air -passages, 
perforation  of  the  lung  in  chest  wounds,  foreign  bodies  carried  in  through 
such  a  wound  (bullets,  shreds  of  clothing,  fragments  of  rib)  ;  opening  of  an 
abscess  into  the  bronchi  from  the  liver,  spleen,  kidney,  etc.  ;  perforation  of 
the  oesophagus  in  cancer,  whether  spontaneous  or  due  to  forcible  catheteri- 
zation. 

All  the  gangrenous  or  suppurative  affections  of  the  bucco-pharyngeal 
cavity — noma,  diphtheria,  bucco-pharyngeal  abscess,  laryngeal  necrosis, 
operations  ujDon  the  mouth  and  throat,  removal  of  lingual  cancer — may  cause 
gangrene  of  the  lung.  It  is  probable  in  the  latter  cases  that  the  obstruction 
to  swallowing  explains  the  entrance  of  infected  particles  mto  the  respiratory 
passages,  an  accident  also  seen  in  lunatics,  patients  suffering  from  labio- 
glosso-laryngeal  and  diphtheritic  paralyses. 

A  pulmonary  infarct,  resulting  from  non-infective  embolism,  may  be 
invaded  secondarily  by  micro-organisms. 

As  regards  lobar  pneumonia,  although  gangrene  is  an  exceptional  ter- 
mination, and  even  denied  by  Laennec,  yet  some  cases  are  found  (Grisolle, 
Andral,  Bouillaud,  Lanceraux).  Gangrene  ls  more  frequent  in  lobular 
pneumonia  ;  but  why  tn  any  given  case  does  the  infection  of  the  lung  tissue 
end  in  gangrene  ?  To  answer  this  question  the  patient's  general  condition 
has  been  called  in  question.  It  is  said  that  in  the  insane,  diabetics,  and 
alcoholics  the  infectious  process,  instead  of  tending  to  resolution,  finds  in 
the  general  state  of  the  subject,  or  perhaps  in  the  then  existing  constitution 
(Graves,  Leudet),  a  reason  for  ending  in  necrosis  and  putrefaction  of  tissue. 
On  this  account  an  individual  already  weakened  by  typhoid  fever,  or  suffering 
from  an  eruptive  fever  (scarlatina,  measles,  variola),  would  run  a  risk  of  the 
pulmonary  inflammation  ending  in  gangrene. 

Syphilis  sometimes  determmes  gangrene  of  the  lung. 

Lastly,  in  certain  cases  a  part  must  be  assigned  to  overcrowding  and  to 
contagion,  especially  in  hospital  wards. 

Bacteriology. — The  microbic  origin  of  this  affection  was  foreseen  as 
early  as  1849  by  Virchow,  but  it  is  chiefly  to  Leyden  and  Jaffe  that  we  are 
indebted  for  the  first  serious  work  on  this  subject.  Without  attributing  to 
the  Leptothrix  pidmonalis — a  microbe  derived  from  the  Leptothrix  huccalis— 


DISEASES  OF  THE  LUNG  153 

as  great  an  importance  as  tliese  authors  would  do,  we  cannot  hesitate  to 
recognize  that  this  micro-organism  exists  in  most  of  the  foci  of  gangrene, 
either  alone  or  in  association  with  the  Monas  lens,  Cercomonas  (Kannen- 
berg),  Proteus  vulgaris,  Micrococcus  tetragenus,  and  many  other  aerobic 
and  anaerobic  microbes.  We  may  note  the  Bacillus  ramosus  (Veillon  and 
Zuber),  the  Bacillus  fragilis  (Veillon  and  Zuber),  and  the  Micrococcus 
fcetidus.  "  Upon  the  whole,  in  the  centres  of  gangrene  the  aerobic  flora  is 
chiefly  and  sometimes  uniquely  represented  by  an  almost  constant  species 
of  streptococcus.  In  all  cases  this  flora  is  less  numerous  than  the  anaerobic 
one.  It  may,  indeed,  be  completely  absent.  The  anaerobic  species  are,  on 
the  contrary,  represented  by  various  and  very  numerous  kinds  "  (Guillemot). 

Symptoms.— Gangrene  of  the  lung  is  sometimes  ushered  in  by  special 
symptoms,  such  as  extreme  rise  of  temperature,  acuteness  of  thoracic  pain, 
and  adynamia  ;  but  in  other  cases  no  hint  may  be  given  of  the  imminence  of 
gangrene.  I  have  seen  two  cases  in  which  the  course  of  events  was  as 
follows  :  An  individual  is  taken  ill  with  chills,  nausea,  and  vomiting  ;  cough, 
dyspnoea,  and  pain  are  next  added  to  the  gastric  symptoms.  Auscultation 
shows  slight  pleural  rub,  scattered  rales,  and  tubular  breathing,  due  to 
pulmonary  congestion  or  to  broncho-pneumonia.  The  fever  is  moderate, 
and  the  general  condition  without  special  significance.  At  the  commence- 
ment the  disease  simulates  an  ill-defined  infection,  but  the  Issue  is  not  long 
in  coming.  The  patient  Is  seized  with  dyspnoea  and  fits  of  coughing,  and  if 
there  is  a  communication  between  the  gangrenous  centre  and  a  bronchus 
(this  is  more  rare  in  the  case  of  embolic  than  of  aerial  gangrene),  he  brings 
up  abundant  blackish  sputum,  which  Is  mixed  with  blood  and  extremely 
foetid.  It  is  then  evident  that  a  gangrenous  focus  has  formed  in  the  lung, 
and  has  just  opened  into  a  bronchus. 

As  soon  as  the  communication  between  the  bronchus  and  the  centre 
occurs,  the  expectoration  and  the  breath  become  horribly  foetid,  and 
haemoptysis  Is  not  uncommon.  The  sputum  is  very  abundant,  diffluent, 
greeuisli,  or  blackish  ;  it  contains  blood,  pus,  mucus,  fat,  crystals  of  mar- 
garine, elastic  fibres,  balls  of  filaments,  and  micro-organisms. 

When  the  expectoration  Is  abundant,  if  collected  in  a  measure-glass, 
it  usually  presents  three  distinct  layers.  The  top  Is  frothy  and  muco- 
j)urul(int ;  the  middle  one,  transparent  and  viscid,  appears  to  be  composed 
of  thickened  saliva  ;  lastly,  at  the  bottom  of  the  sputum-glass  we  find 
yellowish  or  greenish  balls,  giving  off  an  offensive  odour,  and  constituting 
what  are  usually  called  Dittrich's  plugs.  According  to  Charcot,  foetor  of 
the  breath  may  be  lacking  in  diabetic  gangrene  ;  this  feature  is  not  absolute. 
When  a  gangrenous  cavity  forms,  ])rovided  it  is  superficial  or  of  suflirioiit 
extent,  auscultation  yields  the  signs  of  a  cavity — namely,  cavernous  breath- 
ing, gurgling,  and  pectoriloquy.     Gangrene  of  the  pleura,  which  beguis  with 


154  TEXT-BOOK  OF  MEDICINE 

intense  pain  in  the  side,  acute  dyspnoea,  and  the  signs  of  effusion,  is  often 
associated  with  gangrene  of  the  hmg.  This  aspect  of  the  question  will 
be  studied  under  Putrid  and  Gangrenous  Pleurisy.  The  existence  of 
pneumothorax  (by  perforation  or  by  putrefaction)  is  sometimes  recognized. 
The  general  symptoms  are  usually  marked — high  fever,  repeated  chills,  an 
earthy  tint,  loss  of  appetite,  diarrhoea,  and  rapid  wasting.  Death  usually 
ensues  in  gangrene  of  the  lung.  Kecovery  may,  however,  take  place, 
especially  in  the  circumscribed  form,  either  spontaneously  or  after  operation. 

The  diagnosis  of  gangrene  from  bronchiectasis  has  been  already  de- 
scribed. Gangrene  should  not  be  confused  with  foetid  bronchitis,  where  the 
mucous  membrane  alone  is  attacked.  Foetid  bronchitis  has  special 
symptoms.  In  a  person  who  suffers  from  bronchial  catarrh  the  breath  and 
expectoration  become  at  certain  times  terribly  foetid;  but  these  troubles 
are  transitory,  intermittent,  and  perfectly  curable,  and  auscultation  shows 
the  signs  of  bronchitis,  not  those  of  a  gangrenous  cavity. 

The  mouth  must  be  examined  to  make  sure  that  the  foetor  of  the  breath 
is  not  due  to  some  local  affection,  such  as  dental  caries,  ulcero- membranous 
stomatitis,  gangrene  of  the  tonsils,  etc. 

The  treatment  of  gangrene  of  the  lung  is  very  limited.  The  chief  point 
is  to  support  the  patient's  strength  by  means  of  tonics,  quinine,  wine,  and 
alcohol.  Creosote,  balsams,  hyposulphite  of  soda  (Lanceraux)  also  find 
their  indications.  The  patient  should  breathe  an  atmosphere  loaded  with 
the  fumes  of  tar,  and  should  be  made  to  use  sprays  of  carbolic  acid. 

The  gangrenous  focus  should  be  opened  up,  when  it  is  clearly  limited  and 
superficial.  Cases  of  pneumotomy  have  been  followed  by  recovery,  but 
successes  are  rare,  judging  from  the  cases  which  I  have  seen. 


IX.  BRONCHO-PULMONARY  HiEMORRHAGE— HEMOPTYSIS. 

I  shall  describe  in  the  same  chapter  haemorrhages  from  the  bronchi  and 
from  the  lung.  Haemorrhage  from  the  surface  of  the  bronchi  is  called 
bronchorrhagia ;  that  which  occurs  in  the  lung  tissue  itself — that  is,  in  the 
alveolar  cavities — takes  the  name  of  pneumorrhagia.  This  distinction  is 
most  often  artificial.  The  term  pulmonary  apoplexy,  which,  by  an  abuse 
of  language,  was,  and  is  still,  used  to  designate  haemorrhage  of  the  lung, 
should  be  abandoned.*     Spitting  of  blood  after  broncho-pulmonary  haemor- 

*  The  term  pulmonary  apoplexy  was  created  by  Latour  in  1815,  and  adopted  by 
Laennec.  This  abuse  of  language  was  due  to  Rochoux,  who  in  his  wi'itings  on  cerebral 
haemorrhage  had  made  wrong  use  of  the  term  apoplexy,  and  employed  it  as  synonymous 
with  haemorrhage.  Several  authors  have  protested  against  this  faulty  term — for 
example,  Gendrin,  who  coined  the  word  pneumo-haemorrhage,  and  Trousseau,  who 
called  this  lesion  infiltration  of  blood. 


DISEASES  OF  THE  LUNG  155 

rhage,  or  hSBmoptysis,  is  only  a  symptom  which  serves  to  designate  the 
rejection  of  blood  which  comes  from  the  respiratory  passages,  just  as  hajma- 
temesis  designates  the  vomiting  of  blood  which  comes  from  the  digestive 
tract. 

etiology. — Bronchial  haemorrhage  (bronchorrhagia)  is  caused  by  con- 
gestion (strains,  chills,  hysteria).  It  is  sometimes  supplementary  to  a  flux, 
or  to  an  habitual  haemorrhage  (menstruation,  haemorrhoids),  and  it  is  very 
often  associated  with  pulmonary  tuberculosis.  According  to  circumstances, 
haemoptysis  precedes  or  accompanies  the  hatching  of  tubercles ;  later,  it 
may  be  due  to  rupture  of  small  aneurysms  in  the  cavities.  Bronchial 
haemorrhage  may  be  associated  with  enlargement  of  the  arterioles  which 
accompanies  bronchiectasis  ;  it  very  frequently  accompanies  the  growth  of 
hydatid  cysts  in  the  lung.  Under  interlobar  plem-isy  we  shall  see  the  cause 
of  "  interlobar  haemoptysis."  Haemophilia  and  purpura  are  sometimes 
accompanied  by  haemoptysis. 

Pulmonary  haemorrhage  (pneumorrhagia)  is  often  passive  (blood 
stasis),  and  due  to  diseases  of  the  heart  (especially  mitral  lesions).  The 
occurrence  of  haemorrhage  in  heart  affections  has  been  variously  inter- 
preted.* Some  invoke  the  mechanical  obstruction  to  the  pulmonary  circu- 
lation by  the  lesions  at  the  mitral  orifice  ;  others  add  to  this  cause  the 
frequent  hypertrophy  of  the  right  ventricle  and  the  changes  in  the  capillaries 
of  the  lung.  A  more  recent  theory  attributes  the  haemorrhage  to  an  em- 
bolism which,  starting  from  clots  in  the  right  auricle,  reaches  the  small 
branches  of  the  pulmonary  artery,  and,  after  the  fashion  of  capillary 
embolisms,  provokes  a  haemorrhagic  infarct. 

The  eruptive  fevers  (black  small-pox),  icterus  gravis,  etc.,  provoke 
haemorrhage  which  appears  to  be  connected  with  the  alteration  in  the 
capillaries  and  a  pathological  state  of  the  blood,  named,  for  want  of  a  better 
term,  "  state  of  dissolution."  The  causes  of  the  haemorrhage  associated 
with  Bright's  disease  are  ill  understood.  In  the  new-born,  pulmonary 
haemorrhages  connected  with  sclerema  are  seen  (Hervieux). 

In  some  cases  it  is  dilhcult  to  differentiate  the  origin  of  one  haemorrhage 
from  another  :  for  example :  the  haemorrhages  consecutive  to  broncho-pul- 
monary lithiasis,  syphilis,  hydatids  of  the  lung,  gangrene,  cancer,  inter- 
lo])ar  pleurisy,  etc. 

Pathological  Anatomy. — The  changes  in  bronchial  haemorrhage  are 
superficial  ;  the  mucosa  of  the  bronchi  may  be  anaemic  or  congested,  and 
coagula  may  be  present  in  the  lironchi. 

The   lesions  of  pulmonary   haMUorrhage  are  more  important.      If  the 

haemorrhage,  takes  place  by  rupture,  which  is  rare,  the  blood  tears  the  lung 

*  Athcromatoiis  changos  cannot  bo  accused  in  this  case,  as  they  arc  cxtrciiicjy 
rare  in  (he  pulnumary  vessels  (Roki(an.sky). 


156  TEXT-BOOK  OF  MEDICINE 

tissue,  collects  in  a  diffuse  fOCUS,  as  in  the  brain,  and  may  burst  into  the 
pleural  cavity. 

As  a  rule,  however,  the  haemorrhage  proceeds  in  a  different  way.  The 
blood  infiltrates  the  alveoli  and  the  parenchyma  without  much  destruction, 
and  the  infiltration  takes  the  form  of  conical  nodules,  which  show  a  centrally 
directed  apex,  recalling  the  distribution  of  the  bronchi  and  vessels.  These 
hsemoptoic  infarcts,  which  vary  in  size  and  number,  are  clearly  circum- 
scribed and  deeply  situated,  as  a  rule,  in  the  lower  lobes.  The  cut  section 
of  the  nodules  is  blackish  and  granular,  like  the  hepatization  in  pneumonia, 
on  account  of  the  fibrinous  coagula  which  make  the  infundibula  prominent. 
The  bronchi  and  the  pulmonary  vessels  of  the  area  near  the  infarct  are 
obliterated  by  clots.  The  hsemoptoic  nodule  may  undergo  or  provoke  the 
following  changes  :  It  becomes  indurated  and  retains  its  pigmentation  ;  it 
passes  into  fatty  degeneration  ;  it  causes  secondary  pneumonia  at  its  peri- 
phery, or  provokes  limited  gangrene.  When  it  is  subjacent  to  the  pleura,  it 
causes  partial  pleurisy. 

Symptoms. — The  chief  symptom  in  bronchial  haemorrhage  is  haemop- 
tysis. When  the  haemorrhage  is  violent,  the  blood  pours  out  of  the  nose 
and  mouth  ;  it  may  also  flow  into  the  stomach,  whence  it  is  rejected  by 
haematemesis.  As  a  rule,  the  haemoptysis  is  more  moderate,  and  the 
patient  coughs  up  bright,  frothy  blood,  which  in  the  spittoon  has  the 
appearance  "  of  the  foam  produced  in  a  basin  when  an  animal  is  bled  " 
(Trousseau).  It  may  cease  in  a  quarter  of  an  hour  or  half  an  hour,  and 
recur  some  hours  later,  next  day,  or  on  succeeding  days.  The  last  sputum 
coughed  up  has  not  this  frothy  and  bright  red  appearance,  but  is  black  and 
viscid.  It  is  the  remnant  of  the  haemorrhage  which  has  remamed  longer 
in  the  bronchi. 

Haemoptysis  is  sometimes  sudden,  and  the  patient  is  as  much  surprised 
as  scared  by  his  spitting  of  blood.  Sometimes  it  is  preceded  by  a  feeling  of 
warmth  m  the  chest  and  throat ;  at  other  times  it  is  preceded  or  ushered 
in  by  epistaxis.  When  supplementary  to  the  menstrual  flow,  it  is  periodic, 
like  the  haemorrhage  which  it  replaces. 

Bronchorrhagia  has  no  physical  signs.  I  am,  of  course,  referring  to 
signs  directly  related  to  the  haemorrhage,  and  not  "to  those  of  the  lesions  which 
have  caused  the  bleeding. 

When  the  haemorrhage  is  pulmonary,  especially  in  cardiac  cases,  the 
clinical  picture  is  very  different.  The  blood  which  has  infiltrated  the  lung  tissue 
has  not  the  same  tendency  to  burst  into  the  respiratory  channels.  Haemop- 
tysis is  not,  as  in  the  preceding  case,  the  chief  symptom,  but  is  often  absent, 
and  its  characters  distinguish  it  from  haemoptysis  in  tuberculosis.  The 
sputum  in  pneumorrhagia  is  neither  bright  red  nor  aerated ;  it  is  blackish, 
viscid,  and  more  or  less  mixed  with  mucus.     The  quantity  of  blood  brought 


DISEASES  OF  THE  LUNG  157 

up  is  much  less  abundant  than  in  bronchorrhagia.  The  hgemoptysis  may 
last  from  ten  to  twenty  days,  and  Grisolle  considered  this  persistence  as  one 
of  the  best  diagnostic  signs.  The  differential  signs  are,  however,  not 
absolute,  since  the  blood  of  bronchorrhagia,  if  it  has  remained  long  in  the 
bro2ichi,  may  resemble  that  of  pneumorrhagia. 

When  the  bleeding  is  abmidant  or  persistent,  the  patient  presents  the 
usual  symptoms  of  great  haemorrhage  :  pallor  of  the  face,  small  pulse, 
tendency  to  syncope  and  to  dyspnoea,  which  is  proportionate  to  the  extent 
of  the  lesion.  If  the  nodules  of  j)neumorrhagia  are  large  and  superficial, 
percussion  reveals  dullness,  and  auscultation  yields  blowmg  breathing  and 
bronchophony.  Broncho-pneumonia  consecutive  to  pulmonary  haemor- 
rhage is  rare.  Gangrene  and  perforation  of  the  pleura  are  almost  always 
fatal. 

Diagnosis. — The  diagnosis  of  broncho-pulmonary  haemorrhage  has  only 
one  certain  sign — that  is,  haemoptysis.  Given  haemoptysis,  it  is  necessary 
to  distinguish  it  from  other  haemorrhages  (epistaxls,  stomatorrhagia,  haema- 
temesLs)  which  somewhat  resemble  it.  We  must,  therefore,  trace  the  cause, 
and  for  this  purpose  we  inquire  into  the  characters  of  the  blood  coughed  up, 
the  symptoms  accompanying  it,  and  the  circumstances  in  which  it  super- 
vened. The  larynx,  the  aorta,  the'  lungs,  and  the  heart  are  subjected  to  a 
mmute  examination. 

Cancers  of  the  larynx  sometimes  provoke  profuse  h93moptysis. 

Aneurysms  of  the  aorta  may  open  into  the  trachea  or  into  the  bronchi, 
and  cause  sudden  death  from  haemoptysis,  or  only  slight  bleeding,  which 
recurs  for  several  consecutive  days  or  weeks.  These  cases  are  exceptional, 
but  still  they  must  be  recognized,  for  both  prognosis  and  diagnosis  are 
involved.  Spitting  of  blood,  arising  as  a  supplementary  haemorrhage,  must 
not  be  taken  for  haemoptysis  of  tubercular  origin ;  nor  must  we  forget  that 
hysterical  patients  have  congestion  and  haemoptysis,  which  has  nothing  in 
common  with  tuberculosis. 

The  diagnosis  between  the  haemoptysis  of  pulmonary  (tuberculosis)  and 
that  of  cardiac  origin  (mitral  lesion)  is  often  made  easy  by  the  different 
characters  of  the  blood  and  by  the  existence  of  the  respective  lesions  in  the 
lung  or  in  the  heart ;  but  the  matter  is  not  always  so  simple,  and  haemoptysis 
may  appear  as  an  early  sign  before  the  organic  lesions  are  j^erceptible  by 
our  means  of  investigation.  Furthermore,  the  distinctive  characters  of  the 
bloody  sputum  are  not  absolutely  rigid.  Haemoptysis  which  has  the  appear- 
ance of  a  bronchorrliagia  has,  nevertheless,  been  caused  by  heart  disease, 
as  Trousseau  has  clearly  shown. 

The  diagnosis  as  to  the  nature  of  haemoptysis  has  been  greatly  simplified 
since  the  discovery  of  the  tubercle  bacilhis.  Careful  and  repeated  ex- 
amination of  the  sputum  or  of  the  blood  in  lucmoptysii  in  performed,  and 


158  TEXT- BOOK  OF  MEDICINE 

the  presence  of  the  bacillus  sometimes  allows  us  to  state  that  the  lesion  is 
tuberculous. 

Although  there  is  not  absolute  agreement  between  broncho-puhnonary 
haemorrhage  and  haemoptysis,  it  is  difficult  clinically  to  separate  them,  and 
the  gravity  of  the  prognosis  often  betrays  itself  by  the  persistence  or  the 
abundance  of  the  haemoptysis.  Fulminating  haemoptysis  is  caused  by  the 
opening  of  an  aortic  aneurysm  uito  the  trachea  or  hito  the  bronchi,  or  by  the 
rupture  of  a  small  aneurysm  in  a  tuberculous  cavity  (Kasmussen's  aneurysm). 
Febrile  haemoptysis  m  tuberculous  patients  is  more  grave  than  the  apyretic 
form.  The  gravity  of  the  prognosis  depends  also  on  the  causes  (pulmonary 
or  cardiac  lesions)  which  have  produced  the  haemorrhage. 

Treatment. — Bronchial  is  more  accessible  to  treatment  than  pulmonary 
haemorrhage.  The  initial  haemoptysis  of  tuberculosis  may  be  arrested  by 
an  emetic  : 

Ipecacuanha  . .  . .  . .  . .  . .     gr.  xv. 

Tartrate  of  antimony         . .  . .  . .  . .     gr.  ss. 

Give  at  once,  as  soon  as  the  patient  is  seized  with  haemoptysis. 

The  expectoration  of  blood  is  sometimes  arrested  before  the  complete 
effect  of  the  emetic.  Ipecacuanha  may  then  be  admmistered  f  grain  every 
half-hour,  or  every  hour.  Good  results  are  obtained  with  a  mixture  of 
perchloride  of  iron  in  a  dose  of  30  grains  in  4  ounces  of  water. 

Iced  and  acid  druiks  are  given,  and  a  draught  of  the  following  compo- 
sition is  prescribed  : 

Distilled  water  . .         . .  . .  . .  . ,     §iv. 

Syrup  of  rhatany        . .  . .  . .  . .  . .     si. 

Rabel  water     . .         . .         . .         . .         . .         . .     5ss. 

A  tablespoonful  to  be  taken  every  four  hours. 

Pills  of  extract  of  thebaine,  ^  gram  in  each,  may  be  given  nourly — from 
4  to  10  pills  in  the  twenty-four  hours.  Subcutaneous  injections  of  ergotin 
may  be  used.  Chloride  of  calcium,  in  drachm  doses,  may  be  prescribed. 
An  ice-bag  is  kept  in  situ  on  the  chest. 

Blisters  applied  to  the  thorax  or  to  the  actual  seat  of  the  congestion, 
revulsives  to  the  lower  limbs,  dry-cupping  and  sinapisms,  may  also  be 
employed. 

This  treatment  will  be  considered  in  detail  in  the  chapter  on  Pulmonary 
Tuberculosis. 

Digitalis  finds  its  indications  in  haemoptysis  of  cardiac  origin. 


DISEASES  OF  THE  LUNG  159 


X.  PULMONARY  EMPHYSEMA. 

Definition. — Tlie  name  emphysema  is  given  to  the  exaggerated  dilatation 
ot  the  pulmonary  tissue  by  air.  When  emphysema  is  limited  to  the  alveoli 
or  the  lobules,  it  is  said  to  be  alveolar  or  intralobular  ;  but  when  the  lobule 
is  ruptured,  and  the  air  invades  the  interstitial  tiasue  of  the  lung,  the  emphy- 
sema is  interlobular. 

Pathological  Anatomy  and  Mechanism. — On  opening  the  thorax,  the 
lungs  apjjear  distended,  and  have  but  little  tendency  to  collapse.  The 
affected  parts  are  greyish- white,  crepitate  a  little,  and  have  a  downy  feel- 
ing to  the  touch  (Laennec).  Emphysema  usually  involves  the  aj)ices  and 
the  anterior  edges  of  the  lungs.  Spherical  projections  of  different  sizes,  due 
to  the  emphysematous  enlargements  oi  the  infundibula,  are  seen  on  the 
surface.  The  vessels  of  these  parts  are  for  the  most  part  obliterated,  and 
the  circulation  is  deficient,  while  it  is  increased  in  the  neighbouring  parts, 
which  become  the  seat  of  oedematous  congestion.  On  microscopical  ex- 
amination of  sections  from  an  emphysematous  lung  which  has  been  pre- 
viously inflated  and  dried,  the  alveolar  walls  are  often  found  to  be 
atrophied  and  perforated.  The  atrophy  of  the  septa  and  of  the  elastic 
tissue  permits  dilatation  of  the  alveoli  and  of  the  lobules.  The  dilatation 
is  at  first  limited  to  some  alveoli  or  to  an  infundibulum ;  later,  as  the  lesion 
spreads,  the  infundibula  communicate  with  one  another,  and  the  dilatations, 
which  are  at  first  as  large  as  millet-seeds,  finally  exceed  a  nut  in  size.  In  old 
people  the  apex  of  the  lung  is  thus  transformed  into  a  lacunar  tissue,  in 
which  the  air  circulates  freely.  How  are  the  perforation  of  the  septa  and 
the  communication  between  the  infundibula  brought  about  ?  "  Under  a 
still  unknown  influence."  The  thinned  septa  are  transformed  ;  in  tlieii 
interior  and  on  their  surface  they  present  ovoid  masses  of  fatty  granulations, 
which  may  come  from  the  alveolar  pavement  epithelium  or  perhaps  from  the 
capillary  vessels,  and  it  is  probable  that  this  granular  degeneration  plays  a 
large  part  in  the  perforations  of  the  wall  of  the  alveoli. 

The  mechanism  by  which  emphysema  is  produced  has  been  varioursly 
explauied.  Two  orders  of  causes  are  admitted — mechanica'i  ana  trophic. 
Sudden  efforts  of  expiration,  the  fits  of  whooping-cough,  the  cough  of 
croup  and  of  broncho-[)ncumoiiia,  dilate  the  alveoli  to  excess,  and  produce 
acute  emphysema.  It  is  therefore  not  surprising  that  the  same  causes  if 
often  n^pcatod  (usthma,  chronic  bronchitis),  eventually  cause  emphysema  by 
mechanical  means.  In  other  cases — in  the  aged,  for  example — faults  in 
the  nutrition  of  the  lobule,  atrophy  and  perforation  of  the  alveoli,  coincide 
80  closely  with  the  spread  of  emphysema  that  they  appear  to  be  the  principal 
cause.     It  is  therefore  dilfirjult  to  say  exactly  what  part  corresponds  to 


160  TEXT-BOOK  OF  MEDICINE 

mechanical  and  what  to  trophic  action,  in  the  production  of  emphysema. 
In  a  good  many  cases  this  double  process  seems  to  exist.  It  is  perhaps 
favoured  by  some  special  tendency  of  the  lung  tissue  (heredity). 

Rupture  of  the  emphysematous  vesicles  is  a  grave  complication.  If  the 
perforation  involves  the  pleural  cavity,  pneumothorax  results.  If  the 
rupture  occurs  under  the  visceral  layer  of  the  pleura,  or  in  the  interstitial 
tissue  of  the  lung  (interlobular  emphysema),  the  air  travels  along  the  con- 
nective tissue,  reaches  the  mediastinum,  and  invades  the  subcutaneous 
tissue  of  the  neck,  the  thorax,  and  other  regions. 

Symptoms. — The  shape  of  the  thorax  is  peculiar.  The  chest  is  rounded 
and  bulging  in  the  clavicular  regions,  and  when  the  emphysema  is  very  ex- 
tensive, the  intercostal  spaces  appear  dilated,  and  the  chest  is  enlarged  at 
its  base.  In  the  affected  regions  percussion  gives  a  more  ringing  sound  than 
in  health.  This  resonance  may  encroach  upon  regions  which  are  usually 
dull,  so  that  the  area  of  cardiac  dullness  is  replaced  by  hyperresonance.  On 
auscultation,  the  vesicular  murmur  is  feeble,  the  respiration  has  a  harsh 
tone,  inspiration  is  shortened,  and  expiration  is  prolonged.  The  obliteration 
of  vessels  produces  blood  stasis,  which  may  extend  to  the  right  ventricle. 
Dilatation  of  the  ventricle  and  tricuspid  incompetence  sometimes  follow, 
and  troubles  m  the  cardio-pulmonary  circulation  may  come  on  and  increase 
the  obstruction  to  respiration.  The  emphysematous  patient  has  many 
reasons  for  his  difficulty  in  breathing.  The  rarefaction  of  the  lung  tissue, 
the  depression  of  the  diapliragm  by  exaggerated  distension  of  the  lungs,  the 
insufficiency  of  expiration,  and  the  diminution  in  the  field  of  haematosis, 
lower  the  respiratory  capacity  by  50  per  cent.,  or  even  more,  as  shown  by 
spirometry. 

Besides  the  continuous  dyspnoea  which  is  the  result  of  the  emphysema, 
we  must  also  note  attacks  of  suffocation,  which  often  supervene,  and  are 
due  to  the  various  diseases,  such  as  asthma,  pulmonary  congestion,  or  mitral 
lesions,  that  are  so  often  associated  with  emphysema  (Woillez).  These 
various  types  of  dyspnoea  also  exist  when  emphysema  is  associated  with 
tuberculosis. 

The  diagnosis  is  easy,  but  we  must  not  forget  that  emphysema,  instead  of 
constituting  the  whole  disease,  is  often  only  an  episode  in  the  course  of 
another  malady  (asthma,  tuberculosis,  chronic  bronchitis),  which  must  also 
be  diagnosed. 

Treatment. — The  therapeutic  indications  are  chiefly  directed  to  the 
diseases  which  have  produced  the  emphysema.  As  for  the  emphysematous 
lesions  themselves,  we  have  but  little  influence  over  them.  Inhalations  of 
oxygen  and  baths  of  compressed  air  are,  however,  generally  recommended. 


DISEASES  OF  THE  LUNG  161 


XI.  (EDEMA  OF  THE  LUNG— SUPERACUTE  OEDEMA  IN  BRIGHT'S 

DISEASE. 

(Edema  of  the  lung  is  due  to  the  transudation  of  blood-serum  into  the 
alveoli  and  the  interstitial  tissue  of  the  lung.  Congestion  is  sometimes 
present  as  well,  and  plays  a  more  or  less  important  part.  In  cases  due  to 
nephritis  the  oedema  far  outweighs  the  congestion,  while  in  cases  due  to 
cardiac  lesioas  the  congestion  has  the  same  importance  as  the  oedema,  and 
the  lesion  is  called  "  congestive  oedema,"  oi  "  cedematous  congestion  of  the 
lung." 

On  anatomical  examination  of  the  cedematous  lung,  congestion  and 
atelectasis  are  found  in  association  with  oedema.  The  lung  is  heavy,  and 
does  not  float.  On  section,  abundant  frothy,  clear  fluid  exudes  when 
oedema  alone  is  the  cause,  but  red-tinted  when  congestion  is  also  present. 

Many  causes  provoke  oedema  of  the  lung.  It  may  arise  suddenly, 
following  thoracentesis,  when  the  operator  has  made  the  mistake  of  with- 
drawing a  large  quantity  of  fluid  too  rapidly  or  too  completely.  The  opera- 
tion is  scarcely  finished  when  the  patient  is  seized  with  suffocation,  angina, 
and  fits  of  coughing,  and  brings  up  a^rosy,  albuminous,  frothy  liquid,  which 
is  the  result  of  superacute  oedema.  It  is  fortunate  if  this  terrible  accident 
does  not  end  in  death. 

Congestive  oedema  of  the  lung  is  seen  fairly  frequently  in  the  course  of 
diseases  of  the  heart,  and  during  periods  of  asystole.  Many  persons  suffering 
from  ill-compensated  mitral  lesions  are  seized  with  dyspnoea,  due  to  blood- 
stasis,  elevation  of  the  pulmonary  tension,  and  resulting  oedema.  This  con- 
gestive oedema  chiefly  occurs  at  the  bases  of  the  lungs.  On  auscultation, 
numerous  fine  moist  rales  are  heard  ;  tubular  breathing  is  heard  if  pleural 
effusion  accompany  the  oedema.  In  certain  cardiac  cases  congestive  oedema 
of  the  lung  exists,  to  the  exclusion  of  lesions  in  other  organs.  The  lung,  which 
is  the  first  to  receive  the  recoil  of  the  circulatory  embarrassment,  becomes 
congested,  oedema  appears,  and  dyspnoea  is  the  first  indication  of  the  cardiac 
lesion.  In  other  cardiac  cases  the  oedema  is  associated  with  congestion  of 
the  liver  (cardiac  liver),  of  the  kidney  (cardiac  kidney),  or  with  oedema  of 
the  extremities — in  short,  it  forms  part  of  the  asystolic  syndrome.  Appro- 
priate treatment  may  give  good  results,  as  we  shall  see  in  the  chapter  on 
Diseases  of  the  Heart. 

Influenza  (Teissier,  Rendu)  and  aortic  lesions  (Huchard)  may  lead  to 
OL'dema  of  the  lung,  but  the  chief  cause  is  nephritis,*  either  acute  or  chronic. 

*  SiipcracuUi  (rdeiiiii  of  tlic  liint^  may  .suiMTvcno  in  tlio  courso  of  iinyiiaiiry- 
Vinay  (Li/on  Mcdiad.  IS!)7),  whu  ha-s  Btudiid  this  complication,  rightly  cunsicK-LS  it 
due  lo  ni'i^hritis  gravidarum. 

u 


162  TEXT-BOOK  OF  MEDICINE 

GEdema  of  the  Lung  in  Bright's  Disease  :  Slow  Form— Acute  Form— 

Superaeute  Form. 

ffidema  of  the  lung  is  very  frequent  in  the  course  of  acute  and  chronic 
neplu-itis.  In  many  cases  of  acute  scarlatinal  or  of  early  syphilitic  nephritis, 
or  nephritis  a  frigore,  oedema  of  the  lungs  may  be  associated  with  dropsy  of 
other  parts.  Sometimes  the  oedema  affects  the  bronchi  rather  than  the 
lungs,  and  is  the  old  "albuminuric  bronchitis  of  Lasegue";  at  other  titnes 
the  lungs  are  oedematous,  especially  at  the  bases,  and  auscultation  records  a 
multitude  of  fine  rales.  Oldema  as  slight  as  this  scarcely  merits  the  name 
of  a  complication  ;  it  forms  part  of  the  general  dropsy,  hampers  the  breath- 
ing, and  brings  on  dyspnoea,  but  does  not  occupy  the  chief  place  in  the  course 
of  the  acute  nephritis.  The  matter  is  very  different  in  generalized  oedema  of 
the  lung,  and  especially  in  the  superacute  from,  which  is  a  complication  as 
sudden  as  it  is  terrible. 

The  same  remarks  apply  to  oedema  of  the  lung  in  chronic  nephritis.  In 
a  dyspnoeic  patient  with  Bright's  disease  we  often  hear  at  the  bases  the  sub- 
crepitant  rales  of  pulmonary  congestion,  which  remains  stationary  for  weeks 
and  months.  The  patient  who  has  attacks  of  dyspnoea  and  believes  himself 
asthmatic  is  sometimes  the  victim  of  an  error  in  diagnosis,  and  goes  the 
round  of  the  thermal  cures  in  his  search  for  the  best  treatment.  In  such  a 
case  the  oedema  is  not  of  the  first  importance  ;  it  is  more  or  less  extensive, 
more  or  less  obstinate,  takes  its  share  in  the  respiratory  embarrassment,  but 
does  not  focus  all  the  attention  upon  itself.  It  Is  very  different  in  the  other 
variety  of  oedema— superacute  pulmonary  oedema— which  may  burst  forth 
suddenly  in  the  course  of  chronic  nephritis,  or  more  rarely  in  the  com-se  of  the 
acute  disease,  and  in  a  few  hours  endanger  life.  It  is  on  this  superacute 
oedema,  then,  that  we  shall  fbc  our  attention. 

The  following  case  gives  an  exact  idea  of  it : 

A  man  of  forty-five  was  seized  with  such  acute  distress  that  he  was  brought  to 
hospital  at  once.*  On  admission,  death  appeared  imminent :  pale  face,  duU  eyes,  livid 
lips,  bluish  fingers  and  nails,  hurried  breathing,  WTetched  pulse — such  was  the  con- 
dition of  the  moribimd  patient.  Any  interrogation  was  impossible.  The  heart  could 
not  be  examined,  but  both  lungs  were  full  of  fine  subcrepitant  rales. 

At  fu-st  sight  the  condition  recalled  capillary  bronchitis,  suffocative  catarrh,  or  acute 
phthisis.  The  diagnosis,  although  difficult,  was  not  unpracticable.  He  brought  up 
abundant  frothy  sputum,  of  a  rosy  colour.  The  eyelids  were  puffy,  the  legs  slightly 
oedematous  ;  the  temperature  was  subnormal,  and  the  urine  very  albuminous.  The 
o?dema  and  albuminuria  pointed  to  nephi'itis  ;  the  characteristic  expectoration  and  the 
fine  rales  in  the  lungs  indicated  superacute  oedema. 

The  treatment  was  obvious.     Charrier  cupped  the  patient,  and  di-ew  off  10  ounces 

*  This  case  is  taken  from  my  lecture  on  Superacute  CEdema  of  the  Limg  in  Bright's 
Disease,  in  which  I  have  quoted  a  large  number  of  cases  {Clinique  Mcdicah  de  V Hotel- 
Dieu,  1897,  p.  23). 


DISEASES  OF  THE  LUNG  163 

of  blood.  The  effect  was  immediate.  In  less  than  an  hour  the  breathing  was  easier, 
the  expectoration  was  less  profuse,  the  fine  rales  disappeared  from  the  upper  parts  of 
the  lungs,  and  death  was  averted.  Strict  milk  diet  and  lactosed  diinks  were  prescribed, 
and  5  teaspoonfuls  of  Trousseau's  diuretic  wine  were  given  daily. 

Next  day  the  breathing  was  easy,  the  temperature  normal.  The  heart  was  ex- 
amined, and  Ave  heard  a  shglit  bruit  de  galop.  Rilles  were  no  longer  audible  in  the 
lungs  except  at  the  bases.  The  kidneys  commenced  to  act ;  and  the  urine,  though 
almost  supijressed  the  day  before,  amounted  to  8  ounces,  but  was  markedly  albuminous. 

Two  days  later  the  patient  was  able  to  give  us  a  complete  history.  He  told  us  that 
for  some  time  his  health  had  been  faulty,  and  he  had  suffered  from  pollakiuria,  cramps 
in  the  calves,  dead  fingers,  cedema  of  the  eyelids  and  of  the  malleoh. 

Treatment  produced  rapid  improvement.  In  a  few  days  the  situation  had  totally 
changed.  Respiration  became  regular,  except  that  some  rales  persisted  at  the  bases 
of  the  lungs.  The  puffiness  of  the  face  and  the  cedema  of  the  legs  had  completely 
disappeared,  and  the  urine  amounted  to  50  ounces,  although  albumin  wa^  still  present 
and  the  depuration  was  imperfect,  for  the  toxicity  of  the  mine,  as  experimentally 
determined,  was  far  from  reaching  its  normal  value. 

Symptoms. — The  first  point  of  importance  is  the  suddenness  of  this 
cedema.  Reference  to  the  cases  which  I  have  collected  shows  that  super- 
acute  oedema  does  not,  as  a  rule,  result  from  bronchitis  or  some  pulmonary 
condition  which  has  gradually  become  more  severe.  The  onset  is  nearly 
always  sudden  and  unexpected ;  the  unforeseen  accident  comes  on  by  day 
or  by  night.  One  patient  was  seized  with  superacute  cedema  while  I  was 
asking  him  questions,  and  on  auscultation,  I  felt,  so  to  say,  the  rising  of  the 
liquid  in  his  chest.  The  same  sudden  onset  occurred  m  tlu:ee  of  Girau- 
deau's  patients.  His  first  patient  was  seized  while  fast  asleep,  just  as  an 
attack  of  asthma  comes  on,  although  on  the  previous  day  she  was  quite 
well.  Hls  second  patient  was  taken  ill  quite  as  suddenly  in  the  night  with 
superacute  oedema  dui-ing  a  period  of  apparently  good  health.  The  same 
remark  applied  to  his  third  patient,  who  was  stricken  down  two  hours  after 
dinner,  although  there  was  no  premonition  of  such  an  accident.  A  sunilar 
thhig  happened  to  Bouveret's  patients.  In  one  of  them  superacute 
oedema  appeared  suddenly,  and  death  resulted  ;  in  the  other  a  first  attack 
of  cedema  supervened,  it  is  true,  after  a  walk  of  tliree  miles,  but  the  two  other 
attacks  appeared  without  appreciable  caiLse,  when  the  patient  was  at  rest. 

I  do  not  say,  of  course,  that  events  always  have  this  course.  In  some 
cases  superacute  cedema  is  preceded  by  such  prodromata  as  cough,  dyspnoea, 
or  rales.  In  such  a  case  it  seems  that  the  soil  is  prepared ;  it  was  so  in 
my  first  case  and  in  one  of  Giraudeau's  cases.  It  is,  however,  an  exception. 
Superacute  oedema  of  the  lung  in  Bright's  disease  is  hardly  ever  the  result 
of  pro-oxistiug  broncho-fjuimonary  lesions.  It  bursts  out  suddenly,  like 
an  attack  of  asthma,  all  hough  some  hours  previously  no  sus[)icion  has  been 
entertained. 

A  second  point  is  that  superacute  oedema  of  the  lung  is  very  often  an 
isolated  result  uf  Bright's  disease,  for,  paradoxical  as  this  may  ap[)e;ir,  it 

11—2 


164  TEXT-BOOK  OF  MEDICINE 

is  hardly  ever  associated  with  the  severe  manifestations  of  uraemia,  or  with 
the  marked  oedema  of  Bright' s  disease.  Without  knowledge  on  this  point, 
it  would  appear  that  superacute  oedema  ought  to  supervene  in  the  patient 
who  is  suffering  from  anasarca.  This  may  be  so,  especially  in  acute 
nephritis.  Giraudeau's  patient  was  seized  with  superacute  oedema  of  the 
lung  in  the  course  of  acute  nephritis  with  .anasarca.  This,  however,  is  a 
rare  occurrence.  Nearly  all  the  cases  which  I  have  collected  show  that  the 
mischief  appeared  as  an  isolated  accident  in  the  course  of  latent  nephritis. 

It  cannot  be  said,  however,  that  this  oedema  attacks  persons  in  perfect 
health.  Close  examination  will  show  that  they  are  more  or  less  tainted 
with  Brjghtism.  If  the  "  minor  complications  of  Brightism  "  be  carefully 
looked  for,  the  evolution  of  an  insidious  nepliritis  may  be  constructed. 
A  group  of  symptoms,  such  as  the  sensation  of  dead  fingers,  cryaesthesia, 
auditory  troubles,  cramps  in  the  calves,  pollakiuria,  itching,  electric  shocks, 
and  epistaxis,  will  be  found  in  their  past  history.  We  shall  see  that  they 
were  not  exempt  from  such  a  trace  of  oedema  as  puffiness  of  the  eyelids  and 
of  the  alveoli.  We  shall  find  that  their  arterial  tension  is  high,  their  tem- 
poral arteries  are  tortuous,  the  second  sound  accentuated,  and  a  gallop  rhythm 
is  present.  We  shall  find  that  these  patients  were  subject  to  headache,  which 
they  styled  migraine  ;  to  suffocation,  which  they  took  for  asthma  ;  and  to 
colds,  which  they  regarded  as  due  to  ordinary  bronchitis.  If  their  urine  is 
analyzed,  albumin  will  be  found  ;  on  testing  the  toxicity,  it  will  be  low.  We 
shall  find,  in  short,  by  a,n  attentive  and  searching  examination  of  this  con- 
dition— which  for  a  long  time  I  have  named  Brightism — that  the  patient 
whose  health  appears  to  have  been  fairly  good  has  in  reality  been  suffering 
from  mischief  in  his  kidneys ;  the  urinary  depuration  has  been  affected,  and  he 
has  been  exposed  to  the  risk  of  complications  which  gave  more  or  less  warning. 

After  this  digression  as  to  the  onset,  let  us  resume  our  clinical  analysis 
of  the  symptoms.  The  attack  commences  with  a  tickling  in  the  larynx, 
jerky  cough,  and  distress,  which  reaches  its  limit  in  some  minutes,  or 
perhaps  some  hours.  These  symptoms  are  due  to  sudden  blocking  of  the 
pulmonary  alveoli  by  sero-albuminous  fluid.  As  a  rule,  the  inundation 
begins  in  the  bases,  and  may  affect  the  whole  of  the  lungs  more  or  less  rapidly. 
As  the  blood-serum  transudes  into  the  alveoli  and  the  bronchioles  under 
pressure,  the  patient  is  at  once  seized  with  fits  of  coughing,  and  then  brings 
up  the  characteristic  fluid,  which  is  frothy  and  rose-coloured.  Some 
patients  may  bring  up  as  much  as  2  or  3  pints  in  a  few  hours,  or  even 
more.  It  may  be  that  the  bronchi  have  not  the  power  of  expelling  the  fluid 
which  has  thus  accumulated,  and  the  asphyxia  varies  in  indirect  ratio  to  the 
amount  of  expectoration. 

As  soon  as  dyspnoea  appears,  innumerable  fine  subcrepitant  and  sibi- 
lant rales  can  be  heard  over  both  sides  of  the  chest,  testifying  to  the 


1 


DISEASES  OF  THE  LUNG  165 

inundation  of  the  alveoli  and  of  the  bronchioles.  According  to  the  rapidity 
and  the  extension  of  this  inundation,  the  rales  invade  the  whole,  or  nearly 
the  whole,  of  the  lungs. 

In  proportion  as  the  inundation  increases,  and  if  the  expectoration  is 
ever  so  slightly  insufficient,  dyspnoea  increases  rapidly  ;  the  patient  is  pale, 
alarmed,  and  conscious  of  his  extreme  danger  ;  the  pulse  is  small  and  quick, 
the  lips  are  bluish,  the  nails  livid,  the  limbs  cold  ;  and  the  struggle  may  in 
a  few  moments  end  in  death  (fulminant  forni),  in  a  day  (rapid  form),  or  in 
three  or  four  days  (slow  form). 

In  some  patients  the  condition  is  not  absolutely  perilous,  so  long  as  the 
sufferer  can  empty  the  inundated  lungs.  Paresis  of  the  expulsive  muscles 
may  supervene,  expectoration  may  be  quite  absent,  and  death  from 
asphyxia  occurs  at  short  notice.  In  favourable  cases  the  fluid  is  coughed 
up  as  soon  as  it  forms,  the  inundation  Ls  arrested  in  time,  and  after  a  duration 
which  varies  from  some  hours  to  some  days,  the  dyspnoea  improves,  the 
rales  diminish,  and  the  patient  wins  the  struggle.  We  must,  however,  not 
be  too  sanguine,  for  the  danger,  though  averted  for  a  moment,  may  some 
hours  or  some  days  later  recur  and  prove  fatal.  Sometimes  convalescence 
requires  several  days  ;  at  other  times  recovery  comes  on  suddenly,  and  the 
patient  is  able  to  resume  work  on  the  next  day. 

Superacute  oedema  of  the  lung  in  Bright's  disease  is  made  worse  by  the 
fact  that  not  only  may  the  patient  succumb  to  an  attack  in  a  few  hours,  but 
that,  although  liLs  lungs  have  recovered,  he  remains  liable  to  fresh  attacks. 
Several  patients  have  had  two  or  three  repetitions  of  superacute  oedema, 
months  or  years  apart.  Giraudeau's  first  case  had  three  attacks  in  two 
years,  and  Bouveret's  second  case  had  three  attacks  in  six  months. 

Diagnosis. — The  diagnosis  of  superacute  oedema  of  the  lung  in  Bright's 
disease  follows  from  the  description  which  has  just  been  given.  A  patient 
with  Bright's  disease  may  have  severe  attacks  of  dyspnoea,  but  in  this  case 
it  is  a  question  of  uraemic  dyspnoea,  which  often  exhibits  the  Cheyne  Stokes 
type.  It  differs  from  that  of  pulmonary  oedema  in  that  we  do  not  find  rales 
and  the  characteristic  sputum.  Dyspnoea  of  toxic  origin  may,  however,  be 
combined  with  that  due  to  oedema. 

We  see  a  patient  who  is  a  prey  to  the  most  acute  dyspnoea,  but  it  is  a 
case  of  genuine  asthma,  and  the  diagnosis  will  be  easy.  The  number  of 
respirations  is  not  increased,  but  rather  diminished.  Everything  points  to 
spasmodic  dyspnoea  ;  inspiration  is  painful,  expiration  whistling  and  very 
prolonged.  The  prominent  fact  on  auscultation  is  not  the  innumerable 
rales  of  j)ulinonary  rjedema,  but  the  association  of  rales  with  signs  of  acute 
eni[)]iyKema.  Expectoration  is  a})sent,  or  composed  of  shreddy,  mucous, 
or  pearly  sputum,  and  in  any  case  the  frothy,  albuminous,  rosy  expectoration 
of  superacute  oedema  is  not  found.     Prognosis  and  treatment  are  (piite 


166  TEXT-BOOK  OF  MEDICINE 

different,  for  the  attack  of  asthma  is  never  grave,  and  blood-letting  is 
unnecessary. 

I  cannot  review  all  the  varieties  of  dyspnoea  which  may  resemble  that 
of  superacute  oedema.  Such  are  the  severe  cases  of  dyspncea  in  suffocative 
catarrh,  acute  phthisis,  cardiac  asthma,  and  angina  pectoris.  Let  us  not 
forget  that  we  can  always  make  a  correct  diagnosis  in  superacute  oedema 
from  the  following  symptoms :  Sudden  onset  of  the  dyspnoea ;  fine  rales  over 
a  large  area  of,  or  the  whole:,  chest ;  incessant  cough ;  abundant  frothy, 
albuminous,  rosy  expectoration  ;  frequent  oedema  of  the  face  or  of  the  legs  ; 
albuminuria  ;  and  previous  symptoms  of  Brightism. 

Pathological  Anatomy. — In  a  case  reported  by  Bouveret  both  lungs, 
from  base  to  apex,  were  oodematous.  The  fluid  literally  streamed  out  on 
cutting  and  squeezing  a  lobe  between  the  fingers.  The  bronchi  were  full 
of  the  same  frothy  rose-coloured  fluid.  The  kidneys  were  small,  granular, 
and  cystic.  The  heart  was  enormous,  the  aorta  much  dilated,  but  not 
atheromatous  ;  the  sigmoid  valves  were  healthy.  The  coronary  arteries 
presented  yellow  patches  of  endarteritis. 

In  Huchard's  case  nephritis  was  found  post  mortem,  with  small 
granular  kidneys,  weighing  together  5|  ounces,  and  pericarditis,  with  about 
3  ounces  of  sero-fibrinous  fluid  in  the  pericardium.  The  lungs  were  so 
infiltrated  with  serous  fluid  that  two  pints  of  albuminous  rose-coloured 
fluid  were  pressed  out  by  gentle  squeezing. 

At  the  autopsy  on  Giraudeau's  patient  the  lungs  were  bulky  and 
violet-coloured.  On  section  and  on  pressure  a  large  quantity  of  frothy 
rose-coloured  fluid,  like  that  brought  up  in  the  expectoration,  flowed  out. 
The  kidneys  showed  acute  congestive  nephritis  ;  they  were  large  and  violet- 
coloured  ;  the  capsule  stripped  easily,  and  in  places  subcapsular  haemor- 
rhages were  visible.  The  heart  showed  general  hypertrophy,  which  was 
most  marked  in  the  left  ventricle.  The  valvular  and  arterial  orifices  were 
healthy.  The  aorta  presented  no  trace  of  aortitis,  either  at  its  origm  or  in 
the  arch. 

Giraudeau  observed  the  following  lesions  in  the  lungs  of  a  young 
girl  :  The  pulmonary  alveoli  were  filled  with  coagulated  fluid,  which  im- 
prisoned desquamated  epithelial  cells  and  some  red  corpuscles.  The 
capillaries  of  the  septa  were  gorged  with  red  corpuscles.  It  seemed  that 
certain  septa  were  thickened  by  a  true  interstitial  oedema.  At  these  points 
the  bloodvessels  were  less  apparent,  as  if  the  circulation  had  been  impeded 
by  the  compression  of  the  vessels. 

Pathogenesis. — What  is  the  explanation  of  superacute  oedema  m  Bright's 
disease  ?  The  undeniable  clinical  fact  is  that  patients  with  Bright's  disease 
are  liable  to  slight  oedema  in  any  part — in  the  lungs,  the  larynx,  and  the 
cellular  tissue — just  as  they  are  prone  to  effusion  into  the  serous  cavities. 


DISEASES  OF  THE  LUNG  167 

Why,  then,  this  localization  in  the  lungs  ?  I  do  not  know.  As  Brouardel 
remarks,  from  a  medico-legal  point  of  view,  cold  and  alcohol  appear  to  have 
been  important  factors  in  many  persons  who  have  died  from  this  cause.  A 
drunken  man  sometimes  falls  asleep  in  the  open  air  during  intense  cold.  He 
dies,  and  post-mortem  superacute  oedema  of  the  lung  is  found,  with  lesions 
of  nepliritis,  which  are  never  wanting.  Some  authors  (Huchard  and  Renaud) 
assign  the  jsrincipal,  if  not  the  only,  part  to  the  lesions  of  aortitis  and  peri- 
aortitis. According  to  Huchard,  the  needful  intermediary  between  acute 
pulmonary  oedema  and  Brightism  is  aortitis,  and  especially  periaortitis, 
with  its  inflammatory  or  reflex  reaction  on  the  cardio-pulmonary  plexuses. 
I  am  sorry  to  differ  from  this  view.  I  do  not  deny,  of  course,  that  some 
aortic  cases  may  have  congestion  and  oedema  of  the  lungs ;  but  what  I  main- 
tain, .supported  by  undoubted  evidence,  is  that  superacute  oedema  of  the 
lung  has  been  found  in  many  cases  of  Bright's  disease  in  which  neither  aortic 
nor  periaortic  lesions  were  found  during  life  or  post  mortem.  The  subject 
on  whom  Bouveret  made  an  autopsy  had  neither  aortitis  nor  periaortitis  ; 
Giraudeau's  two  cases  showed  neither  of  these  lesions.  My  patient  had 
neither  aortitis  nor  periaortitis.  Brouardel,  who  at  the  Morgue  performed 
post-mortems  on  patients  who  died  of  superacute  oedema  of  the  lung,  says 
that  the  aortic  lesions  are  far  from  being  constant,  while  the  renal  ones  are 
never  lacking.  He  noted,  among  others,  the  autopsy  of  a  man  who  suffered 
from  latent  nephritis,  and  succumbed  to  superacute  a^dema  of  the  lung. 
The  autopsy  revealed  the  integrity  of  the  aorta,  but  showed  the  lesions  of 
nephritis. 

To  the  anatomical  let  us  add  the  clinical  proofs.  Many  patients  with 
Bright's  disease,  whose  cases  I  have  reported,  have  neither  before  nor  after 
their  attacks  of  pulmonary  oedema  had  any  sign  of  aortitis.  The  question 
seems  to  me  settled. 

We  do  not  know  by  what  mechanism  superacute  oedema  in  Bright's 
disease  is  produced.  I  do  not,  however,  reject  the  idea  of  pulmonary  vas- 
cular troubles  of  vasomotor  origin,  the  return  circulation  being  for  the 
moment  annihilated,  and  favouring  considerable  hypertension  in  tlie 
afferent  vessels. 

Loeper  blames  the  increase  of  the  l)lood  concentration ;  Widal  tlie 
increase  f)f  the  clHoride  of  soda  in  the  blood. 

Treatment. — The  urgent  indication  is  bleeding.  In  spite  of  the  cokl- 
ncss  of  the  patient  and  the  threatening  collapse,  which  would  at  first  appear 
as  contra-indications,  there  must  be  no  delay,  and,  without  losing  an  instant, 
10  to  15  ounces  of  blood  must  be  withdrawn.  The  marvellous  results  of 
bleeding  must  have  been  seen  to  make  its  imporfance  clear.  I  do  not 
exaggerate  in  saying  that  it  produces  in  the  patient  a  visible  change.  In  a 
case  at  the  Necker  Hospital  o^flema  came  on  with  such  ra])i(lity  that  death 


168  TEXT-BOOK  OF  MEDICINE 

would  have  speedily  followed  unless  bleeding  had  been  performed  at 
once.  The  patient,  who  had  not  lost  consciousness,  told  us  that  he  felt 
himself  dying  and  recovering  in  the  space  of  a  few  moments.  In  my  patient 
at  the  Hotel-Dieu  blood-letting  had  such  a  marvellous  result  that  imminent 
death  was  arrested,  and  the  rales  which  filled  his  chest  from  apex  to  base 
disappeared  as  by  magic,  leaving  only  a  residue  at  the  bases.  Bleeding  gave 
a  similar  result  in  Giraudeau's  first  case.* 

Of  all  methods  of  blood-letting  bleeding  is,  without  doubt,  the  most 
favourable  ;  but,  in  default  of  bleeding,  wet -cupping  over  the  chest  may  be 
made,  or,  better  still,  two  dozen  leeches  may  be  applied.  Dry-cupping  of 
the  thorax  and  of  the  lower  limbs  is  also  useful. 

Subcutaneous  injections  of  caffeine  or  ether  are  often  indicated.  We 
must  remember,  however,  that  the  kidneys  are  inactive,  and  therefore  use 
caffeine  with  caution.  We  may  start  with  an  injection  of  a  grain,  and  be 
ready  to  repeat  it  several  times  during  the  following  hours.  Oxygen  in  large 
doses  may  also  render  some  service.  The  patient's  strength  must  be 
supported  by  milk  and  weak  tea,  with  a  little  alcohol. 

We  must  also  know  what  to  avoid.  Blisters  must  not  be  used,  for  the 
patient  has  Bright's  disease,  and  the  action  of  cantharides  on  the  kidneys 
will  rapidly  make  the  situation  worse. 

For  the  acute  dyspncea  our  thoughts  turn  to  morphia,  but  caution  is 
necessary,  for  morphia  in  such  conditions  may  cause  grave  mishaps.  As 
Brouardel  says  :  "  These  are  cases  which  it  has  been  my  lot  to  see  fairly 
frequently.  A  patient  begins  to  choke.  It  is  evening,  and  one  of  the 
physicians  on  night  duty  is  called.  He  gives  an  injection  of  morphia, 
following  an  only  too  common  rule  ;  the  patient  gets  no  relief.  A  second 
and  third  injection  at  length  bring  quiet ;  some  minutes  or  hours  later 
the  patient  succumbs,  and  the  family  blame  the  physician  who  has  given 
the  injections.  Autopsy  and  inquest  follow.  It  is  found  that  death  was 
due  to  superacute  oedema  of  the  lung." 

Danger  once  averted,  do  not  lose  sight  of  the  patient.  Absolute  milk 
diet  must  be  prescribed,  chloride  of  soda,  which  favours  oedema  (Widal), 
avoided,  and  the  urinary  secretion  closely  watched.  In  short,  he  must  be 
treated  as  a  case  of  Bright's  disease,  and  be  advised  to  avoid  with  the 
greatest  care  every  cause  of  overwork  and  chill. 

*  In  my  wards  I  have  recently  seen  two  more  cases  of  superacute  oedema,  in 
which  bleeding  suddenly  arrested  asphyxia  that  was  threatening  the  patient's  life. 


DISEASES  OF  THE  LUNG  169 

XII.  ON  TUBERCULOSIS  IN  GENERAL— BACILLUS  TOXINES. 

Local  Tuberculosis. 

Nature  of  Tuberculosis. — By  his  immortal  work  on  pulmonary  phthisis, 
Laennec  bequeathed  to  tlie  medical  world  such  an  exhaustive  description  of 
this  disease,  with  its  lesions,  its  forms,  and  its  signs,  that  we  must  all  do 
homage  to  his  genius. 

On  December  5,  1865,  Villemin  read  a  paper  before  the  Academic  de 
Medecine,  and  upset  all  previous  theories  as  to  the  nature  of  tuberculosis. 
By  numerous  and  well-conducted  experiments,  Villemin  showed  that  tuber- 
culosis is  a  virulent,  infectious,  and  inoculable  disease. 

As  soon  as  Villemin's  discovery  was  known,  inoculation  of  tuber- 
culosis was  repeated,  and  varied  to  infinity  in  France  and  abroad.  The 
tuberculous  material  was  introduced  into  the  serous  cavities  of  the  pleura 
and  of  the  peritoneum.  Cohnheim  practised  inoculation,  by  means  of  a  fine 
needle,  mto  the  anterior  chamber  of  the  eye,  and,  owing  to  the  transparency 
of  the  cornea,  was  day  by  day  able  to  follow  the  evolution  of  the  tubercular 
process,  and  in  some  cases  show  the  generalization  of  tuberculosis  m  the 
animal  under  experiment.  Chauveau  produced  tuberculosis  in  the  bovine 
species  by  mixing  tuberculous  material  with  their  food,  and  observed  in 
several  cases  that  the  intestine,  which  had  served  as  the  point  of  entrance 
for  the  virus,  was  much  changed  by  the  lesion.  Tappeiner  and  Wcichsel- 
baum  produced  tuberculosis  in  dogs  by  making  them  breathe  the  powdered 
s])utum  of  phthisical  patients.  Krishaber  and  myself  have  experimented 
upon  the  monkey,  in  order  to  deal  with  the  animal  which  nearest  approaches 
man,  and  in  the  numerous  experiments  made  with  my  intimate  and  lamented 
friend  I  was  struck  at  the  autopsy  with  the  severity  of  the  infectious 
pror-ess.  Three-quarters  of  our  inoculated  monkeys  died  of  tuberculosis 
in  a  few  weeks,  while  out  of  twenty-eight  monkeys  kept  away  from  all  con- 
tamination, and  not  inoculated,  only  one  died  of  tuberculosis.* 

So  great  was  the  importance  of  Villemin's  discovery  that  it  completely 
changed  our  ideas  of  tuberculosis,  and  gave  it  a  place  in  the  list  of  infectious 
diseases.  It  had  also  the  result  of  sanctioning,  in  irrefutable  fashion, 
Laennec's  doctrine  of  the  identity  and  the  unity  of  tuberculo-caseous 
l<'sions,  and,  at  the  same  stroke,  destroyed  the  German  teaching,  which, 

*  Our  comploto  researches  concern  scventy-eiglit  monkeys.  Out  of  sixteen  monkeys 
inoculated  with  human  tubercle,  twelve  died  with  tubercular  lesions  ;  out  of  Iwenfyfour 
monkeys  win'eh  were  not  inoculated,  but  wliieli  livi-d  witli  the  inoculated  monkeys,  live 
died  from  tuberculosis  ;  out  of  ten  monkeys  which  wc^re  inoculated  with  purulent  matter, 
only  one  died  tulwrculous  ;  out  of  twenty-eight  nionki-ys  which  wen^  i.solatcd  from  ••v«'ry 
Rource  of  contamination,  only  one  died  from  tubercular  disease  {Arch.de  I'/ii/siologic, 
Mars,  1884,  No.  ."J). 


170  TEXT-BOOK  OF  MEDICINE 

under  the  eminent  patronage  of  Virchow  and  Niemeyer,  differed  from  the 
work  of  Laennec,  and  looked  upon  tuberculous  infiltrations  of  the  lung  as 
simple  caseous  degeneration,  or  so-called  scrofulous  phthisis.  This  latter 
part  of  the  question,  however,  with  its  developments,  will  be  treated  in 
one  of  the  following  chapters. 

Bacillus  of  Tuberculosis.— The  infectious  nature  of  tuberculosis  being 
demonstrated,  the  question  was  to  discover  the  microbe  of  the  disease.  The 
work  of  Pasteur  and  his  culture  methods,  which  had  given  such  marvellous 
results  in  the  study  of  other  diseases  (antlu-ax),  served  as  a  guide.  The  work 
was  begun,  and  in  May,  1882,  Koch  discovered  the  bacillus  of  tuberculosis. 
This  bacillus  may  be  revealed  in  the  sputum  by  the  process  described 
below.*  It  forms  a  very  slender,  straight,  or  bent  rod,  in  length  equal  to 
the  third  part  of  a  blood-corpuscle— that  is  to  say,  2  or  3  //. 

The  bacillus  is  of  uniform  size  throughout  its  whole  length,  but  ovoid 
swellings,  which  may  be  due  to  the  presence  of  spores,  are  seen.  The 
small,  colourless,  oval  vacuoles  in  the  interior  of  the  bacillus  have  also  been 
looked  upon  as  spores. 

In  order  to  stain  Koch's  bacillus,  Ziehl's  method  is  employed  at  the 
present  day.  It  consists  m  leaving  the  slides  for  ten  to  twenty  minutes  in 
a  solution  of  carbol-fuchsin  which  is  prepared  as  follows  : 

Fuchsin  . .  1  gtamme 


Carbolic  acid 
Absolute  alcohol 
Distilled  water  . 


5  grammes 
10 
90 


The  preparation  is  then  decolorized,  either  with  a  30  per  cent,  solution  of 
nitric  acid,  or  by  a  mixture  of  five  parts  of  absolute  alcohol  with  one  of  nitric 
acid.  In  order  more  clearly  to  define  the  bacilli,  the  slide  is  stained  a  second 
time  with  methylene  blue  in  a  solution  of  water  and  alcohol.  By  this 
process  the  bacilli  are  stamed  red,  while  the  tissue  and  other  microbes  are 
of  a  blue  colour. 

These  characters  distinguish  it  from  all  other  micro-organisms.  It  is 
analogous  only  with  that  of  leprosy. 

The  so-called  pseudo-tuberculous,  or  acid-resisting  bacilli,  are  more  thick- 
set, and  are  less  resistant  to  decoloration  by  acids,  especially  nitric  acid.f 


* 


Some  of  the  most  purulent  sputum  is  taken  with  a  needle  and  spread  out  on  a 
slide,  which  has  previously  been  washed  in  diluted  nitric  acid,  and  afterwards  in  alcohol. 
A  second  slide  is  placed  upon  the  first,  and  the  two  are  rubbed  together  so  as  to  form  a 
film  on  each  of  the  slides.  The  albumen  is  then  coagulated  by  passing  the  slide  three 
times  through  the  flame  of  a  Bimsen  burner,  or  by  placing  upon  it  a  few  drops  of  a 
mixture  of  alcohol  and  ether  in  equal  parts.  The  slides  may  then  be  put  in  the  staining 
fluid. 

•1-  Tlie  tubercle  bacillus  is  not  the  only  one  which  remains  stamed  by  Ziehl  s  method 
after  decoloration  with  acids.     A  group  of  other  baciUi  possesses  the  same  property ; 


DISEASES  OF  THE  LUXG  171 

The  bacilli  in  tubercular  sputum  are  usually  free,  and  are  rarely  found 
enclosed  in  the  leucocytes  or  the  epithelial  cells.  They  may  be  single  or  in 
pairs,  or  grouped  en  masse. 

In  histological  preparations  the  bacilli  are  found  en  masse  in  the  giant 
3ells. 

The  discovery  of  the  tubercle  bacillus  has  been  of  the  highest  importance, 
for  its  presence  is  a  sure  sign  of  tuberculosis.  The  proof  that  the  bacillus 
is  indeed  the  active  agent  of  tuberculosis,  as  the  bacterium  is  the  active 
agent  of  anthrax,  is  that  the  tubercle  bacillus  has  been  successfully  isolated, 
cultivated,  and  inoculated.  Koch,  inspired  by  his  culture  methods,  pro- 
ceeded in  the  following  manner  :  He  took  a  small  piece  of  tubercular 
material,  and  placed  it  on  sterile  gelatinized  serum,  which  was  then  put  in 
an  oven  at  99^  F. 

Roux  and  Nocard  have  introduced  glycerinated  media,  which  are  an 
excellent  culture  material.  Good  results  are  obtained  by  the  addition  of 
1  to  2  per  cent,  of  glucose  to  the  glycerinated  media. 

After  twelve  days  or  a  fortnight  the  appearance  of  dry  or  scaly  particles, 
"omposed  of  colonies  of  bacilli,  is  noticed.  These  colonies  are  whitish  or 
yellowish,  not  shining,  clearly  isolated  from  one  another,  and  but  little 
adherent  to  the  culture  medium. 

The  tubercular  particles,  transported  to  another  culture  medium,  re- 
produce new  colonies  of  barilji,  and  so  on,  through  several  successive  cultures. 

Bezan^on  and  Griffon  have  extolled  the  use  of  glycerinated  blood-agar 
and  yolk  of  egg  with  agar,  which  give  earlier  and  more  certain  cultures 
than  other  media. 

From  the  point  of  view  of  diagnosis,  the  discovery  of  the  tubercle  bacillus 
has  had  considerable  influence.  We  know  how  difficult  the  diagnosis  often 
is  between  pulmonary  phthisis  and  other  diseases,  such  as  bronchitis,  clu-onic 
catarrh,  chronic  pneumonia,  bronchiectasis,  chronic  laryngitis,  pulmonary 
Byphilis,  hydatids  of  the  lung,  etc.  In  these  different  cases  the  presence  of 
the  bacillus  in  the  sputum  furnishes  the  proof  of  tuberculosis  ;  and  its  absence, 
after  several  sucx^.essive  examinations,  enables  us  to  deny,  in  a  more  or  less 
certain  fasliion,  the  existence  of  tuberculosis. 

In  cases  where  the  search  for  the  bacillus  is  fruitless  recourse  is  had 


they  aro  tliorofon^  callod  arid-re.v,stin/j,  or  p.s('iido-tul)frculniis.  Thoy  arc  mot  with  in 
milk  anrl  in  butter,  and  aro  found  in  pianta,  in  earth,  and  manure.  They  may  l)e  patho- 
genic in  animals.  In  man  acid-resisting  bacilli  are  found  in  the  smegma,  the  cerumen, 
the  nasal  mucus,  in  certain  affections  of  the  eyes,  of  the  uro-genital  system,  and  of  <ho 
iiings,  especially  gangrene.  They  may  therefore  give  rise  to  errors  in  diagnosis,  'riioy 
can  be  distinguished  from  the  tubercle  l)acillus  by  (he  following  characters  :  They  nre 
not  so  resistant  to  decfdoralion  by  acids  :  'AO  jkt  cent,  nitric  acid,  which  does  not  affect 
Koch's  bacillus,  renders  them  colourless;  lliey  are  more  squat,  grow  in  all  eiilturo 
media,  and  cannot  produce  tubercles  by  inoculation  of  animala  (Creuzen  el  Villaret, 
lievue  dc  la  Tuberculofie,  HtO.l,  p.  188). 


172  TEXT-BOOK  OF  MEDICINE 

to  inoculation  of  animals — a  procedure  which  gives  most  excellent  results. 
The  guinea-pig  is  usually  chosen.  A  fragment  of  suspected  tissue  is  inocu- 
lated under  the  skin  of  the  animal's  belly.  A  few  days  later  a  nodule 
appears,  breaks  down,  and  ends  in  a  tubercular  chancre.  The  neighbouring 
glands  enlarge  ;  the  tuberculosis  becomes  general,  and  the  animal  dies  one 
or  two  months  later.  To  gain  time,  it  is  better  to  inoculate  the  peritoneal 
cavity,  provided,  however,  pyogenic  germs  be  not  associated  with  Koch's 
bacillus. 

The  reaction  is  still  more  rapid  if  the  suspected  product  be  injected  under 
the  mamma  of  a  female  guinea-pig  during  lactation  (Nattan-Larrier). 

Every  inoculated  animal  (guinea-pig,  rabbit,  dog)  presents  a  blood 
reaction,  characterized  at  first  by  polynuclear  leucocytosis,  and  later  by 
lymphocytosis. 

In  some  special  cases,  in  order  to  prove  tuberculosis,  recourse  may  be 
had  to  the  reaction  produced  by  the  injection  of  tuberculin,  which  will  be 
discussed  in  the  chapter  on  Pulmonary  Phthisis. 

As  regards  tuberculin,  I  will  content  myself  for  the  moment  with 
pointing  out  the  researches,  the  object  of  which  is  the  extraction  and  the 
isolation  of  the  soluble  products  secreted  by  Koch's  bacillus.  These  toxines 
cause  vaso-dilatation,  convulsions,  and  necrosis,  and  play  a  considerable 
part  in  the  symptoms  of  tuberculosis. 

Pathological  Anatomy. — The  tubercular  lesions,  in  whatever  organ  or 
tissue  they  be  situated,  present  two  chief  forms — the  one  circumscribed 
and  nodular  (tubercular  granulation) ;  the  other  diffuse  (tubercular  infil- 
tration). These  two  forms  are  frequently  associated,  and  I  would  point  out 
here  that  the  anatomical  peculiarities  and  texture  of  the  tissue  in  which 
the  lesions  develop  may  modify  their  external  appearance. 

1.  The  tubercular  granulation,  which  corresponds  to  the  macroscopic 
unit,  or  the  tubercle,  properly  so  called,  is  a  promment  rounded  nodule, 
hard  to  the  touch,  grey  and  semitransparent  when  it  is  young,  opaque  and 
yellow  when  it  is  old.  It  is  visible  with  the  naked  eye  or  with  a  lens  ;  its 
size  is  variable,  but  it  does  not  exceed  tjV  millimetre  in  diameter. 

This  tubercular  granulation  is  formed  of  one  or  of  several  smaller  parts, 
called  tubercular  follicles,  which  correspond  to  the  microscopic  unit,  so  that 
there  may  be  ten,  fifteen,  or  thirty  follicles  massed  together  to  form  the 
granulation. 

The  tubercular  follicle  (Schiippel),  or  elementary  granulation  (Malassez), 
or  tubercle  proper,  has  the  following  structure :  When  a  section  is  made, 
we  find  at  the  centre  a  giant  cell,  containing  several  nuclei,  which  are  most 
often  set  like  a  crown  at  the  periphery.  Its  dimensions  have  gained  for  it 
the  name  of  giant  cell  (Langhans).  The  giant  cell  is  surrounded  by  a  zone 
of  fairly  large  cells,  known  as  epithelioid,  and  by  rounded  closely-packed 


DISEASES  OF  THE  LUNG  173 

cells  belonging  to  the  embryonic  type — that  is  to  say,  having  a  nucleus 
which  is  large  as  compared  with  the  protoplasm. 

All  these  elements  are  bound  together  by  a  fibrillary  or  granular  ground 
substance.  The  circulation  is  imperfect  or  absent  in  the  granulations,  for  the 
vessels  here,  as  in  every  tubercular  product,  are  arrested  in  their  develop- 
ment, or  obliterated  by  endarteritis  or  capillaritis. 

The  manner  in  which  the  tubercle  is  formed  in  the  tissues — that  is,  its 
histogenesis — is  still  disputed.  According  to  Koch,  the  tubercle  is  formed 
chiefly  by  white  corpuscles  from  the  blood,  the  vessels,  or  the  lymph. 
According  to  MetchnikofE  and  his  pupils,  the  tubercle  is  really  composed 
of  leucocytes,  and  represents  a  defensive  reaction  against  the  bacillus.  The 
epithelioid  and  giant  cells  of  the  tubercle  are  formed  entirely  at  the  expense  of 
the  phagocytes^that  is  to  say,  of  the  large  wandering  mononuclear  leuco- 
cytes— and,  secondarily,  of  the  endothelial  and  connective  cells.  No  epi- 
thelial cell  ever  contributes  to  the  formation  of  the  tubercle.  "  The  tubercle 
is  composed  of  a  collection  of  phagocytes  of  mesodermic  origin,  which  pass 
towards  the  spots  where  they  find  and  envelop  the  bacilli."  According  to 
Baumgarten,  Ziegler,  Cornil,  Straus,  Brissaud  and  Toupet,  Kostenisch 
and  Wolkon,  the  primary  and  fundamental  lesion  of  the  tubercle  is  a  reaction 
of  the  fixed  cells  of  the  tissues,  coniiective  and  also  epithelial  cells,  which 
proliferate  by  karyokinesis,  and  become  converted  into  epithelioid  and  giant 
cells,  elements  that  are  very  rich  in  glycogen — a  fact  which  clearly 
indicates  their  activity  (Loeper).  The  lesion  is  only  secondarily  invaded 
by  migratory  leucocytes. 

The  bacilli  are  more  or  less  abundant  in  the  tubercular  follicle  ;  they 
are  found  in  variable  numbers  in  the  giant  cells  and  the  periphery  of  the 
follicle.  The  follicle  may  be  considered  as  the  primary  element ;  the  follicles, 
by  their  aggregation,  form  the  tubercle,  and  the  tubercles,  in  their  turn, 
by  their  aggregation,  may  form  those  large  tubercles  which  may  be  as  large 
as  an  egg,  and  are  found  in  the  lung,  the  brain,  or  at  times  in  other  organs. 
All  these  products  have  a  common  character  (but  it  is  not  confined  to  them)  '* 
they  undergo  caseous  degeneration  from  the  centre  to  the  periphery.  Tho 
central  part  of  the  follicle  or  of  the  granulation  is  infiltrated  with  fatty 
granules,  becomes  opaque,  and  this  degeneration  extends  to  the  middle 
zone  of  large  cells  and  to  the  external  one  of  small  embryonic  cells.  The 
tubercle  now  becomes  yellow,  softens,  and  tends  to  the  formation  of  ulcers. 

It  miLst  not  be  thought,  however,  that  caseation  is  the  only  termina- 
tion :  the  tubercle  may  become  calcified ;  it  may  be  converted  into 
fibro-plastic  tissue,  and  become  fibrous — that  is  to  say,  harmless.  Most 
often  the  tubercular  change  seems  to  begin  in  the  small  vessels  or  capil- 
laries (tuberculous  endarteritis) ;  the  vascular  origin  of  the  tuberculosis  is, 
however,  not  absolute. 


174  TEXT-BOOK  OF  MEDICINE 

2.  The  tuberculous  infiltration  represents  the  diffuse  form  of  tuber- 
culosis. The  follicles  have  no  tendency  to  aggregate  into  granulations, 
but  are  spread  out  "  like  a  sheet,"  and  infiltrate  the  tissues,  which  become 
thickened,  and  sometimes  take  on  a  lardaceous  aspect.  These  tuberculous 
infiltrations  comprise  :  infiltration  of  the  lung,  which  plays  so  large  a  part 
in  pulmonary  phthisis ;  hifiltration  of  the  larynx,  confounded,  quite 
wrongly,  for  several  years  with  oedema  ;  infiltration  of  the  lymphatic  glands, 
considered  until  lately  as  bemg  of  a  scrofulous  nature  ;  infiltration  of  the 
synovial  membranes,  joints,  and  bones,  which,  under  the  name  of  fungous 
synovitis,  white  swellmg,  and  caries,  were  too  often  regarded  as  of  scrofulous 
origin. 

The  tubercular  infiltrations  described  by  Grancher  may  show  the 
same  changes  as  the  granulations ;  they  pass  into  the  same  caseous  state, 
become  softened,  have  a  greyish  or  a  yellowish  colour,  and  when  the  caseous 
change  is  complete  differential  cellular  elements  are  no  longer  found.  The 
bacilli  themselves  are  present,  but  only  in  very  small  numbers.  Nodules 
and  infiltration  are  often  found  together  in  the  same  tissue  or  organ,  and 
are  associated  with  the  usual  products  of  inflammation  ha  different  pro- 
portions, accordmg  to  the  soil  in  which  they  develop.  Such  are  the  different 
forms  which  tuberculosis  may  assume,  and,  in  spite  of  the  importance  and 
of  the  value  of  numerous  works,  it  may  be  asserted  that  pathological 
anatomy  alone  would  often  have  been  unable  to  affirm  or  to  deny  the  nature 
of  a  tubercular  product. 

Recognition  of  the  bacillus  and  inoculation  with  the  suspected  product 
allow  us  to  affirm  its  tubercular  nature.  We  can  now  distinguish  between 
tuberculosis  and  changes  which  resemble  it;  scrofula  will  no  longer 
encroach  upon  a  domain  which  does  not  belong  to  it,  nor  will  true  bacillary 
tuberculosis  be  confounded  with  false  tuberculosis. 

It  is  convenient  to  mention  the  rare  but  undoubted  association  of  cancer 
and  tuberculosis  in  the  same  tissue.  The  old  ideas  as  to  the  antagonism 
of  tubercular  and  cancerous  lesions  must  be  abandoned,  and  hybrid  forma- 
tions admitted.  Tuberculosis  may  be  grafted  upon  cancer,  but  more  often 
cancer  is  grafted  upon  tuberculosis. 

Local  Tuberculosis. — By  assigning  to  tuberculosis  some  of  the  lesions 
which  had  been  included  under  scrofula,  the  question  of  tuberculosis  has 
latterly  assimied  a  slightly  different  aspect.  We  find  local  manifestations 
of  tuberculosis  which  are  confined  to  the  glands,  the  synovial  membranes, 
the  jomts,  the  prostate,  testicle,  scrotum,  ovary,  uterus,  nipple,  skm,  pleura, 
meninges,  cerebellum,  eyes,  or  tonsil. 

Certain  of  these  local  manifestations  appear  in  patients  already  suspected 
of  pulmonary  tuberculosis,  and  do  not  merit  the  name  of  "  local,"  but 
others    appear    as    an    isolated    manifestation.     Some  remahi  stationary, 


I 


DISEASES  OF  THE  LUNG  175 

without  becoming  general  or  affecting  the  lung  ;  they  may  even  be  cured. 
Others  attack  the  lung,  and  may  be  followed  by  slow  phthisis  or  by  acute 
tuberculosis.  Many  people  suffer  from  suppurative  adenitis,  white  swelling, 
or  ossifluent  abscess,  which  were  formerly  regarded  as  scrofulous,  but  are 
manifestly  tuberculous  !  These  folk  were  considered  scrofulous,  because 
the  lesion  apjieared  localized  and  curable,  because  their  lungs  were  free,  and 
because  physicians  held  to  the  Louis  law,  wliicli  taught  that  pulmonary 
tuberculosis  must  be  accompanied  by  that  of  other  organs.  This  question 
must  to-day  be  looked  upon  in  a  different  light,  and  I  refer,  therefore,  to  the 
article  on  Scrofula. 

Tuberculosis  in  Animals. — Monkeys,  oxen,  and  pigs  are  very  subject 
to  tuberculosis.  It  is  fairly  common  in  the  monkey  ;  it  is  rare  in  the  horse, 
sheep,  and  goat. 

The  carnivorous  animals,  such  as  dogs  and  cats,  are  not  liable  to 
tuberculosis. 

Tuberculosis  in  gallinaceous  birds — that  is,  avian  tuoerculosis— differs 
in  several  respects  from  the  disease  in  man. 

Cadiot,  Gilbert,  and  Royet  arrive  at  the  following  conclusions  :  '"  Avian 
tuberculosis,  which  is  very  frequent  in  the  Gallinacese,  is  inoculable  in 
hens,  pigeons,  and  rabbits ;  it  is  transmissible,  but  with  more  difficulty,  to 
the  guinea-pig  ;  it  may  be  seen  in  the  ox  and  in  man  "  (Kruse,  Pansmi). 

"  Tuberculosis  of  the  Mammiferse  attacks  mankind,  the  dog,  the  ox, 
and  the  horse  ;  it  is  easily  transmissible  to  the  guinea-pig  and  to  the  rabbit, 
which,  however,  is  perhaps  less  sensitive  to  it  than  to  avian  tuberculosis ; 
it  is  inoculable  in  the  parrot,  and  sometimes  in  the  hen. 

"  Both  poisons,  therefore,  attack  the  same  animals,  and  the  terms 
which  designate  them  are  not  exact,  since  the  so-called  tuberculosis  of 
Mammiferaj  is  also  seen  in  parrots ;  and  the  so-called  avian  tuberculosis 
is  not  seen  in  all  birds,  and  may  sometimes  be  met  with  in  the  Mammifera3. 
Parrots  infected  by  human  beings  become,  in  their  turn,  a  permanent 
centre  of  tuberculous  infection." 

The  doctrine  of  the  unity  of  human  and  bovine  tuberculosis  (Nocard, 
Arlohig)  has  recently  been  attacked  by  Koch,  who,  in  a  famous  paper  read 
before  the  London  Congress  in  1901,  attempted  to  establish,  first,  that 
bovine  differs  from  human  tuberculosis,  as  the  latter  cannot  be  transmitted 
to  the  bovine  species ;  secondly,  transmission  by  the  milk  or  the  flesh  of 
infected  animals  is  hardly  more  frequent  than  hereditary  tuberculosis, 
which,  according  to  Koch,  is  almost  exccjjtional.  Tiiese  assertions  have 
been  opposed  by  Arloing,  and  during  the  last  two  years  many  works  have 
been  written  refuting  them  (Kavcnul,  Spronck,  Orth). 


176  TEXT-BOOK  OF  MEDICINE 

XIII.  PULMONARY  PHTHISIS— COMMON  CHRONIC 
TUBERCULOSIS. 

The  word  phthisis  is  not  synonymous  with  tuberculosis.  It  repre- 
sents the  ultimate  or  last  phase  of  tuberculosis,  and  characterizes  the 
consumption  period  of  phthisiogenous  lesions.  These  lesions  vary.  Some 
are  clearly  circumscribed — viz.,  the  tubercular  granulation,  or  tubercle  ; 
others  are  diffuse — viz.,  tuberculous,  or  caseous  infiltration;  but  their 
nature  is  identical,  and  they  are  essentially  tubercular.  When  the  lesions 
are  slow  in  growth  and  ulceration  of  the  lung  (cavity)  occurs  late,  the 
patient  dies  of  consumption.  This  essentially  chronic  form,  which  is  the 
most  common  of  all,  is  called  pulmonary  phthisis,  without  other  designation. 
If  the  tubercular  products  grow  rapidly  and  lead  to  early  ulceration,  the 
disease  then  takes  the  name  of  acute  phthisis.  Lastly,  the  tubercular 
granulations  may  be  confluent,  killing  the  patient  before  softenmg  and 
ulceration  have  time  to  occur ;  in  this  case  the  disease  is  called  acute  miliary 
tuberculosis — that  is,  there  is  tuberculosis,  but  not  phthisis. 

Pathological  Anatomy. — Lesions,  which  vary  accordmg  to  their  form 
and  their  age,  are  found  in  the  lungs,  especially  at  the  apices :  tubercular 
granulations  and  infiltrations,  ulcers,  cavities,  interstitial  pneumonia, 
bronchial  dilatations,  pleural  adhesions,  etc.,  may  be  present. 

We  find  in  the  lung,  as  elsewhere,  two  chief  forms — the  granulation  or 
the  infiltration — which  may  be  isolated  or  combmed. 

Tubercular  Granulations. — The  tubercular  granulations  in  the  lung  show 
two  slightly  different  forms — the  grey  granulation  and  the  miliary  tubercle. 

The  grey  granulation  (so  named  by  Bayle)  is  a  small,  hard,  prominent, 
rounded,  transparent  nodule,  that  is  much  smaller  than  the  miliary  tubercle. 
It  is  sometimes  only  visible  with  the  lens,  and  it  does  not  exceed  ^V  milli- 
metre in  diameter.  This  greyish  granulation  may  take  on  a  yellowish  tint, 
from  degeneration  of  its  elements  ;  it  is  composed  of  tubercular  follicles, 
which  have  been  described  in  the  previous  chapter.  The  grey  granulation 
may  arise  in  several  spots,  but  its  seat  of  election  is  the  wall  of  the  blood- 
vessels and  of  the  lymphatics.  It  is  especially  found  in  the  case  of  acute 
miliary  tuberculosis,  where  it  is  confluent  and  generalized  through  both 
lungs,  while  it  is  more  rare  in  pulmonary  phthisis.  The  miliary  tubercle 
(Laennec)  is  the  form  found  in  chronic  phthisis,  and  is,  as  a  rule,  localized 
the  apex  of  the  lung,  invading  later  the  lower  regions. 

The  miliary  tubercle  is  about  as  big  as  a  millet-seed  :  its  diameter 
varies  from  |  to  1 J  millimetres ;  it  is  prominent,  rounded,  greyish,  and 
semitransparent — at  first  yellowish  and  opaque,  when  it  is  degenerating. 
Like  all  tubercles,  it  is  adherent  to  the  neighbouring  tissues,  and  cannot 
be  removed  without  tearmg  away  particles  of  them. 


I 


DISEASES  OF  THE  LUNG  177 

The  description  of  the  little  tubercular  granulation  does  not  quite  apply 
to  the  miliary  tubercles,  which  have  a  more  complex  structure,  because  "  the 
contents  of  the  alveoli  and  of  the  bronchioles,  and  the  neoplastic  infiltration 
of  the  connective  tissue  of  the  walls  of  the  bronchi  and  the  vessels,  take  part 
in  their  formation."  The  miliary  tubercle  appears  to  have  a  well-defined 
origin  ;  the  tubercular  follicles,  which  take  the  chief  part  in  its  formation, 
develop,  according  to  Rindfleisch,  around  the  terminal  intralobular  bron- 
chiole, at  a  point  where  it  becomes  acinous  and  joins  the  alveolar  ducts  of 
the  acinus.  Such  is  said  to  be  the  origin  of  the  miliary  tubercle,  named 
by  Charcot  the  peribronchial  tubercular  nodule.  It  is  necessary  to  add 
that  slightly  larger  bronchioles  may  be  the  centre  of  formation  of  the 
tubercle. 

This  little  mass  assumes  various  shapes.  Sometimes  it  takes  that  of  a 
crescent,  and  does  not  completely  surround  the  bronchiole  ;  at  other  times 
it  leaves  one  of  the  segments  free,  or  sheathes  the  bronchus  like  a  muff, 
and  the  diffuse  tubercular  elements  only  present  at  distant  intervals  "the 
agglomerated  and  circumscribed  form,  usually  regarded  as  the  characteristic 
of  the  tubercle."  From  the  bronchus,  the  tubercular  infiltration  gradually 
reaches  the  neighbouring  alveoli,  and  thus  the  tubercular  nodule  arises. 
Embryonic  infiltration  occurs  in  the  walls  of  the  bronchi  and  of  the  alveolus, 
while  the  mucosa  of  the  bronchus,  affected  by  inflammation,  loses  its 
epithelium,  and  its  cavity  is  filled  with  large  cells,  of  which  some  show 
fatty  degeneration  ;  in  other  words,  we  find  tubercular  peribronchitis  and 
catarrhal  bronchitis.  Moreover,  obliterating  endobronchitis  is  met  with, 
the  tubercular  nodules  projecting  into  the  interior  of  the  bronchus,  and 
finally  obliterating  its  lumen. 

The  tubercular  granulations  which  develop  in  the  walls  of  the  alveoli 
have  the  following  disposition  :  A  granulation  always  envelops  several  rows 
of  alveoli,  and  the  extension  of  the  tubercular  agglomeration  takes  place 
by  cellular  infiltration  of  the  walls  and  the  cavities  of  the  alveoli.  The 
endothelium  of  the  alveolus  undergoes  changes  analogous  to  those  of 
catarrhal  pneumonia.  In  the  midst  of  this  tubercular  invasion  the  walls  of 
the  alveoli  remain,  and  form,  as  it  were,  the  sketch  of  the  tubercular  nia.ss, 
while  the  ela.stic  fibres  still  indicate  the  skeleton  of  the  alveohis. 

The  bronchial  vessels  dilate  and  may  become  varico.se,  while  progressive 
obstruction  by  embryonic  proliferation  occurs.  The  condition  Is  really  an 
obliterating  endarteritis,  or  capillaritis  (Martin). 

Tubercular  Infiltration— Caseous  Inflammations.— Granulations  and 
miliary  tubercles  do  not  form  the  chief  lesion  :  we  first  notice  a  substance 
which  may  be  greyish  and  semitransparent,  or  yellowish  and  opat^uc,  or  at 
times  amorphous  and,  as  it  were,  infiltrating  the  pulmonary  tissues,  though 
it  more  often  forms  centres  of  variable  dimensions.      Laennec  called  this 

12 


178  TEXT-BOOK  OF  MEDICINE 

tubercular  infiltration,  and  it  has  since  been  named  caseous  material, 
because  of  its  resemblance  to  cheese  (caseum).  It  is  composed  of  crystals 
of  fatty  matter,  epithelial  cells,  and  more  or  less  degenerated  lymphatic 
corpuscles.     What  is  the  nature  and  origin  of  this  caseous  material  ? 

Speaking  generally,  tubercular  granulations,  whatever  be  theh-  situation 
(pleura,  peritoneum,  meninges,  or  lungs),  cause  a  surrounding  zone  of 
inflammation  (Herard  and  Cornil).  If  tuberculosis  develops  upon  the  walls 
of  the  bronchi,  the  lesions  of  endobronchitis  result;  if  it  affects  the 
pulmonary  alveoli,  the  changes  of  catarrhal  pneumonia,  as  well  as  the 
embryonic  infiltration,  result. 

Is  the  caseous  substance  due  to  metamorphoses  of  the  ordmary  inflam- 
matory products  ?  or  is  it  the  remains  of  broncho-pneumonia  arising  by 
contact  with  the  tubercle  ?  or,  indeed,  is  it  not  a  tubercular  mfiltration, 
just  as  the  miliary  tubercle  and  the  grey  granulation  are  ? 

Far  too  much  importance  has  been  assigned  to  the  pneumonic  products  ; 
indeed  the  products  of  ordinary  inflammation  are  not  wanting  m  essentially 
tubercular  lesions,  but  they  are  only  of  secondary  importance.  The  infil- 
trations called  caseous  are  true  tubercular  infiltrations,  which  have  under- 
gone the  degeneration  common  to  a  large  number  of  tubercular  productions. 
Some  caseous  masses  are  simply  an  agglomeration  of  miliary  tubercles, 
and  we  shall  see  later,  when  dealing  with  "  caseous  pneumonia,  that  the 
tubercular  infiltrations,  which  are  apparently  diffuse,  are  really  composed 
of  a  more  or  less  confluent  aggregation  of  tubercular  products.  The  tuber- 
cular products,  which  are  present  either  in  a  chrcumscribed  form  (granula- 
tion, miliary  tubercle)  or  in  an  apparently  diffuse  and  infiltrated  form,  are 
therefore  only  the  result  of  a  specific  mflammatory  process;  and  ordinary 
phthisis  has  for  its  most  common  lesions  the  isolated  or  aggregated 
miliary  tubercle  and  chronic  tubercular  broncho-pneumonia. 

It  is  to  be  noted  that  all  these  mflammations  of  tubercular  nature  and 
origm  are  destined  to  undergo  the  same  process :  The  vessels,  prunarily  or 
secondarily  invaded  (endarteritis,  capillar itis),  become  obliterated ;  the 
inflammatory  products,  which  are  greyish  at  first,  become  opaque,  yellow, 
and  caseous  ;  they  break  down,  pass  into  a  neighbouring  bronchus,  and  leave 
an  ulceration  in  their  place. 

There  is,  however,  a  process  which  tends  to  cure— viz.,  the  cretaceous, 
or  fibrous,  change  in  the  tubercular  products. 

Pulmonary  Cavities.— The  formation  of  a  cavity  is  preceded  by  dilata- 
tion of  the  neighbouring  bronchi.  This  dilatation  leads  to  the  destruction 
of  the  walls  which  lose  their  resistance  ;  also,  when  the  softened  tubercle 
empties  itself  into  the  bronchus,  the  latter  is  already  dilated,  and  forins 
part  of  the  excavation.  The  primary  excavations  which  result  from  the 
breakmcx  down  of  the  mUiary  tubercles  might  be  called  acinous  cavities; 


DISEASES  OF  THE  LUNG  179 

the  union  of  several  acinous  cavities  would  form  lobular  cavities,  which, 
in  their  turn,  would  form  lobar  or  large  cavities. 

Cavities  vary  in  size  from  a  pea  to  a  nut,  or  larger.  They  are  often 
anfractuous,  divided  into  compartments,  and  traversed  by  bands  of  connec- 
tive tissue  and  by  vessels  which  have  resisted  the  ulceration.  The  cavity 
is  lined  with  a  membrane  formed  of  embryonic  tissue  and  granulations. 
This  surface  secretes  a  purulent  liquid,  rich  in  toxmes,  and  their  absorption 
leads  to  hectic  fever.  The  surface  of  the  cavity  is  sometimes  converted 
into  cicatricial  tissue  ;  this  change  may  end  in  cure.  The  cavity  may  be 
filled  with  blood.  Aneurysmal  dilatations  of  the  pulmonary  artery  at 
times  project  into  the  cavity,  and  may  rupture,  causing  fatal  haemorrhage. 
The  shell  of  the  cavity,  which  is  rich  in  fibro-plastic  tissue  and  granulations, 
is  deprived  of  pulmonary  blood  (functional  blood),  but  vessels  which  com- 
municate with  the  bronchial  arteries  (nutritional  blood)  are  present  in  it 
(Natalis  Guillot). 

The  localization  of  the  tubercular  products  and  their  extension  in  the 
lung  take  place  in  the  manner  so  graphically  described  by  Laennec  :  "  We 
very  often  find  in  the  same  lung  evident  proofs  of  two  or  three  successive 
eruptions,  and  we  can  then  nearly  always  make  out  that  the  primary  eruption 
at  the  apex  of  the  lung  has  already  become  excavated ;  that  the  second, 
situated  around  the  first,  but  a  little  lower,  is  formed  by  tubercles  which, 
in  most  instances,  are  already  yellow,  though  still  small ;  that  the  third, 
formed  by  grey  miliary  tubercles,  with  some  yellow  points  in  the  centre, 
occupy  a  still  lower  zone." 

The  secondary  eruptions  are  not  confined  to  the  lung ;  similar  lesions 
develop  in  other  organs  at  the  same  time. 

The  lesions  of  the  lung  are  not  always  incurable  ;  they  may  end  in 
recovery  by  calcification  or  by  fibrosis.  In  persons  who  have  died  from 
some  other  disease,  and  especially  among  the  elderly,  old  tubercular  masses 
are  found,  varying  in  size  from  a  pin's  head  to  a  pea,  and  converted  into 
calcified  tissue. 

Fibrous  change  is  also  a  method  of  cure  which  may  occur  in  the  granu- 
lations and  cavities.  Fibrous  granulations  were  clearly  noted  by  Cruveilhier, 
who  called  them  curative  ;  they  have  lately  been  carefully  studied.  The 
granulations,  both  in  chronic  and  acute  tuberculosis,  may  pass  into  the 
fibrous  state.  The  walls  of  the  cavities  may  also  be  surrounded  by  a  fibrous 
zone,  continuous  with  the  fibrous  bands  in  the  lung,  and  part  of  the  apex 
may  thus  be  converted  into  fibrous  tissue. 

Pleura. — The  changes  in  the  pleura  (dry  pleurisy,  or  pleurisy  with 
effusion,  adhesic^ts,  perforation,  and  pneuinotiiorax)  occupy  an  important 
place  in  tlio  history  of  pulmonary  phthisis.  The  j)leurisy  is  sometimes 
encysted  and  apical,  interlobar,  or  diaphragmatic.     Often  the  pleurwy  is 

12—2 


180  TEXT-BOOK  OF  MEDICINE 

dry  (false  membranes  and  adhesions)  ;  in  some  cases  there  is  a  considerable 
effusion  of  an  extremely  variable  nature,  and  the  fluid  may  be  serous,  sero- 
fibrmous,  hsemorrhagic,  or  purulent.  The  more  or  less  adherent  false 
membranes  which  line  the  pleura  are  composed  of  fibrinous  lamellae, 
separated  by  masses  of  round  cells.  The  superficial  layers  contain  no  bacilli. 
Giant  cells  are  met  with,  as  well  as  cellular  masses  and  bacilli  in  the  deeper 
layers,  and  the  vessels  of  the  pleura  often  show  numerous  bacilli  in  their 
walls.  Bacilli  are  sometimes  found  in  the  lymphatic  spaces.  The  granula- 
tions are  situated  on  the  surface  of  the  lung,  or  in  the  pleura. 

Tuberculosis  of  other  organs  will  be  studied  elsewhere.  Tuberculous 
adenopathy  of  the  axilla  is  sometimes  seen  in  pleuro-pulmonary  tuberculosis. 

Bacteriology. — The  tubercle  bacillus  has  been  already  described.  I 
shall  therefore  only  refer  to  it  briefly.  Bacilli  are  found  in  all  tubercular 
granulations,  "  between  the  fibrillse  and  the  coagulated  fibrin,  in  the  interior 
of  the  alveoli,  and  in  the  thickened  connective  tissue  of  the  septa  ;  they 
are  especially  numerous  at  the  points  where  the  cells  become  caseous  or 
granular,  and  where  it  is  difficult  to  distinguish  the  limit  of  the  alveoli — 
that  is  to  say,  in  the  central  parts  of  the  tubercles."  Bacilli  exist  m  numbers 
in  the  intravascular  clots,  in  the  altered  walls  of  the  vessels,  and  in  the  peri- 
vascular connective  tissue. 

They  are  also  found  on  the  surface  of  the  pulmonary  cavities,  but  are 
always  associated  with  other  microbes.  A  veritable  flora  develops  in  the 
walls  of  the  cavities,  and  we  find  streptococci,  staphylococci,  zoogloese,  sar- 
cinse,  the  Proteus  vulgaris,  the  Proteus  mirahilis,  the  bacillus  of  green  pus, 
etc.  These  pathogenic  agents  play  a  very  active  part.  Some  cause  sup- 
puration and  necrosis  ;  others,  by  their  toxines,  produce  septicaemia  and 
hectic  fever  ;  and,  lastly,  they  all  hasten  and  complete  the  work  of  destruc- 
tion commenced  by  the  bacillus.  Many  observers,  having  recognized  the 
streptococcus  m  the  blood  of  phthisical  patients,  have  asserted  that  it  plays 
a  great  part  in  the  production  of  hectic  fever.  Straus  has  shown  that  this 
assertion  is  exaggerated. 

Symptoms. — Pulmonary  phthisis  is  often  preceded  by  prodromata  of 
long  duration — viz.,  repeated  attacks  of  laryngitis  or  repeated  bronchitis  ; 
pleurisy,  which  is  sometimes  of  long  standing,  or  which  has  recurred  several 
months  or  years  apart ;  haemoptysis,  which  has  arisen  without  appreciable 
cause,  while  the  patient  was  apparently  in  good  health.  Many  patients 
complain  of  what  they  call  "  a  neglected  cold,"  or  have  suffered  for  months 
from  bronchitis,  and  have  never  regamed  their  health.  They  are  often 
anaemic  ;  they  cough,  grow  thin,  lose  strength,  and  bring  up  sputum  streaked 
with  blood  ;  they  easily  get  out  of  breath,  and  suffer  from  clu-onic  hoarseness 
and  loss  of  voice  ;  the  appetite  is  bad,  dyspepsia  is  present,  and  at  times 
accompanied  by  regurgitation  or  vomiting. 


I 


DISEASES  OF  THE  LUNG  181 

On  auscultation,  we  find  signs  of  commencing  tuberculosis,  such  as 
some  roughness  on  inspiration  (Grancher) ;  some  dry  crackling,  which  is 
limited  to  one  apex,  or  very  slight  impairment  of  resonance  at  the  same 
level.  The  expectoration  is  examined,  and  the  tubercle  bacillus  is  often 
found  in  it. 

At  this  early  pei-iod  the  disease  may  remain  stationary  for  an  almost 
indefinite  period,  may  improve,  or  be  cured,  but  more  often  it  pursues  its 
way.  Its  course,  though  slow  as  a  rule,  is  sometimes  interrupted  by  acute 
attacks  of  laryngitis,  bronchitLS,  fever,  or  slight  haemoptysis,  and  the  patient 
only  too  often  enters  the  second  stage  of  the  disease. 

During  this  period  of  onset  the  nutrition  has  suffered  but  little  :  the  appe- 
tite has  been  fair,  and  wasting  has  not  made  rapid  progress  ;  but  if  the  disease 
continues  to  develop,  the  lesion  extends  and  softens,  large  moist  rales 
appear,  the  lung  tissue  ulcerates,  the  exj)ectoration  becomes  muco-puru- 
lent,  and  the  mischief  is  no  longer  limited  to  one  side,  but  begins  to  invade 
the  other  lung.  In  spite  of  the  gravity  of  this  condition,  improvement  and 
cure  are  still  possible. 

Later,  sometimes  after  many  years,  consumption  appears,  and  sets  its 
seal  on  the  body.  The  patient  has  a  special  facies  :  his  cheeks  and  temples 
become  hollowed,  with  a  tinge  of  colom*  over  the  malar  bones  ;  the  eyebrows 
and  eyelashes  grow  long  ;  the  conjunctiva  takes  on  a  bluish  tint ;  the  fingers 
become  clubbed.  The  symptoms  present  comprise  fever,  profuse  sweats 
(especially  during  sleep  or  on  waking),  vomiting  of  food,  palpitation  of  the 
heart,  pain  in  the  side  (intercostal  neuralgia  or  pleurisy),  vocal  troubles, 
and  dysphagia  (laryngeal  phthisis).  The  fever  rises  every  evening  (hectic 
fever) ;  diarrhoea  is  frequent  (cachectic  diarrhoea,  or  intestinal  tuberculosis)  ; 
the  wasting  is  extreme  ;  the  feet  are  swollen  (cachectic  oedema)  ;  and  the 
tongue  is  sometimes  covered  with  thrush.  In  the  midst  of  this  general 
break-up  the  intellectual  faculties  are  usually  intact ;  illusion  is  sometimes 
complete,  and  it  is  in  this  state  of  consumption,  with  death  at  hand,  that 
tiie  patient,  trusting  in  recovery,  or  believing  himself  affected  by  a  benign 
bronchitis,  gives  himself  up  to  the  hap))iest  thoughts. 

Such  is  the  course  of  pulmonary  plithisis,  when  it  has  not  been  arrested 
by  a  curative  process.  Let  us  now  study  in  detail  the  signs  which  correspond 
to  the  three  })erio(ls  f)f  its  course. 

During  the  first  period  we  find  duUuess  at  one  apex  ;  on  auscultation, 
rough  breathijig,  with  prolonged,  jerky  expiration,  is  heard  in  the  supra- 
spinous fossa  or  in  the  clavicular  region,  together  with  dry,  subcrepitant  rales 
(dry  crackling)  or  sibilant  ronchi.  These  last  signs  are,  however,  often 
absent,  and  some  dry  crepitations  may  be  only  heard  at  a  limited  point  after 
the  patient  has  been  made  to  cough. 

The  lesion,  at  its  commencement,  often  appears  to  be  confined  to  the 


182  TEXT-BOOK  OF  MEDICINE 

most  external  part  of  the  supraspinous  regions  ;  in  many  cases  I  have  found 
slight  duUness  and  dry  crackling  at  this  point — i.e.,  almost  upon  the 
shoulder. 

During  this  period,  which  may  be  of  very  long  duration,  many  patients 
scarcely  consider  themselves  as  invalids.  They  cough,  but  bring  up  little 
expectoration ;  they  have  little  or  no  fever.  They  believe  themselves 
affected  by  simple  bronchitis,  and  make  no  change  in  their  manner  of 
living,  until  haemoptysis  gives  them  warning,  or  an  aggravation  of  symptoms, 
that  must  be  reckoned  with,  supervenes. 

In  the  second  period  the  lesions  are  more  extensive  :  the  tubercular 
tissue  softens ;  the  ulceration  of  the  lung  commences  ;  the  expectoration 
is  more  abundant ;  the  sputum  is  nummular,  and  often  mixed  with  blood ; 
fever  may  appear  ;  the  appetite  fails,  and  wasting  begins.  Percussion 
shows  more  extensive  dullness ;  on  auscultation,  mucous  rales  are  percep- 
tible ;  the  dry  crackling  of  the  first  period  has  become  moist ;  the  breathing 
is  rough  and  blowing,  and  bronchophony  is  heard.  Pleural  friction  sounds 
are  often  heard  in  various  regions,  and  tubercular  lesions  often  appear  in  the 
apex  of  the  other  lung.  Laryngitis  and  tracheo -bronchitis  are  frequent. 
The  patient  always  puts  them  down  to  a  chill  or  to  some  imprudence ;  as 
a  matter  of  fact,  they  are  tubercular. 

The  lesions  end  in  the  third  period — that  is  to  say,  ulcers  and  cavities 
in  the  lung.  The  signs  of  cavity  are  then  evident,  their  mtensity  being  in 
proportion  to  the  size  of  the  cavity.  If  the  cavity  be  only  in  process  of 
formation,  a  single  sign  may  exist  alone — namely,  gurglmg.  If  the  cavity 
be  of  sufficient  size,  new  signs  are  evident — namely,  on  percussion,  the 
cracked-pot  sound  ;  on  auscultation,  gurglmg,  cavernous  breathing,  and 
pectoriloquy.  If  the  cavity  be  very  extensive,  it  may  give  the  same  signs 
as  pneumothorax  :  amphoric  breath  and  voice  sounds,  and  metallic  tinkling. 
This  period  corresponds  to  the  term  "  phthisis,"  or  consumption  with  hectic 
fever,  profuse  sweats,  extreme  wasting,  and  cachectic  oedema. 

I  must  now  dwell  at  greater  length  on  some  symptoms,  such  as  expectora- 
tion, fever,  and  haemoptysis,  which  are  of  great  importance. 

The  expectoration,  which  has  no  special  characters  at  the  onset,  becomes 
gradually  thick  and  opaque  ;  the  sputum  is  homogeneous  and  nummular 
(from  its  resemblance  to  the  shape  of  a  coin) ;  it  floats  in  a  clear  liquid. 
During  the  last  period  the  expectoration  is  quite  puriform  (liquid  froml 
cavities).     Nummular  sputum  is  also  seen  in  the  bronchitis  of  measles  orj 
of  influenza,  and  in  bronchiectasis.     In  order  that  muco-purulent  sputum! 
may  take  the  nummular  form,  it  is  sufficient  to  expectorate  into  a  sputum- 
glass  containing  water.     The  sputum  of  phthisical  patients  contains  a  large! 
amount  of  phosphates  and  of  chloride  of  soda. 

Under  the  microscope  pus  corpuscles,  epithelial  cells,  and  elastic  fibresj 


DISEASES  OF  THE  LUNG  183 

all  indicating  destruction  of  the  lung  parenchyma,  are  seen  in  the  sputum. 
The  microbes  met  with  in  the  sputum  are  very  numerous  ;  I  may  mention 
the  staphylococcus,  the  streptococcus,  the  pneumococcus,  the  pneumo- 
bacillus,  the  Bacillus  fyocyaneus,  sarcinae,  leptothrix,  and  micro-organisms 
which  colour  the  sputum  green,  etc.  ;  but  the  important  microbe  is  Koch's 
bacillus.  In  the  preceding  chapter  I  have  given  a  description  of  this  bacillus, 
and  the  means  of  detecting  it  in  the  sputum,  so  I  shall  not  reproduce  it  here. 
We  shall  see  later  that  the  presence  of  Koch's  bacillus  in  the  sputum  is 
sometimes  the  only  positive  proof  of  tuberculosis.  The  bacillus  may  exiat 
in  the  sputum  from  the  onset  of  pulmonary  tuberculosis  ;  it  is,  however, 
more  abundant  a  little  later.  As  a  rule,  the  gravity  of  the  disease  is  in 
proportion  to  the  number  of  the  bacilli. 

Fever. — Fever  is  of  very  great  importance,  for  it  is  the  almost  certain 
index  of  the  gravity  of  the  prognosis.  Febrile  tuberculosis  is  always 
grave,  while  the  non-febrile  form  may  go  on  for  an  indefinite  period  without 
compromising  life.  Fever  usually  shows  itself  during  the  second  period, 
with  softening  of  the  tubercles  or  with  broncho -pulmonary  inflammation ; 
it  may,  however,  appear  at  the  onset  of  tuberculosis.  Some  patients,  indeed, 
have  fever,  before  the  apparent  onset  of  the  lesions  ;  in  their  case  it  may  be 
said  that  the  fever  comprises,  for  a  time,  almost  the  entire  disease,  and  may 
tlierefore  be  called  pretubercular  fever. 

The  early  fever  in  tuberculosis  is  due  to  successive  crops  of  tubercles, 
and  also  to  the  special  virulence  of  the  bacillus  and  the  poisoning  of 
the  economy  by  tuberculin,  so  that  the  patients  in  question  are  rather 
tuberculinized  than  tuberculized.  It  is  certain,  I  repeat,  that  every 
tuberculosis  which  is  febrile  at  its  onset  is  very  grave  ;  every  haemoptysis 
which  is  febrile  is  very  serious  ;  fever  is  an  unfavourable  element  in  the 
prognosis. 

The  symptoms  of  fever  are  rise  of  temperature,  abundant  perspiration, 
and  an  acceleration  of  the  pulse,  which  may  reach  100  or  120  beats,  while 
the  temperature  may  be  but  little  elevated.  The  local  temperature  on  the 
diseased  side  is  higher  than  at  a  symmetrical  point  on  the  healthy  side. 

At  a  later  stage,  during  the  period  of  softening,  with  ulcerations  and 
cavities,  the  fever  grows  worse  ;  it  is  intermittent,  usually  begins  about 
five  or  six  o'clock  in  the  evening,  and  ends  during  the  night  with  profuse 
sweating.  The  attack  is  sometimes  ushered  in  by  a  feeling  of  cold,  and  the 
thermometer  frequently  reaches  104°  F.  This  variety  is  hectic  fever,  which 
is  usually  accompanied  or  followed,  at  a  more  or  less  early  interval,  by 
diarrhoea,  wasting,  and  consumption — in  short,  phthisis. 

The  fever  of  the  advanced  period  of  tuberculosis  is  due,  not  only  to  the 
causes  already  mentioned,  but  also  to  the  association  of  other  microbes 
wliich  give  rise  to  most  complicated  infections.     The  cavities  and  caseous 


184  TEXT-BOOK  OF  MEDICINE 

centres  are  invaded  by  an  army  of  microbes  ;  they  establish  themselves  in 
the  conquered  country,  and  produce  secondary  infections,  which  are  largely 
responsible  for  the  symptoms  of  this  period. 

Haemoptysis. — Spitting  of  blood  is  one  of  the  most  important  symptoms 
in  pulmonary  tuberculosis,  and  causes  the  patient  the  most  distress.  It 
may  supervene  at  any  period  of  phthisis,  but  it  is  usually  an  early  symptom, 
or  appears  late  in  the  stage  of  cavity. 

Early  haemoptysis  shows  different  forms.  Sometimes  the  patient  brings 
up  only  sputum  tinged  with  blood ;  at  other  times  the  fits  of  coughing  are 
very  violent,  and  he  brings  up  bright  red  frothy  blood,  which  in  the  sputum- 
glass  has  the  appearance  "  of  the  foam  that  is  present  in  a  basin  into  which 
an  animal  has  been  bled  "  (Trousseau).  The  duration  is  variable  :  it  may 
cease  after  a  quarter  of  an  hour  or  half  an  hour  ;  it  may  reappear  some  hours 
later,  on  the  next  day,  or  on  the  following  days.  The  last  sputum  brought 
up  has  not  a  bright  red,  frothy  appearance,  but  is  viscid  and  dark,  and 
represents  the  remains  of  the  haemorrhage  which  has  remained  longer  in  the 
bronchi. 

In  some  cases  haemoptysis  is  from  the  outset  very  profuse.  The 
patient  starts  coughing  ;  warm  fluid  rises  in  the  throat,  and  the'  blood  gushes 
forth  in  such  quantity  that  the  patient  does  not  appear  to  spit,  but  rather 
to  vomit,  blood. 

Haemoptysis  may  supervene  without  prodromata,  and  the  patient  is  as 
surprised  as  he  is  frightened  by  his  spitting  of  blood.  Sometimes  it  is 
preceded  by  oppression,  by  a  feeling  of  warmth  in  the  chest  or  tickling  in 
the  throat,  pufiiness  of  the  face,  and  epistaxis.  Before  or  during  the 
bleeding,  and  as  long  as  the  hsemorrhagic  phase  has  not  ended,  the  pulse  is 
usually  hard  and  tense  ;  in  some  cases  fever  is  marked,  and  the  prognosis 
is  usually  bad. 

Haemoptysis  may  precede  the  other  symptoms  by  many  years,  and  may 
be  repeated  during  apparent  good  health,  while  auscultation  shows  no  sign  of 
the  mischief.  This  proves  that,  in  its  embryonic  stage,  the  tubercle  produces 
congestion,  which  may  extend,  directly  or  reflexly,  to  the  respiratory 
channels,  or  even  to  the  nasal  mucosa  ;  and  it  is  a  notable  fact  that  tubercular 
patients  sometimes  have  attacks  of  epistaxis  which  precede  or  accompany 
the  haemoptysis.  It  is  the  molimen  hcemonhagicum  associated  with  the 
formation  of  tubercles. 

Pulmonary  congestion  of  tubercular  origin  is,  then,  a  cause  of  haemop- 
tysis. This  assertion  must  be  admitted  without  dispute,  as  it  rests  on  facts, 
verified  post  mortem  ;  but  it  is  more  probable  that  the  obliteration  of  vessels 
by  the  tubercular  products  produces  collateral  congestions,  which  are  largely 
responsible  for  the  bronchial  haemorrhages.  Perhaps  the  violent  congestion 
which  results  in  the  rupture  of  capillaries  and  in  haemoptysis  is  favoured 


I 


DISEASES  OF  THE  LUNG  185 

by  the  vaso-dilatory  toxine  of  the  tubercle  bacillus,  to  wiiich  Bouchard 
has  given  the  name  of  ectasine. 

It  is  upon  cases  of  early  haemoptysis  that  Morton's  theory  was  based — 
Ab  h(B)no'pt(B  tabes.  According  to  this  theory,  the  haemorrhage  itself 
becomes  the  starting-point  of  the  tubercularization  of  the  organ.  This 
theory  is  dead.  When  an  individual  who  has  had  haemoptysis  becomes 
phthisical  two  or  three  years  after  the  spitting  of  blood,  the  bronchorrhagia 
is  not  the  cause  ;  it  is  only  an  early  sign  of  the  tubercular  lesion.  We  have, 
besides,  the  proof  of  this  in  the  examination  of  the  semisanguineous  sputa 
which  follow  haemoptysis.  Tubercle  bacilli  have  several  times  been  recog- 
nized in  the  sputum,  although  other  signs  of  tuberculosis  were  absent. 

Let  us  now  consider  late  haemoptysis,  which  occurs  in  the  period  of 
cavities.  This  late  haemoptysis  may  be  due  to  the  various  causes  which  I 
have  just  enumerated  above,  and  is  then  the  result  of  new  attacks  of  tuber- 
culosis ;  but  sometimes,  also,  it  is  caused  by  the  rujiture  of  small  aneurysms 
in  the  wall  of  the  cavities.  These  aneurysms,  which  we  call  Rasmussen's 
aneurysms,  from  the  name  of  the  Danish  physician  who  first  clearly  described 
them,  are  found  in  the  pulmonary  and  bronchial  arterioles,  whose  calibre  is 
from  1  to  5  millimetres.  They  vary  in  size  from  a  pin's  head  to  an  almond. 
The  ruptiu-e  of  the  aneurysm  may  be^  delayed  by  the  formation  of  clots,  but 
when  the  aneurysm  bursts,  the  haemorrhage  is  so  abundant  that  the  patient 
vomits  mouthfuls  of  blood,  and  death  may  supervene  in  a  few  minutes.  I 
have  seen  such  a  case  :  the  young  girl  was  seized  with  fulminating  haemor- 
rliage,  and  succumbed  in  less  than  five  minutes. 

The  above  description  gives  an  idea  of  the  early  and  late  haemorrhages 
of  pulmonary  tuberculosis.  The  early  cases  never  prove  fatal  by  their  abun- 
dance, but  the  late  ones  may  carry  off  the  patient  in  a  few  minutes.  The 
absence  or  presence  of  fever  is  important  in  prognosis.  Non-febrile  haemop- 
tysis, especially  if  early,  is  not  severe  ;  but  haemoptysis  which  is  febrile  or 
associated  with  the  febrile  forms  of  tuberculosis  has  an  exceptional  gravity. 

Haemoptysis  is  present  in  about  60  per  cent,  of  cases,  and  may  be  for  years 
the  sole  symptom  of  almost  latent  tuberculosis.  The  case  quoted  by  Andral 
is  well  known  :  A  man  who  had  haemoptysis  all  his  life  died  of  a  disease  other 
than  phthisis ;  at  the  autopsy  cretaceous  tubercles  were  found.  All  his 
children  died  of  phthisis.  I  have  often  seen  such  cases  ;  more  often  than 
we  tliink,  haemoptysis  is  the  only  evidence  of  pulmonary  tuberculosis. 
ii;i'moptysis  is  not  one  of  the  symptoms  of  tuberculosis  in  infancy,  and  is 
rare  in  patients  under  fifteen  years  of  age.  It  is  more  fr»H[uent  in  women 
than  in  men,  antl  many  ca.ses  of  so-called  supplementary  hiiMnoj)tysis  are 
tubercular. 

The  genital  functions  are  less  affected  in  men  than  in  wom(>ii.  At  a 
more  or  less  advanced  stage  in  phthisis  the  menses  become  irregular,  and 


186  TEXT-BOOK  OF  MEDICINE 

may  be  suppressed,  or  at  times  replaced  by  Icucorrhoea.  These  troubles 
explain  why  pregnancy  is  rarer  in  phthisical  women.  The  puerperal  and 
nursing  states  have,  furthermore,  a  bad  influence  on  the  course  of  the  disease. 

The  oedema  seen  in  phthisis  is  of  diverse  origin :  cachectic  oedema, 
which  begins  in  the  lower  extremities  ;  painful  oedema,  which  is  due  to  venous 
coagulation  (phlegmasia  alba  dolens),  and  is  generally  limited  to  one  limb  ; 
and  diffuse  oedema,  with  lesions  of  the  kidney  and  albuminuria,  are  seen. 

Lesions  of  Other  Organs. — I  have  so  far  described  the  lesions  of  the 
lung,  and  discussed  the  most  usual  symptoms  of  pulmonary  phthisis.  There 
is  hardly  an  organ  which  escapes  tubercular  infection.  Whether  tubercular 
infection  be  present  alone,  or  whether  it  be  aided  in  its  work  of  destruction 
by  secondary  infections  from  the  toxines  of  other  microbes,  many  and 
varied  troubles  result,  modifying  the  picture  of  the  disease  or  hastening  its 
course.  The  study  of  these  complications  will  be  discussed  fully  when 
dealing  with  the  tuberculosis  of  each  organ ;  I  shall  here  content  myself  with 
a  rapid  enumeration. 

1.  Digestive  System.  —  The  changes  in  the  digestive  system  com- 
prise tubercular  ulcerations  of  the  tongue,  the  mouth,  and  the  larynx ; 
tuberculosis  of  the  tonsils  ;  gastritis,  which  is  sometimes  ulcerating ;  all 
varieties  of  dyspepsia  ;  chronic  enteritis  ;  ulceration  and  fistula  of  the  anus  ; 
tuberculosis  of  the  mesenteric  glands  ;  acute  and  chronic  peritonitis. 

The  lesions  of  the  liver  present  the  most  diverse  forms  ;  for  the  liver,  like 
every  other  organ,  has  its  own  peculiar  tuberculosis.  The  tubercular  granu- 
lation is  not  the  only  lesion  present.  We  find  also  tubercular  lesions  affecting 
the  type  of  cirrhosis  or  of  fatty  or  amyloid  degeneration. 

2.  Circulatory  System.  —  The  troubles  of  the  circulatory  system  in- 
clude palpitation,  which  is  very  frequent ;  dilatation  of  the  right  heart ; 
tubercular  pericarditis  and  endocarditis  ;  the  formation  of  clots  in  the  veins 
of  the  limbs ;  and  thrombosis  of  the  pulmonary  artery,  which  is  a  possible 
cause  of  rapid  death. 

3.  Genito-Urinary  System.  —  The  testes,  the  prostate,  the  bladder, 
the  kidney,  the  ovaries,  and  the  uterus,  may  be  affected  by  tuberculosis. 
It  may  remain  as  a  local  condition,  or  precede  that  of  the  lung. 

4.  Nervous  System. — Here  we  find  extensive  or  localized  meningitis ; 
lesions  of  the  cerebrum,  with  all  their  train  of  symptoms  ;  tubercular  lesions 
of  the  mesoencephalon  and  the  bulb,  and  those  of  the  spinal  cord  (tuber- 
cular leptomyelitis),  which  do  not  differ  in  their  clinical  description  from 
other  varieties  of  myelitis. 

In  opjjosition  to  these  lesions  of  the  nervous  centres,  I  would  mention 
peripheral  neuritis,  which  has  of  late  been  carefully  studied.  Clinically, 
it  shows  itself  by  sensory  (neuralgia,  hypersesthesia,  anaesthesia),  motor 
(paralysis,  paresis),  and  trophic  troubles  (amyotrophia,  zona). 


DISEASES  OF  THE  LUNG  187 

5.  Organs  of  the  Senses. — Otitis  in  phthisical  patients  is  a  catarrh 
of  the  drum  (otorrhoea),  with  perforation  of  the  membrana  tympani.  The 
ulceration  of  the  mucosa  causes  caries  and  necrosis  of  the  petrous  bone. 
This  otitis  may  be  consecutive  to  pharyngeal  catarrh,  which  has  spread  to  the 
drum  through  the  Eustachian  tube  (Belliere).  Tuberculosis  of  the  nose  and 
of  the  nasal  fossse  has  been  already  described. 

Tuberculosis  in  Children. — I  shall  now  mention  tuberculosis  in  children 
and  elderly  people.  Children  may  become  tubercular  at  all  ages,  but  the 
very  young  child  (one  from  a  few  days  up  to  two  years  old)  presents  a 
familiar  form  of  tuberculosis.  It  has  been  summed  up  by  Landouzy  and 
Queyrat  as  follows  :  Infantile  tuberculosis  often  appears  as  a  broncho- 
pneumonia. It  may  show  all  the  lesions  of  tuberculosis  seen  in  adults, 
including  cavities  surrounded  by  fibrous  tissue  and  aneurysms,  which  pre- 
dispose to  fatal  haemoptysis.  Tuberculosis  is  transmitted  to  the  new-born 
either  by  mediate  contagion  or  by  heredity. 

In  elderly  people  tuberculosis  is  more  frequent  than  is  usually  supposed, 
but  it  has  not  the  cliaracteristics  of  phthisis  in  the  adult.  It  is  more  torpid, 
and  its  symptoms  are  less  marked. 

Course — Prognosis — Termination. — The  course  and  duration  of  pul- 
monary phthisis  are  extremely  variable.  One  individual,  for  example,  may 
for  many  years  bear  the  growth  of  tubercular  products  without  passing 
into  the  third  stage  ;  while  another,  after  six  or  eight  months'  illness,  is 
already  a  victim  to  sweating,  wasting,  diarrhoea,  and  hectic  fever.  Some 
people  who  have  had  apparently  insignificant  haemoptysis  show  no  symp- 
toms of  proved  tuberculosis  until  ten  or  fifteen  years  later.  Others  may 
have  had  several  attacks  of  haemoptysis  and  inveterate  bronchitis,  but  yet 
have  dragged  out  a  more  or  less  invalid  existence,  without  ever  reaching 
the  third  stage.  Many  causes  hasten  or  retard  the  course  of  pulmonary 
phthisis.  Firstly,  there  is  the  nature  of  the  soil  on  which  the  disease  has 
developed  ;  then  there  are  the  cares  of  every  kind,  hygiene,  questions  of 
climate,  nourishment,  and  comfort,  and  hence  the  much  quicker  course  of 
tuberculosis  amongst  the  poorer  classes,  while  among  those  in  easy  circum- 
stances we  can  often  check  or  modify  its  progress.  It  has  been  said  that 
when  emphysema  occurs  in  a  tubercular  lung,  it  arrests  the  progress  of  the 
tuberculosis  for  the  time  being. 

Between  the  local  changes  in  the  lung  and  the  general  condition  of  the 
patient  there  is,  of  nece.ssity,  some  parallelism.  We  see  people  with  local 
.signs  of  advanced  tuberculosis  (softening  and  cavities),  but  they  live  on, 
without  reaching  the  stage  of  consumption.  These  examples  must  be  known 
in  order  to  avoid  grave  errors  in  prognosis. 

The  natural  end  of  pulmonary  tuberculosis  is  often  death  by  i»hthisis ; 
yet  cases  of  cure  are  frequent  (({rancher).      I  have  often  s(!en  recovery  from 


188  TEXT-BOOK  OF  MEDICINE 

pulmonary  tuberculosis  when  it  is  treated  at  an  early  period.  The  tubercle 
may  recover  (cretaceous  and  fibrous  condition),  and  the  small  cavities  may 
cicatrize.  In  certain  conditions  death  supervenes  from  complications,  such 
as  laryngeal  phthisis,  purulent  pleurisy,  pneumothorax,  enteritis,  perito- 
nitis, meningitis,  etc.  Syncope,  embolism,  or  thrombosis  of  the  pulmonary 
artery  are  causes  of  sudden  death. 

iEtiology. — Heredity  and  contagion  are  the  two  great  causes  of  pul- 
monary phthisis,  and  in  this  respect  tuberculosis  shows  an  analogy  with 
syphilis.  In  both  heredity  may  betray  itself  by  early  or  by  late  manifesta- 
tions. The  early  ones  are,  in  the  one  case,  syphilis  in  the  new-born  ;  in  the 
other,  tuberculous  broncho -pneumonia  of  infancy,  meningitis,  and  tuberculi- 
zation of  the  peritoneum  and  of  the  bronchial  glands.  The  late  manifesta- 
tions are,  in  the  one  case,  the  multiple  lesions  of  hereditary  syphilis  ;  in 
the  other,  pulmonary  phthisis  and  the  various  local  tubercular  lesions  till 
lately  considered  as  scrofulous. 

Sometimes  the  parents  are  notably  phthisical ;  at  other  times  they 
show  only  such  imperfect  evidences  of  tuberculosis  as  inveterate  bronchitis 
or  suppurating  adenitis,  wrongly  regarded  as  scrofulous ;  they  drag  out  a 
more  or  less  invalid  existence,  without  going  on  to  confirmed  phthisis.  They 
may  be  cured,  or  think  themselves  cured.  These  troubles  favour  tuber- 
culosis, and  children  born  of  such  stock  may,  unfortunately,  inherit 
the  original  taint.  Sometimes,  in  a  family  where'  tuberculosis  or  scrofula 
reigas  (and  they  are  identical),  the  parents  in  whom  the  germ  is  latent  beget 
children  who  develop  tuberculosis,  while  the  parents  themselves  are  only 
affected  later. 

We  may  consider  heredity  in  two  ways :  either  the  subject  inherits  the 
infectious  principle — that  is  to  say,  the  seed  ;  or  he  only  inherits  the  predis- 
position to  contract  tuberculosis — that  is  to  say,  the  nature  of  the  soil 
which  is  favourable  to  its  growth.  Many  authors  mcline  to  this  latter 
opinion.  Peter  says  that  people  are  not  born  tubercular,  but  tuberculizable. 
Bouchard  says  that  the  tuberculosis  which  parents  transmit  to  their 
children  is  prospective,  and  not  actual. 

This  opinion  is  admissible,  but  it  is  none  the  less  true  that  the  hereditary 
lesion  has  been  caught  red-handed  in  the  foetus.  The  inoculation  of  guinea- 
pigs  with  blood  from  a  foetus  conceived  by  a  phthisical  mother  has  caused 
tuberculosis  analogous  to  that  which  a  fragment  of  tubercular  lung  produces. 
We  possess  to-day  undeniable  cases  of  congenital  tuberculosis.  In 
two  cases  out  of  five,  Koch's  bacillus  has  been  found  in  the  blood  of  the 
umbilical  vein  of  infants  born  of  tubercular  mothers  (Bar  and  Renon). 
Tuberculosis  has  been  recognized  in  the  foetus  at  various  ages.  It  may  be, 
says  Kuss,  that  the  germs  reach  the  foetus  a  little  before  delivery,  or  at 
the  moment  of  birth  (thanks  to  placental  depletion,  produced  by  the  first 


DISEASES  OF  THE  LUNG  189 

inspirations),  and  only  succeed  in  setting  up  appreciable  foci  at  the  end  of 
several  months.  It  is  therefore  reasonable  to  admit  that  hereditary  tuber- 
culosis Ls  transmitted  directly  by  the  germs.  The  whole  question  consists 
in  recognizing  what  the  conditions  will  be  which,  sooner  or  later,  will  favour 
the  growth  of  the  germs,  which  may  long  remain  in  a  latent  state.  This 
latency  of  the  bacilli  is  not  at  all  surprising. 

The  contagious  nature  of  tuberculosis  had  been  long  supposed,  but  it 
was  clearly  established  by  Villemm.  To-day  it  is  based  upon  a  consider- 
able number  of  cases.  Cases  of  contagion  between  husband  and  wife  are 
relatively  frequent :  a  healthy  husband  becomes  tubercular  through  contact 
with  his  wife  who  is  dymg  of  phthisis.  He  marries  again,  and,  in  his  turn, 
gives  tuberculosis  to  his  second  wife,  who  was  quite  well.  I  could  give 
many  more  cases  ;  the  more  intimate  the  living  in  common  with  phthisical 
persons,  the  more  is  contagion  to  be  dreaded.* 

In  the  preceding  chapter  I  describe  the  modes  of  transmission  of  tuber- 
culosis by  experimental  measures.  How  can  we  explam  its  transmission 
in  the  human  species  ?  It  is  possible  that  the  bacillus  enters  the  digestive 
tract  by  means  of  food  and  drink,  and  in  this  connection  milk,  both  from  a 
tubercular  animal  and  from  a  tubercular  wet-nurse,  has  been  incriminated. 
Calmette  thinks  that  the  intestinal  tract  is  often  the  entrance-gate  of 
pulmonary  tuberculosis.  Verneuil  thinks  that  the  contagion  may  take  place 
through  the  genital  tract.  In  some  cases  the  bacillus  has  entered  the  economy 
through  a  wound  in  the  skin. 

The  respiratory  passages  are  the  usual  entrance  gateway  of  the  infectious 
germ  (spore  or  bacillus),  and  in  most  cases  the  lung  Is  the  first  organ  attacked. 
The  germs  exist  in  abundance  in  the  sputum  of  phthisical  patients,  and 
experience  has  proved  that  the  sputum  may  be  dried,  powdered,  and  kept 
for  several  weeks  without  losing  its  virulence,  since  the  dust,  when  uihaled 
by  animals,  causes  tuberculosis  (Tap}>einer).  Transmission  to  man  prob- 
ably occurs  in  this  way  :  the  debris  of  sputum,  reduced  to  powder,  floats 
in  the  air  and  enters  the  bronchi.  In  order  that  the  germ  may  produce  its 
noxious  effect,  the  bronchus  must  have  first  lost  its  epithelium,  and  it 
may  be  asked  if  bronchitis  and  broncho-pneumonia  (measles,  whooping- 
cough)  do  not  especially  favour  the  entrance  of  the  germ.  In  all  cases  the 
contaminated  person  must  be  in  a  condition  of  receptivity,  for  in  case  of  con- 
tagion we  find  favourable  soils  and  soils  refractory  to  the  growth  of  germs. 

Children  of  tubercular  stock,  patients  with  diabetes  or  convalescent  from 

*  These  propositionH  are  general,  and  ajjply  equally  to  animals  and  to  man.  Krid- 
haber  and  myself,  in  1883,  made  exix-rimental  researches  upon  tuberculosis  in  the  ape, 
and  lost  only  one  monkey  out  of  eighteen  which  were  living  together,  but  wen*  kept 
isolated  from  every  source  of  contaminatif)n,  while  we  lost  five  monkeys  from  tuber- 
culosis out  of  twenty-four  which  lived  with  tubercular  animals.  They  had  cunt  rated 
tuberculosis  by  contagion  (Arch,  de  Fhysiulogie,  1883). 


190  TEXT-BOOK  OF  MEDICINE 

acute  diseases  (measles,  whooping-cough,  typhoid  fever)  are  in  a  state  of 
receptivity.  The  soil  is  prepared  by  malnutrition,  failing  health,  excesses  of 
every  kind,  exhaustion,  fatigue,  trouble,  and  repeated  pregnancies.  "  It 
may  be  said  that  tuberculosis  is  the  common  end  of  all  constitutional 
degenerations  in  families  as  well  as  in  individuals  "  (Jaccoud). 

Traumatism  and  contusions  of  the  thorax  may  be  placed  in  the  category 
of  predisposing  causes,  by  tilling  the  soil  in  which  the  bacillus  \$as  in  a  latent 
condition.  Since  attention  has  been  called  to  this  point  many  cases  have 
been  collected,  and  I  know  of  several  in  which  injury  to  the  thorax  has  been 
followed  by  tuberculosis. 

Tuberculosis  is  most  common  in  youth ;  it  appears,  however,  at  other 
periods.  It  is  fairly  common  in  advanced  age  and  in  children  during  earliest 
infancy.  It  is  more  common  in  warm  climates,  and  is  comparatively  rare 
in  high-lying  countries. 

Diagnosis. — The  diagnosis  of  pulmonary  phthisis  is  sometimes  difficult, 
not  only  at  the  onset  of  the  disease,  but  even  at  more  advanced  periods. 
See  divides  the  disease  into  latent,  larval,  and  pseudo-  phthisis.  In  latent 
phthisis  we  find  ill-marked  symptoms,  such  as  pallor,  wasting,  with  or  with- 
out fever,  catarrhal  cough,  or  haemoptysis.  The  cases  of  larval  phthisis  are 
those  which  assume  the  mask  of  an  acute  affection  of  the  respiratory  tracts, 
such  as  bronchitis,  pleurisy,  broncho-pneumonia,  or  laryngitis.  The  cases 
of  pseudo-phthisis  are  diseases  such  as  bronchial  dilatation,  syphilitic 
gummata  of  the  lungs,  hydatid  cysts  of  the  lung,  aspergillary  tuberculosis, 
and  neoplasms  of  different  kinds  that  simulate  phthisis,  but  are  not  of 
tubercular  origin.  In  these  different  cases  the  diagnosis  is  not  always 
simple,  and  the  recognition  of  Koch's  bacillus  renders  the  greatest  service. 

As  regards  diagnosis,  I  think  it  useful  to  state  the  following  precepts  : 

Every  youth  or  adult  who  wastes  much  or  rapidly,  with  or  without  fever, 
must  be  suspected  of  having  tuberculosis,  in  the  absence  of  diabetes  or 
Basedow's  disease. 

Every  girl  or  young  woman  who  has  neither  genuine  chlorosis,  Bright's 
disease,  nor  syphilitic  anaemia,  but  yet  has  the  apjjearance  of  chloro-ansemia, 
must  be  suspected  of  having  tuberculosis. 

Every  individual  who  has  haemoptysis  must  be  suspected  of  tuberculosis. 
The  cases  of  so-called  supplementary  haemoptysis  are  very  often  tubercular  ; 
but,  on  the  other  hand,  we  must  remember  that  there  is  a  group  of  non- 
tubercular  cases,  such  as  haemoptysis  in  bronchitis,  hydatids,  or  syphilis  of  J 
the  lung,  false  tuberculosis,  etc. 

Koch's  tuberculin  has  undoubted  value  in  diagnosis,  and  may  reveal 
even  the  most  hidden  trace  of  tuberculosis.  It  has  therefore  attracted  the 
attention  of  hygienists,  and  has  been  employed  in  veterinary  practice  forj 
the  early  diagnosis  of  tuberculosis  in  cattle. 


DISEASES  OF  THE  LUNG  191 

In  man  great  care  must  be  taken  in  using  injections  of  tuberculin  for 
purposes  of  diagnosis.  The  amount  must  not  be  more  than  yV  or  t  milli- 
gramme ;  two  or  three  injections  may  be  made  at  intervals  of  two  or  tlu:ee 
days.  In  case  of  positive  reaction,  the  temperature  rises  about  1°  or  more. 
The  rise  is  often  accompanied  by  lassitude  and  headache. 

The  cuti-reaction  does  not  give  constant  results.  I  have  verified  this  fact 
at  the  Hotel-Dieu. 

Prognosis. — I  shall  not  dwell  at  length  on  the  prognosis  of  pulmonary 
phthisis.  The  preceding  description  sliows  how  serious  the  disease  is. 
There  is,  however,  a  point  to  which  I  would  call  attention — viz.,  that  tubercu- 
losis is  cured  much  more  often  than  we  suppose.  Not  only  is  it  curable  at  its 
onset,  but  it  is  still  curable  at  an  advanced  period.  In  people  who  have  died 
from  quite  another  disease  we  often  find  old  fibrous  or  cretaceous  tubercular 
lesions,  which  prove  that  they  have  at  some  time  been  affected  by  tuberculosis. 

Treatment. — Let  us  first  consider  prophylactic  treatment,  the  object 
of  which  is  :  (1)  To  modify  as  far  as  possible  the  evil  results  of  heredity  in  a 
person  of  tubercular  stock ;  (2)  to  remove  the  causes  of  contagion.  The 
individual  should  from  infancy  live  in  the  open  air,  in  the  country,  and  in  a 
high-lying  locality,  take  much  exercise,  have  abundant  nourishment,  and 
avoid  all  causes  of  contagion  ;  for,  thanks  to  his  origin,  he  is,  above  all  others, 
in  a  state  of  receptivity. 

The  means  employed  to  avoid  contagion  are  as  follows  :  Choose  for  the 
child  a  nurse  who  has  no  tubercular  taint ;  never  permit  a  child  to  sleep 
in  a  room  with  phthisical  parents ;  do  not  allow  husband  and  wife  to  share 
the  same  room.  Collect,  as  far  as  possible,  the  products  of  expectoration 
in  a  basin,  which  is  emptied  and  washed  several  times  a  day ;  and  do  not 
allow  sputum  to  be  left  on  linen,  pocket-handkerchiefs,  or  on  the  floor, 
where  it  dries,  is  reduced  to  dust,  and  becomes  a  potent  cause  of  contagion. 
Purify  rooms  and  bedding  after  the  death  of  a  phthisical  patient ;  expose 
clothing  which  the  patient  has  used,  to  steam  at  a  temperature  of  212°,  or, 
better  still,  jjurn  it.  If  these  precautions  were  taken,  the  balance-sheet  of 
phthisis  would  be  much  diminished. 

We  may  next  consider  the  different  medicines  and  their  respective 
efficiency  in  phthisis. 

Cod-liver  oil,  in  suflioient  doses,  builds  up  the  constitution.  Intolerance 
on  the  part  of  the  stomach  and  diarrhoia  are  contra-indications.  Tolerance 
may  sometimes  be  established  by  giving  the  oil  in  increasing  doses,  after  it 
has  been  well  cooled  in  a  freezing  mi.xture.  I  have  obtained  excellent  results 
with  cod-liver  oil  in  large  doses — e.g.,  a  tumblerful.  Some  patients  take 
10  to  15  ounces  daily  for  several  weeks.  I  repeat  that  the  results  obtained 
are  often  surprising.  When  the  oil  disagrees,  I  substitute  fatty  and  oily 
foods :  caviare,  sardines  in  oil,  tunny-fish,  slices  of  bread  and  butter,  pdte  de 


192  TEXT-BOOK  OF  MEDICINE 

foie  cjras,  etc.  Excellent  results  are  sometimes  obtained.  I  would  especially 
recommend  eggs  and  raw  meat  in  large  quantities. 

Meat- juice  has  been  used  with  benefit.  The  good  effects  of  this  regime 
do  not  rest  solely  upon  pure  and  simple  super- alimentation,  but  on  the 
particular  quality  of  the  food. 

Glycerine  is  a  very  useful  and  economical  drug,  and  is  given  daily  in 
doses  of  1  to  2  ounces,  with  a  little  rum,  and  flavoured  with  a  drop  of  essence 
of  peppermint  (Jaccoud).  Preparations  of  arsenic,  because  of  their  trophic 
action,  are  much  indicated  :  arseniate  of  soda  is  given  in  doses  of  ^V  to  yV 
grain  daily  in  distilled  water  ;  or  arsenious  acid,  in  doses  of  -oV  to  yV  grain 
daily,  in  the  form  of  granules,  each  containing  -^^  grain.  Cacodylate  of 
soda,  in  daily  injections  of  about  1  grain  or  more,  is  an  excellent  medicine. 
(See  Appendix  on  Therapeutics.) 

Creosote  stimulates  the  appetite  and  lessens  the  bronchial  secretion  ; 
it  is  given  in  capsules  or  in  pills,  each  containing  1  minim  creosote.  The 
patient  takes  as  many  as  ten  or  twenty  during  his  meals. 

Counter-irritation,  by  repeated  blisters  or  by  the  cautery,  is  useful  in 
dealing  with  inflammation  and  congestion.  In  my  own  practice  I  make 
much  use  of  counter-irritants.  It  is  well  to  use  the  cautery,  and  to  allow 
suppuration  to  go  on  as  long  as  possible.  A  good  way  is  to  apply  the 
cautery-point  200  or  300  times  a  week,  and  to  continue  this  treatment  for  a 
long  period. 

The  fever  of  tuberculosis,  especially  in  the  hectic  form  (absorption  fever), 
may  be  checked  by  salicylic  acid  (Jaccoud's  method).  Twenty  grains  of 
salicylic  acid  are  given  during  the  morning  in  three  cachets,  at  intervals  of 
half  an  hour.  According  to  circumstances,  the  dose  is  diminished,  stopped, 
or  repeated  some  days  after. 

Aspirin  (acetyl-salicylic  acid)  in  5-grain  doses,  repeated  three  or  four 
times  a  day,  is  useful  for  the  fever  of  phthisis  (Renon)  ;  abundant  perspiration 
limits  its  use. 

Cryogenin,  in  doses  of  two  or  three  cachets,  each  containing  1  grain, 
has  a  remarkable  antithermic  action. 

Antip}Tin  is  efficacious,  in  daily  doses  of  30  to  40  grains.  For  the  fever, 
I  have  often  prescribed  bathing  with  tepid  water  or  cold  baths,  with  great 
benefit  to  the  patient. 

Haemoptysis  should  be  dealt  with  in  the  following  manner  :  If  very 
abundant,  it  is  sometimes  arrested  by  an  emetic,  such  as  ipecacuanha  (30 
grains).  If  it  is  more  trifling,  ipecacuanha  is  prescribed  in  nauseating  doses, 
and  one  or  two  of  the  following  pills  are  administered  every  hour,  or  every 
two  hours  : 

Ipecacuanha    . .  . .  . .         . .         . .         . .     gr.  i. 

Extract  of  opium        . .  ...         . .         . .         •  •     gr.  uV 


DISEASES  OF  THE  LUNG  193 

Other  means  are  also  used  for  haemoptysis  :  subcutaneous  injections  of 
ergotin,  solutions  containing  perchloride  of  iron,  and  counter-irritation  to 
the  chest  by  means  of  blisters.  The  patient  should  be  kept  absolutely  at 
rest,  given  iced  and  acidulated  drinks,  and  have  abundant  cold  nourish- 
ment,  which  should  be  administered  in  small  quantities.  The  following 
tbaught  may  also  be  prescribed,  in  tablespoonfuls,  every  three  hours  : 

Distilled  water  . .  . .  . .  . .  . .     ^iv. 

Syrup  of  rhatany        . .  . .  . .  . .  . .     51. 

Rabel  water     . .  . .  . .  . .  . .  . .     ni  xlv. 

The  sweats  are  relieved  by  white  agaric  (Trousseau),  in  doses  of  .'3  grains, 
taken  every  evening,  in  a  cachet ;  by  atropin  ( Vulpian),  in  doses  of  Jg  grain  ; 
or  by  cam}»horate  of  pyramidon,  in  doses  of  from  6  to  8  grains,  in  a  cachet. 

Diarrhoea,  which  is  often  profuse,  may  be  treated  with  chalk  in  largo 
doses  ;  by  opiates  (five  to  ten  pills,  each  containing  J-  grain  opium,  given  in 
the  course  of  twenty-four  hours) ;  by  methylene  blue,  given  daily,  in  three 
cachets,  each  containing  3  grains  of  lactose  and  1  grain  of  methylene  blue. 

Vomiting  may  be  relieved  in  some  cases  by  2  drops  of  laudanum,  taken 
before  a  meal ;  or  by  a  tablespoonful  of  lime-water,  with  the  addition  of 
uV  grain  of  hydrochlorate  of  cocaine  ;  at  other  times  by  lavage  of  the 
stomach,  or,  better  still,  by  artificial  feeding.  This  artificial  feeding  (super- 
alimentation, gavage),  used  by  Debove,  has  often  proved  effective,  not 
only  in  vomiting,  but  also  in  malnutrition.  Milk,  lentil-flour,  and  powdered 
meat  are  given  through  a  tube.  Some  patients  will  swallow,  without  the 
help  of  the  tube,  6  ounces  of  powdered  meat  in  the  twenty-four  hours,  the 
powder  being  suspended  in  milk  or  broth,  given  at  short  intervals.  Super- 
alimentation sometimes  produces  remarkable  effects. 

Koch's  Tuberculin.— I  must  now  give  some  details  of  treatment  by 
K<nh\s  tuberculin. 

On  November  13,  1800,  Koch  announced  that  he  had  found  an  efficient 
remedy  for  tuberculosis  of  the  skin,  bones,  glands,  or  lungs  ;  and  this  remedy 
—  Koch's  lymph  —  which  was  immediately  tried  by  many  physicians, 
remained  a  secret  until  the  beginning  of  1891,  when  Koch,  in  a  second  paper, 
stated  that  it  was  tuberculin. 

Tuberculin  is  a  glycerine  extract  of  })ure  cultures  of  the  tubercle  bacillus. 
It  is  a  clear  l)ro\vnisli  fluid,  without  action  when  introduced  by  the  mouth, 
but  very  active  when  injected  under  the  skin  or  into  the  blood-stream.  In 
a  healthy  man  a  dose  of  0-25  c.c.  produces  very  nuirked  effects,  while  in  a 
guinea-pig  a  dose  of  2  c.c.  remains  inactive.  The  human  being  is  therefore 
1,300  times  more  seasitivc  to  its  action  than  the  guinea-pig. 

In  a  tubercular  guinea-pig  tuberculin,  given  in  gradually  increasing 
doses,  has  no  action  on  the  bacilli,  but  produces  a  mafked  effect  on  the 

J  3 


J94  TEXT- BOOK  OF  MEDICINE 

tissues  around  the  tubercle.     These  tissues  show  abunaant  exudation  of 
r;  fluid  and  active  diapedesis.    The,  may  or  .ay  -' >'--"-^^ 
When  necrosis  occurs,  the  cast-of5  tissue  contams  bacilli  in  more  or  les 
Isiderable  numbers,  and  the  ulceration  ^^us  produced  -ay  te  -       f^^^^^ 
into  a  simple  wound,  covered  with  fleshy  granulations,  which  may  form  scat 


tissue. 


In  a  healthy  man  1  c.c.  of  lymph  is  necessary  to  produce  a  rise  of  tem- 
perate to  100"  F,    In  a  tubercular  man  a  dose  of  from  1  to  3  c..  o  lymph 
is  sufficient  to  produce,  at  the  end  of  two  or  three  hours,  a  r  go  ,  a  tempe  a 
ture  of  104°  F.,  cough,  vomiting,  acute  pain,  enlargement  of  the  spleen, 
a^d  Iht  delirium.     These  symptoms  last  twelve  to  fifteen  hours.     In 
he  c:lf:f  lupus,  local  reaction  can  be  made  out  at  the  site  of  the   — ' 
lesions.     At  the  end  of  five  or  six  hours  the  lupoid  areas  swell  ^^^^^'>^^^- 
and  sometimes  necrose.     The  redness  diminishes  after  two  or  three  days 
and  is  accompanied  by  scaling.     Two  or  three  -*s  la        the     scha 
become  detached,  leaving  in  favourable  cases  a  '-t'^g  <=;^*^- J  '^^  ^n 
thing  happens  in  tuberculosis  of  the  glands,  bones,  "'J^*^' *>"**"*  J 
is  less  clear.     In  favourable  cases  of  pulmonary  tuberculosis,  after  sub- 
1  talus  injections  of  lymph  in  very  small  doses  the  cough  is  less    re 
quent,  the  expectoration  becomes  mucous,  the  baolh  diminish,  and  finally 
disappear,  and  the  general  condition  improves. 

Such  are  the  results  of  tuberculin  in  favomrable  cases ;  ^ut  these  cases  are 
exceptional,  and.  after  many  well-conducted  observatior.  the  infatuation 
first  aroused  has  given  place  to  the  most  profound  '^^''f'-  i„„eulati«ns 
Most  serious  accidents,  and  even  death,  have  occurred  after  'no™l''t»m 
of  tuberculin  Amongst  these  accidents,  I  would  note  meningitis  endo- 
Xlema  of  thfglottis  and  of  the  l-S-  ^™-'^°-P"--:"'j\:': 
After  inoculations  performed  in  my  wards  with  the  grea  es  care^  I  have 
seen  perforation  of  the  tympanic  membrane  from  7ff'™.°*'*f  ,  ,^,'^  f, 
gloomy  results  have  caused  the  use  of  mjections  of  tuberculm  m  phthisis 

"  \^"mtion  of  physicians  at  the  St.  Louis  Hospita,  which  for  two 
months'and  a  half  tried  tuberculin  on  thirty  patients  ^-^^^^-l^Z^^^l^' 
decided  aoainst  Koch's  method  of  treatment.  In  some  cases  temporary 
reductt n  °of  the  lupoid  mass  and  temporary  attenuation  of  the  tuberculous 
lesion  were  seen,  but  cure  was  never  obtained.  In  the  course  of  these 
xT^iments  no  patient,  fortunately,  succumbed,  >>-*-,  gravyompa^ 
tions  were  seen  in  the  heart,  brain,  and  kidneys,  as  well  as  the  most  a  a^n 
^neral  symptoms.  In  some  cases  tubercular  centres  m  the  lung,  tUl  the 
latlCwere  reawakened,  and  it  was  very  difiicult  to  arrest  the  lesion  wh.cl 

had  once  more  become  acute.  •     •  i  o  a,.r1  nlUa 

Tuberculocidin.-Klebs  has  separated  the  noxious  principles  and  alka 


DISEASES  OF  THE  LUNG  195 

loids  of  Kocli's  tuberculin  from  the  active  principle  which  is  an  albumose. 
This  purified  lymph,  or  tuberculocidin,  does  not  give  rise  to  febrile  reaction  ; 
it  causes  retrogression  in  the  tubercular  tissues,  without  necrosis,  and  brings 
about  the  destruction  of  the  bacilli.  The  dose,  at  the  commencement  of 
treatment,  is  ^^  grain,  and  it  may  be  raised  to  7  grains  later.  The  results 
are  encouraging. 

C.  Spengler  (of  Davos)  has  combined  the  action  of  tuberculin  with  tuber- 
culocidin. He  injected  a  mixture  of  from  5^^^  grain  of  tuberculin  with 
^  grain  of  tuberculocidin.  Injections  were  made  several  days  following, 
and  in  some  cases  the  fever  yielded. 

Denys  has  used  bouillon,  freed  from  the  tubercle  bacillus  by  filteriug^ 
in  the  treatment  of  tuberculosis  in  man.  He  gives  hypodermic  injections 
in  doses  varying  from  1  to  25  c.c.  He  has  seen  good  results,  but  the  value  is 
not  yet  exactly  known. 

Let  us  now  consider  thermal  and  climatic  treatment  in  pulmonary  tuber- 
culosis. Speaking  generally,  thermal  cures  are  absolutely  contra-indicated 
while  the  patient  is  suffering  from  haemoptysis  or  from  fever.  In  patients 
affected  with  slow  tuberculosis,  who  are  but  little  prone  to  sharp  reaction, 
haemoptysis,  or  broncho-pneumonia,  Mont-Dore,  la  Bourboule,  and  the 
sulphur- waters,  such  as  Cauterets,  Luchon,  Eaux  Bonnes,  etc.,  may  be  recom- 
mended ;  but  in  patients  suffering  from  pulmonary  tuberculosis  in  the  irrita- 
tive form,  the  warm  alkaline  springs  of  Royat  and  Ems,  or  the  cold  sulphur 
springs  of  Allevard,  are  advisable. 

A  similar  distinction  should  be  made  when  choosing  a  place  of  residence 
for  tubercular  patients.  In  cases  liable  to  febrile  attacks  and  palpitations 
of  the  heart,  high  altitudes,  such  as  Davos  and  Saint-Moritz,  will  be  most 
beneficial.  These  elevated  situations  give  wonderful  results,  as  regards 
improvement  and  cure,  from  the  purity  of  the  air  and  the  activity  which 
they  cause  in  the  breathing.  All  forms  of  phthisis,  however,  are  not  suited 
to  these  high  altitudes  ;  stations  of  moderate  altitude,  or  the  maritime  ones 
of  Cannes,  Mentone,  Arcachon,  Algiers,  Madeira,  or  Pan,  are  then  to  be 
considered. 

Surgical  treatment  of  tubercular  lesions  of  the  lung,  interstitial  injections 
of  drugs,  and  pneumotomy,  are  questions  which  are  under  consideration, 
and  upon  which  it  would  be  premature  to  pronounce  an  opinion. 

XIV.  FIBROID  PHTHISIS. 

The  tubercles  in  the  lung,  instead  of  undergoing  caseation,  may  be  con- 
verted into  fibrous  tissue.  They  form  isolated  granulations,  which  aro 
proiniiicut  and  very  hard  to  the  touch  ;  thiur  structure  is  completely  niodilied 
by  the  fibrosis.     Fibrous  tubercles  had  already  been  noted  by  Baylc,  but 

io— 2 


jgg  TEXT-BOOK  OF  MEDICINE 

Cruveilhier  was  the  first  to  show  the  importance  of  this  change  :  "  Pulmonary 
tubercles  are  too  generally  considered  as  being  inc^able;  ^W  -7  become 
cicatrized"     He  noted  "granulations  and  tubercles  of  recovery    -that 
inert  granulations  and  tubercles-perfectly  distinct  from  those  m  process 
of  development,  with  which  they  had  been  confounded.     Cruvem^ier  a^^^^^^ 
noted  that  tubercular  lesions  may  recover  at  any  stage,  ^^^^  "^  ^ 
granulation  to  the  cavity,  by  a  fibrous  change  ;  and  that,  fiirthe  ,     part  of  the 
Lg  tissue  around  the  tubercles  may  be  converted  mto  fibrous  tissue^ 
This  change  constitutes  a  means  of  isolation  and  cure  of  the  tubercular 
centres      The  condition  constitutes  the  curative  phlegmasia,  or  dark  slaty 
induration  which  we  now  call  interstitial  pneumonia  in  phthisical  patients. 
Later   Grancher  and  Charcot  showed  that  this  fibrous  change  is  very 
common,  and  may  occur  at  a  very  early  stage  ;  it  must  be  considered  as  one 
of  the  modes  of  evolution  of  the  tubercle. 

Furthermore,  the  works  of  these  authors,  and  those  of  Renaut,  Bard, 
Cornil,  and  Thaon,  made  it  plain  that  Cruveilhier' s  dark  f^^  ^^^^'[Z 
may  end  in  true  pulmonary  fibrosis  or  fibroid  phthisis  ;  and  that  while  the 
fibrous  change  in  the  young  tubercle  is  a  true  process  of  recovery,  the 
puhnonary  cirrhosis  which  surrounds  the  caseous  tubercles  has  not  always 
that  happy  result.  Indeed,  we  now  know  that  Koch's  bacillus  may  remain 
aUve  foTfvcry  long  time  in  caseous  tubercles  surrounded  by  fibrous  tissues, 
and  that  pulmonary  fibrosis  of  an  invading  character  may  cause  disastrous 
results,  and  be  in  itself  a  serious  condition.  •  n     • 

Lastly    Cruveilhier  showed  that  large  fibrous  tubercles,  especially  in 

old  people,  may  contain  not  only  caseous  substance,  resembling  dry  putty 

but  also  stony  granules.     Very  small  calcareous  granules  have  been  noted 

by  Schlippel  and  by  Ziegler  in  the  tubercular  follicles,  where  they  assume 

quite  a  special  disposition,  and  are  made  up  of  concentric  layers      Metch- 

dkolf  found  calcareous  bodies  of  the  same  character  m  the  tubercles  of 

Algerian  gerbil  {Meriones  Shawi),  an  animal  in  which  the  infection  spreads 

very  slowly  after  inoculation.     In  the  centre  of  these  calcareous  bodies  we 

find  tubercle  bacilli,  which  in  the  early  stages  of  the  lesion  appear  perfectly 

normal,  and  are  surrounded  by  a  layer  of  amorphous  substance.     Later  they 

lose  their  faculty  for  taking  stains,  degenerate,  and  disappear.     According 

to  Metchnikoff,  the  stratified  layers  are  multiple  cuticles,  secreted  by  the 

bacillus  for  defensive  purposes,  and  the  phosphate   of   lime   is   probably 

deposited  in  this  cuticle  by  the  giant  cell  itself,  in  its  reaction  against  the 

*'''' Although  these  facts  are  not  applicable  to  the  calcareous  bodies  in  the 
tubercle  of  man,  they  are  very  interesting  as  reconciling  the  tubercles  o^ 
recovery  with  the  ideas  we  have  concerning  them. 
The  histological  changes  are  as  follows  : 


DISEASES  OF  THE  LUNG  197 

1.  Fibrous  Tubercle. — When  the  tubercle  reaches  its  stationary  stage, 
we  find  new  connective  fibres,  which  interpose  themselves  between  the  cells, 
and  finally  make  up  most  of  the  granulation  in  which  giant  cells  may  still 
be  met  with  at  the  centre  or  at  the  periphery.  "  These  giant  cells  are  often 
situated  in  a  cavity  which  holds  them  exactly,  and  is  made  up  of  fibrous 
Dundles,  forming  a  circle  around  them.  The  isolated  fibrous  tubercles, 
and  the  periphery  of  the  large  confluent  tubercles  of  the  same  nature, 
have  in  their  interior  capillary  vessels  permeable  by  the  blood.  The 
wall  of  the  vessel  is  often  thickened,  especially  in  the  sclerosed  tissues. 
While  the  tissue  of  the  granulation  becomes  fibrous,  "  the  septa  of  the  pul- 
monary alveoli  have  a  tendency  to  become  thickened,  and  interstitial 
pneumonia  develops  around  the  granulations  that  have  become  fibrous." 
In  the  thickened  walls  of  the  alveoli,  small  round  cells,  which  infiltrate  the 
bundles  of  the  connective  tissue,  are  seen  in  large  numbers.  In  the  oldest, 
and  especially  the  confluent,  fibrous  tubercles  the  giant  cells  disappear  at  the 
centre  of  the  islet,  which  is  now  only  formed  of  fibrillary  connective  tissue, 
without  vessels  and  cellular  infiltration ;  fibrous  tubercles,  with  giant  cells 
and  permeable  vessels,  are  found  at  the  periphery. 

The  old  fibrous  tubercles  may  be  infiltrated  with  black  pigment.  Those 
black  granulatioiLS,  composed  of  particles  of  carbon,  and  also  of  altered  blood- 
pigment,  may  occupy  the  whole  granulation,  or  only  a  part  of  it.  They  are 
then  situated  at  the  periphery,  for  they  are  found  chiefly  in  the  cells  ;  they 
may  be  seen  in  the  giant  cells. 

These  fibrous  tubercles,  even  when  they  contain  giant  cells,  may  be 
considered  as  absolutely  arrested  in  their  evolution. 

2.  Interstitial  Pneumonia.— The  fibrous,  pigmented  tubercles  otten 
cause  thickening  of  the  septa  of  the  lung,  so  that  they  may  be  situated  in  the 
middle  of  an  indurated  connective  tissue  which  no  longer  presents  alveolar 
cavities.  Around  these  masses,  where  the  lung  structure  has  quite  perished, 
the  pulmonary  tissues  show  the  lesions  of  interstitial  pneumonia  :  thicken- 
ing of  the  alveolar  septa,  which  are  made  up  of  fibres  of  connective  tissue 
and  flat  cells  containing  black  pigment ;  alveolar  exudate,  made  up  of 
leucocytes  and  pigmental  epithelial  cells  ;  alveolar  septa  covered  with  layers 
of  large  swollen  epithelial  cells  ;  narrowing  of  the  alveoli,  which  may  take 
an  elongated  form,  while  their  direction  is  perpendicular  to  that  of  the 
thickened  interlobular  septa.  In  certain  places  distended  vessels,  which 
form  a  kind  of  cavernous  tissue,  are  found  in  the  connective  tissue.  Side 
by  side  with  the  lesions  of  interstitial  pneumonia  we  sometimes  see  opaque 
formations,  which  to  the  naked  eye  resemble  tubercles.  This  condition 
IS  really  one  of  venous  thrombosis,  surrounded  by  fibrous  zones,  possessing 
a  rich  collateral  circulation  (Cornil).  This  interstitial  ])n('unioni:i  may 
be  found  around  caseous  centres  and  healed  cavities  with  thickened  walls. 


198  TEXT-BOOK  OF  MEDICINE 

This  condition  is  seen  in  the  lung,  where  the  fibrosis  has  made  slow  progress. 
In  these  cases  it  is  often  found  associated  with  chronic  adhesive  pleurisy  and 
thickening  of  the  subpleural  connective  tissue.  In  this  way  arises  pulmonary 
fibrosis,  which  not  only  deprives  a  part  or  the  whole  of  the  lung  of  all  function, 
but  which  may  also  result  in  deformity  of  the  chest  and  dilatation  of  the 
bronchi. 

In  other  cases  fibroid  phthisis  does  not  run  the  same  course.  The 
induration  may  affect  a  whole  lobe,  or  even  both  lungs,  in  the  form  of  islets, 
or  of  large  masses  around  indurated  or  caseous  miliary  tubercles  without 
or  with  merely  small  cavities.  Interstitial  pneumonia  then  presents  a  form 
of  subacute  phthisis,  and  at  times  matures  fairly  rapidly  :  m  six  months  or 
in  a  year  (Cornil). 

To  sum  up :  the  fibrous  change  may  affect  young,  isolated  tubercles, 
and  thus  bring  about  a  true  cure  of  these  lesions.  The  interstitial  pneu- 
monia which  is  often  present,  and  the  fibrous  change  in  the  more  advanced 
lesions,  are  frequently  of  good  omen.  On  the  one  hand,  however,  they  do 
not  always  arrest  the  course  of  the  lesions  ;  and,  on  the  other  hand,  they 
may  go  beyond  the  mark,  and  give  rise  to  pulmonary  fibrosis,  with  its  results. 

XV.  PNEUMONIC  PHTHISIS— TUBERCULAR  PNEUMONIA- 
CASEOUS  PNEUMONIA. 

Since  Laennec  traced  the  anatomical  and  clinical  history  of  phthisis  two 
chief  schools  of  thought  have  arisen — the  one  affirming  the  unity,  and  the 
other  the  duality,  of  phthisiogenous  lesions. 

According  to  the  former,  pulmonary  tuberculosis  and  caseous  pneumonia 
are  one  disease  ;  they  are  both  traceable  to  heredity,  go  on  to  the  same 
termination — i.e.,  phthisis— and  if  their  lesions,  tubercular  granulations 
and  caseous  infiltrations  present  any  difference,  such  difference  concerns 
only  the  form  of  their  morbid  products,  and  not  their  nature.  Laennec 
therefore  bequeathed  to  us  the  doctrine  of  their  unity,  both  from  the 
anatomical  and  the  clinical  point  of  view. 

According  to  the  dualists,  on  the  other  hand,  pulmonary  tuberculosis 
and  caseous  pneumonia  represent  two  distinct  diseases.  In  1850  Reinhardt 
affirmed  that  the  lesion  described  by  Laennec  as  tubercular  infiltration 
was  nothing  else  than  "caseous  pneumonia."  According  to  the  dualists, 
the  pathological  anatomy,  course,  and  prognosis  were  different  in  the  two 
cases.  Tubercular  granulations  and  caseous  infiltration  had  neither  the 
same  origin  nor  the  same  nature  ;  heredity  was  the  chief  element  in  the 
case  of  the  tubercular  patient,  while  in  the  case  of  the  patient  with  caseous 
disease,  he  got  off  with  a  pneumonia  which  Virchow  called  scrofulous, 
he  had  not  the  ill-luck  to  become  tubercular  "  (Niemeyer). 


DISEASES  OF  THE  LUNG  199 

You  see,  said  the  dualists,  that  this  scrofulous  pneumonia  (Virchow's) 
has  nothing  in  common  with  pulmonary  tuberculosis,  since  there  is  a  differ- 
ence in  form,  seat,  origin,  and  nature  between  the  two  maladies — difference  in 
form,  becaiLse  the  tubercular  granulation  is  nodular,  while  caseous  pneu- 
monia Ls  diffuse  ;  difference  in  situation,  because  the  granulation  arises 
outside  the  alveolus,  while  caseous  pneumonia  arises  inside  ;  difference  in 
origin,  because  the  tubercular  granulation  develops  at  the  expense  of  the 
connective  tissue,  and  caseous  pneumonia  at  the  expense  of  the  pulmonary 
endothelium. 

Such  were  the  anatomical  and  histological  arguments  invoked  by  the 
duahsts,  and  it  is  on  this  ground  that  each  of  their  conclusions  has  been 
vigorously  attacked  and  successfully  routed  in  various  works,  and  notably 
by  Grancher,  in  a  thesis  which  forms  an  eloquent  plea  in  favour  of 
Laennec's  work. 

But  what  definitely  ruined  the  dualist  doctrine  and  confirmed  the 
triumph  of  the  French  school  is  Villemin's  discovery,  on  the  one  hand,  and 
Koch's  discovery,  on  the  other.  Since  Villemin  made  his  memorable  experi- 
ments, we  know  that  all  tubercular  products  are  virulent  and  inoculabie, 
whatever  their  form  may  be ;  and  we  know  also,  since  Koch's  great  dis- 
covery, that  all  these  products  contain  the  specific  bacillus  of  tuberculosis. 

The  experiments  of  Auclair  deserve  quoting  :  In  the  rabbit  caseous 
pneumonia  follows  the  intratracheal  injection  of  an  ethereal  extract  of 
bacilli  from  tubercular  patients  ;  interstitial  pneumonia  may  be  the  result  of 
inoculation  with  a  chloroform  extract  of  the  same  bacilli.  The  double 
fibro-caseous  evolution  of  the  tubercle  appears,  then,  to  depend  upon  a 
double  toxine,  whicli  explains  the  incidence  of  the  lesions  to  one  or  to  the 
other  process,  or  to  both  at  once. 

There  is  no  longer  any  reason  for  preserving  the  term  "  caseous  pneu- 
monia." The  infectious  malady  called  tuberculosis,  which  runs  an  acute,  sub- 
acute or  chronic  course  in  the  lung  and  other  organs,  shows  itself  anatomically 
by  products  of  a  tubercular  nature.  The  products  are  sometimes  of  small 
size  and  nodular  in  shape  (grey  granulations,  miliary  tubercles)  ;  at  other 
times  they  are  of  large  size  (discrete  or  confluent  nodules,  tubercular  infil- 
tration). The  granular  form  may  exist  alone — i.e.,  acute  granular  tuber- 
culosis. The  pneumonic  form,  whether  discrete  or  confluent,  may  exist 
alone — i.e.,  caseous  pneumonia,  or,  better,  tubercular  broncho-pneumonia, 
which  may  more  or  less  quickly  give  rise  to  acute  and  subacute  phthisis. 

Pathological  Anatomy. — Tubercular  ])neumonia  is  usually  limited  to 
one  lung  ;  it  may  be;  limited  to  a  few  lobules  or  invade  a  whole  lobe.  It 
attacks  the  lower  as  well  as  the  upper  lobe. 

The  lung  presents  different  appearances,  according  as  the  lesion  is  more 
or  less  advanced.     In  the  more  advanced  stage  the  lung  tissue  resembles 


200  TEXT-BOOK  OF  MEDICINE 

Roquefort  cheese — hence  the  name  "  caseous  pneumonia  " — and  the  greyish 
areas  form  with  the  yellowish  and  brownish  ones  a  kind  of  mosaic.  The  cut 
section  does  not  present  the  granular  condition  of  lobar  pneumonia,  but  is 
more  opaque,  smooth,  dry,  homogeneous  and  angemic. 

The  lesions  of  commencing  tubercular  pneumonia  are  seen  side  by  side 
with  the  caseous  masses.  We  find  masses  of  rosy-coloured,  quivering, 
and  semitransparent  substance,  called  by  Laennec  "  colloid  infiltration," 
but  since  termed  "  caseous  colloid  pneumonia  "  (Thaon)  ;  masses  of  greyish 
homogeneous  substance  are  also  seen  :  this  is  Laennec's  grey  infiltration. 
These  tubercular  infiltrations  may  go  on  to  caseation. 

If  we  study  caseous  infiltration  closely,  we  see  that  it  is  not  disseminated 
at  random  through  the  lung  ;  it  is  composed  of  more  or  less  confluent  nodules, 
leaving  between  them  lung  tissue  that  is  healthy,  or  showing  the  lesions  of 
ordinary  broncho-pneumonia.  The  caseous  nodules  have  a  special  texture, 
and  are,  for  the  most  part,  developed  around  a  small  bronchus,  which  is  the 
centre  of  their  formation  (peribronchial  nodules).  They  are  composed  of  (1) 
a  central  region,  and  (2)  a  peripheral  zone.  The  older  the  central  zone,  the 
more  caseous  it  is.  Some  vestiges  of  lung  are  seen — i.e.,  arterioles — rings 
and  bands  of  elastic  tissue,  which  represent  the  bronchioles  and  the  alveolar 
walls.  Around  this  central  region,  which  comprises  the  caseous  centre  of 
the  tubercular  follicle,  we  see  a  zone  that  is  well  defined  on  the  side  of  the 
central  region,  but  irregular  at  the  periphery.  This  embryonic  zone 
(Grancher)  is  formed  of  embryonic  cells,  that  infiltrate  the  walls  of  the 
alveoli  and  their  cavities ;  and  giant  cells  that  are  irregularly  disposed  in 
the  form  of  a  crown  (Charcot),  and  complete  the  analogy  between  the 
caseous  nodule  and  the  tubercular  follicle.  Here,  as  in  the  tubercle,  the 
degeneration  begins  at  the  centre,  and  the  lesion  extends  at  the  circumfer- 
ence. These  caseous  nodules  which  are  seen  in  the  different  varieties  of 
caseous  pneumonia  are  collections  of  a  tubercular  nature  ;  the  condition 
is  Laennec's  tubercular  infiltration  in  its  most  absolute  sense.  The  caseous 
inflammation  is  tubercular,  and  contains  Koch's  bacillus. 

The  softening  of  the  caseous  substance,  the  ulceration  that  results, 
and  the  cavity,  are  produced  by  the  process  we  have  already  described 
in  the  case  of  tubercle.  Caseous  pneumonia,  however,  may  last  a  long 
while,  without  giving  rise  to  ulceration  of  the  lung  ;  considerable  masses 
may  long  remain  in  the  same  condition,  although  the  lung  is  impermeable 
to  air  and  blood  (Cornil  and  Ranvier). 

Chronic  caseous  pneumonia,  like  chronic  tuberculosis,  is  always  accom- 
panied by  interstitial  pneumonia  (Grancher),  and  often  by  fibrinous  pleurisy. 
We  shall  see  later  in  what  relation  tubercular  granulations  are  associated, 
mth  it. 

Bacteriology. — The   tubercle   bacillus   has   always   been   met  with   ii 


DISEASES  OF  THE  LUNG  201 

caseous  pneumonia.  In  the  lobar  form  the  bacilli  are  found  in  the  centre 
of  the  infundibula,  in  the  embryonic  cells  that  fill  the  alveoli,  and  in  the 
walls  of  the  alveoli.  A  similar  distribution  obtains  in  the  lobular  forms. 
The  tubercle  bacillus,  however,  is  not  alone  in  evidence  in  the  lesions  of 
tubercular  pneumonia  and  broncho-pneumonia.  Mixed  infections  are 
present,  just  as  in  all  broncho-pneumonias  ;  the  pneumococcus,  the  pneumo- 
bacillus,  and  the  streptococcus  predominate  in  the  diseased  zone  around 
the  caseous  masses.  This  peripheral  zone  represents  the  less  advanced 
stage  of  the  lesion,  while  the  caseous  centre  represents  its  completion.  The 
secondary  or  associated  microbes  predominate  in  the  peripheral  zone,  and 
it  is  probable  that  they  engender  centres  of  broncho-pneumonia  and  start 
the  lesion,  which  the  bacillus  finally  casefies. 

Description. — Tubercular  pneumonia  may  be  lobular  or  pseudo-lobar 
(Vulpian).  A  lobar  form  has  also  been  described,  but,  according  to  Charcot, 
tubercular  pneumonia  is  never  lobar,  and  the  cases  which  have  been  called 
lobar  are  confluent  lobular  or  pseudo-lobar. 

Tubercular  pneumonia,  whether  it  be  lobular  or  pseudo-lobar,  some- 
times resembles  an  acute  phlegmasia,  and  at  other  times  a  chronic  disea.se  ; 
but  all  intermediate  forms — notably  the  subacute  variety — are  found 
between  these  two  extremes. 

The  acute  pseudo-lobar  form  begins  suddenly  with  fever,  chill,  pain  in  the 
side  ;  and,  indeed,  the  violence  of  the  chill,  the  high  temperature,  the  coloured 
and  viscid  sputum,  may  closely  resemble  the  onset  of  true  lobar  pneu- 
monia. I  saw,  some  years  ago,  a  medical  student  who  was  carried  off  in  a 
few  weeks  by  tubercular  pneumonia  of  the  middle  lobe  ;  his  sister  had  died 
some  time  before  from  chronic  tuberculosis.  The  acute  lobular  form,  in  its 
initial  symptoms,  resembles  broncho-pneumonia. 

The  acute  forms  may  carry  off  the  patient  very  quickly,  within  a  few 
weeks,  even  before  pulmonary  ulceration  has  had  time  to  develop.  At  other 
times  cavities  appear  early,  and  auscultation  allows  us  to  follow  the  course  of 
events.  Wiieti  thf  progress  of  the  disease  is  a  little  slower,  the  clinical  picture 
of  subacute  tubercular  pneumonia  is  seen.  These  acute  and  subacute  forms 
answer  to  the  terms  "  acute  phthisis  "  and  "  acute  pneumonic  phthisis." 

Chronic  tubercular  pneumonia  may  follow  the  acute  condition,  or  be 
ciirouic  from  tlie  first.  In  the  latter  case  the  disease  begins  silently, 
preceded  or  not  by  some  suspicious  symptoms,  such  as  laryngitis,  bronchitis, 
or  hffimoplysis.  The  patient  coughs  and  complains  of  distress,  which  is 
often  paroxysmal,  and  comparable  to  the  dyspncea  of  heart  disease,  or  of 
an  attack  of  astliina.  He  loses  strength  and  wastes.  On  auscultation,  we 
find  in  one  or  in  several  lobes  tubular  breathing,  subcrepitant  rales,  and 
marked  diniinutioii  of  the  vesicular  ninrmur.  These  signs  are  sometimes 
predominant ;    ihey  remain  stationary  in  the   invaded   regions  ;    but    the 


202  TEXT-BOOK  OF  MEDICINE 

lesion,  in  spite  of  its  extent,  may  only  canse  moderate  fever,  and  trifling,  or 
purely  catarrhal,  expectoration. 

It  is  exceptional  for  caseous  pneumonia  to  recover  ;  in  most  cases  the 
chronic  form  leads  to  ulceration  of  the  lung,  cavities,  slow  consumption, 
and  phthisis,  in  the  true  sense  of  the  word.  In  other  circumstances,  and  in 
spite  of  several  months'  duration,  the  patient  succumbs  without  ulceration 
of  the  lung.  He  is  carried  off  by  asphyxia,  with  symptoms  of  hectic  fever, 
sweating,  and  diarrhoea.  I  have  seen  two  cases  of  this  kind :  one,  with 
Tardieu,  in  a  young  girl  whose  brother  died  two  months  later  of  ordinary 
tuberculosis  ;  the  other,  with  Krank  and  Leudet,  in  a  young  woman  in 
whom  caseous  pneumonia  complicated,  as  often  happens,  fibrinous  pleurisy. 
In  both  patients  almost  the  whole  of  the  right  lung  appeared  to  be 
converted  into  a  huge  caseous  block  ;  the  dullness  was  absolute,  and  the 
absence  of  every  normal  and  abnormal  sound  alternated  in  places  with 
slight  tubular  breathing,  or  with  subcrepitant  rales.  The  growing  dyspnoea 
and  the  asphyxia  were  the  chief  symptoms  throughout  the  disease. 

During  infancy,  as  I  have  said  in  the  chapter  on  Pulmonary  Phthisis, 
tuberculosis  often  shows  itself  as  a  broncho-pneumonia. 

Diagnosis. — The  diagnosis  of  tubercular  pneumonia  is  exceedingly  diffi- 
cult at  the  commencement.  The  acute  forms  simulate  broncho -pneumonia 
or  genuine  pneumonia,  and  it  is  soon  evident  that  we  are  dealing  with  acute 
phthisis.  It  must  be  said,  however,  that  cases  of  acute  caseous  pneumonia 
rarely  show  the  symptoms  of  genuine  inflammation.  Thus,  in  the  form 
which  simulates  lobar  pneumonia  the  sputum  contains  more  blood,  or  is 
accompanied  by  genuine  haemoptysis  ;  defervescence  does  not  occur  ;  wasting 
is  rapid  ;  signs  of  cavities  appear  in  some  cases,  and  the  patient  is  carried 
off  by  acute  consumption. 

The  chronic  and  subacute  forms  of  caseous  pneumonia  are  quite  as  in- 
sidious in  their  course.  The  inflammation  is  ill  defined ;  the  stethoscopic 
signs,  rales,  and  tubular  breathing  remain  stationary  ;  secondary  pneumonia 
is  thought  of,  and  the  primary  cause  is  sought  elsewhere.  The  question  is 
asked  whether  the  patient  may  not  be  diabetic,  or  suffering  from  Bright's 
disease,  or  cardiac  mischief ;  but  the  appearance  of  further  symptoms  soon 
makes  the  diagnosis  clear. 

In  these  doubtful  and  difficult  cases  too  much  information  cannot  be 
obtained.  The  patient's  antecedents  (haemoptysis,  suspicious  bronchitis), 
and  the  question  of  heredity  (phthisis  among  forebears  or  relatives)  will^ 
have  great  weight  in  diagnosis. 

The  presence  of  tubercle  bacilli  in  the  sputum  of  patients  with  caseous! 
pneumonia  is  less  frequent  than  in  cases  of  common  tuberculosis.  Bacilli] 
may  be  wanting  in  the  expectoration,  although  they  may  be  found  in  the^ 
lung  tissue  at  the  autopsy. 


DISEASES  OF  THE  LUNG  203 

XYI.  ACUTE  GRANULAR  TUBERCULOSIS— ACUTE  GENERALIZED 

TUBERCULIZATION. 

The  terms  "galloping"  and  "acute,"  applied  to  phthisis  and  tubercu- 
losis, have  been  variously  interpreted  by  authorities,  and  this  confusion  has 
certainly  complicated  the  study  of  these  diseases.  We  must  abandon  the 
term  "galloping,"  and  keep  only  the  epithet  "acute,"  in  opposition  to 
that  of  "  chronic."  Phthisis  is  chronic  when  the  lesions  slowly  and  gradu- 
ally end  in  ulceration  of  the  lung,  cavities,  and  consumption  ;  it  is  sub- 
acute or  acute  when  these  lesions  run  a  rapid  course,  as  in  certain  cases  of 
tubercular  pneumonia :  the  patient  then  passes  through  the  stages  of  phthisis 
in  a  few  months  or  weeks,  instead  of  several  years. 

These  different  forms — chronic  phthisis,  which  is  the  most  common, 
subacute  and  acute  phthisis — have  been  described  in  the  preceding  chapters. 
I  shall  now  give  the  description  of  another  form  of  tubercular  infection — 
viz.,  acute  granular  tuberculosis,  acute  granulosis,  or  granulia. 

In  the  different  varieties  of  phthisis  which  we  have  already  reviewed, 
the  grey  granulation  was  of  minor  importance,  while  the  miliary  tubercles 
and  the  diffuse  or  circumscribed  tubercular  inflammations  almost  entirely 
made  up  the  lesion.  In  acute  granular  tuberculosis  the  chief  lesion  is  the 
tubercular  granulation,  while  the  hyperaemia  and  broncho-pulmonary 
infection  only  occupy  a  second  place.  The  tubercles  are  so  confluent, 
asphyxia  and  death  arc  so  rapid,  that  the  secondary  degenerations  and  the 
ulcerations  of  the  lung  that  accompany  phthisis  have  not  time  to  develop. 
We  must,  however,  remember  that  the  different  forms  of  tubercular  infec- 
tion may  exist  simultaneously  in  the  same  subject,  in  which  case  we  find  post 
mortem  the  lesions  of  chronic  phthisis  or  of  acute  tubercular  pneumonia, 
and  the  confluent  granulations  of  acute  tuberculosis. 

Pathological  Anatomy. — The  lesions  of  acute  tuberculosis  differ  accord- 
ing as  the  granulations  are  or  are  not  accompanied  by  congestion,  bron- 
'liitis,  broncho-pneumonia,  pleurisy,  or  old  tubercular  lesions. 

1.  In  some  cases  the  granulations  constitute  the  only  lesion,  or,  at  least, 
the  neighbouring  inflammation  which  accompanies  them  is  insignificant ; 
the  parenchyma  of  the  lung  is  riddled  with  granulations,  both  on  its  surface 
and  in  its  deep  parts.  On  section,  the  lung  appears  riddled  with  granula- 
tions ;  these  are  almost  always  quite  young,  grey,  and  somitransparont ; 
wlien  they  are  older  they  undergo  degeneration  in  the  centre.  In 
chronic  tuberculosis  (ordinary  phthisis)  the  miliary  tubercle  develops  chiefly 
around  the  bronchiole,  which  serves  as  its  centre  of  formation  ;  but  in  acute 
tuberculosis  the  grey  granulation  develops  chiefly  around  the  l)loodvessels 
and  the  lymphatics.  The  structure  of  the  granulations  has  been  described 
elsewhere. 


204  TEXT-BOOK  OF  MEDICINE 

2.  In  other  cases  the  granulations  of  acute  tuberculosis  are  accom- 
panied by  intense  congestion,  capillary  bronchitis,  broncho-pneumonia,  and 
pleurisy.  If  the  disease  has  lasted  some  time,  the  tubercular  granulations 
and  the  broncho-pulmonary  infiltrations  have  already  undergone  initiatory 
softening  and  caseation. 

3.  In  a  large  number  of  autopsies  we  find  both  acute  and  quite  recent 
crops  of  granulations,  and  an  old  tubercular  lesion,  or  a  caseous  nodule  of 
broncho-pneumonia.  On  these  facts  Blihl  founded  his  theory,  according 
to  which  the  crops  of  acute  tuberculosis  are  only  secondary  lesions, 
grafted  on  the  chronic  lesion  which  has  favoured  their  develop- 
ment. 

Cases  of  secondary  infection,  well  known  from  Laennec's  time,  are 
very  frequent ;  they  demand  serious  consideration,  and  prove  that  an  indi- 
vidual attacked  by  acute  tuberculosis  has  been  already  in  the  power  of  the 
tubercular  infection,  because  old  silent  lesions  are  found  in  the  lung,  the  brain, 
or  other  organs.  Cases  of  secondary  acute  tuberculosis  have  been  noted  in 
patients  primarily  affected  with  tuberculosis  of  the  eye,  or  with  tubercular 
infiltration  of  the  spine,  of  the  lymphatic  glands,  etc.  Still,  acute  tabercu- 
losis  may  be  primary,  as  has  been  noted,  in  a  large  number  of  cases. 

Acute  tuberculosis  does  not,  as  a  rule,  remain  limited  to  the  respiratory 
system.  It  often  invades  other  organs  and  systems,  and  then  merits  the 
name  of  acute  tuberculization.  Few  organs  escape  ^  peritoneum,  meninges, 
pericardium,  endocardium,  synovial  membranes,  liver,  spleen,  kidneys, 
choroid,  thyroid  gland,  bronchial  and  mesenteric  glands,  etc.,  may  be 
invaded  by  the  tubercular  granulations. 

The  glands  may  rapidly  reach  an  enormous  size,  and  cause  certain  com- 
plications, such  as  "  compression  of  the  bronchi,  with  symptoms  of  asphyxia  ; 
compression  of  the  mesenteric  arteries,  with  intestinal  gangrene  ;  compres- 
sion of  the  common  bile-duct,  with  jaundice." 

In  acute  tuberculosis  the  granulations  are  usually  found  in  the  vascular 
and  lymphatic  tissue.  Giant  cells  and  bacilli  have  been  recognized  in  the 
internal  coat  of  the  meningeal  vessels  and  in  the  fibrinous  thrombi  of  the 
vessels  ;  they  have  been  seen  in  the  lining  membrane  of  the  pulmonary 
veins  (Miigge)  ;  in  the  tunica  intima  of  the  endocardium  of  the  right  heart ; 
in  the  vegetations  of  the  endocardium  ( Weigert) ;  in  the  walls  of  the  veins  ;  in 
the  tunica  intima  of  the  inferior  vena  cava  ;  in  the  blood  ;  in  the  wall  of  the 
thoracic  duct  (Ponfick) ;  and  in  the  walls  of  the  lymphatic  vessels :  so  that 
acute  tuberculosis  "  results,  in  all  probability,  from  the  entrance  of  bacteria 
into  the  general  circulation  of  the  blood  or  lymph  plasma." 

Description. — Acute  tuberculosis  shows  such  different  forms  that  an 
attempt  has  been  made  to  classify  them,  either  by  the  anatomical  lesion  or 
by  the  leading  symptom.     Although  the  different  classifications  proposed 


DISEASES  OF  THE  LUNG  205 

may  be  purely  fanciful  and  but  little  in  agreement  with  the  clinical  data, 
I  feel  that  they  are  necessary  for  a  pathological  description. 

1.  There  is  a  catarrhal  form,  of  benign  appearance,  in  which  acute  and 
almost  latent  tuberculosis  (Leudet)  resembles  a  seasonal  fever,  with  some 
pulmonary  or  gastric  symptoms  ;  but  the  patient  is  rapidly  carried  ofi  by 
attacks  of  suffocation  or  of  syncope  after  a  more  or  less  lengthy  illness, 
which  did  not  appear  serious,  and  was  supposed  to  be  bronchitis  or  influenza. 
These  latent  forms  are  the  more  insidious  inasmuch  as  they  may  be  apyretic. 
I  have  seen  a  case  at  the  Necker  Hospital. 

2.  The  suffocative  form,  which  Graves  calls  acute  tubercular 
asphyxia,  and  which,  says  Andral,  resembles  an  acute  attack  of  asthma,  is 
characterized  by  increasing  dyspnoea  and  asphyxia,  which  come  on  without 
warning,  or,  at  least,  in  the  midst  of  trifling  symptoms.  Pain,  cough,  and 
expectoration  are  absent ;  the  fever  is  moderate,  and  auscultation  shows  only 
some  rales.  This  form,  which  is  often  accompanied  by  broncho-pulmonary 
congestion,  may  carry  off  the  patient  in  four  or  five  days.  If  an}i:hmg 
can  give  a  clue  to  the  diagnosis,  it  is  precisely  the  absence  of  sigas,  or,  at 
least,  the  disproportion  between  the  gravity  of  the  symptoms  and  the  levity 
of  the  physical  signs. 

3.  Acute  tuberculosis  may  be  'associated  with  the  infections  of  the 
respiratory  system  (diphtheria),  and  is  then  partly  masked  by  them.  Thus 
when  it  takes  the  form  of  capillary  bronchitis,  we  find  cough,  dyspnoea, 
and  expectoration.  There  are  the  same  fine,  sibilant  and  subcrepitant 
rales ;  and  if  other  symptoms,  such  as  bloody  sputum,  enlargement  of  the 
spleen,  abdominal  or  cerebral  troubles,  are  not  present,  the  diagnosis  is  most 
difficult.  When  acute  tuberculosis  is  associated  with  broncho-pneumonia 
(acute  phthisis),  the  difficulties  in  diagnosis  are  the  same  as  in  the  preceding 
case.  The  disease  runs  its  course  in  a  few  weeks,  or  in  two  to  three  months  ; 
we  see  the  rapid  formation  of  ulcers  in  the  lung  and  the  consumption  of  the 
patient,  and  this  variety  is  confounded  with  pneumonic  phthisis. 

In  some  cases  the  broncho-pulmonary  inflammations  give  place  to  pleural 
inflammation,  and  the  sero-fibrinous  or  haemorrhagic  pleurisy  is  so  promi- 
nent that  the  acute  tuberculosis  passes  unnoticed,  until  it  shows  itself  by 
symptoms  that  have  nothing  in  common  with  simple  pleurisy. 

A.  The  typhoid  form  answers  especially  to  acute  generalized  tubercu- 
lization, and  closely  resembles  typhoid  fever  :  headaciii^,  insomnia,  pul- 
monary congestion,  epistaxis,  abdominal  and  cerebral  troubles,  and  lenticular 
rose  spots,  are  present.  There  exist,  nevertheless,  some  distinctive  signs 
which  may  assist  in  the  diagnosis.  In  acute  tuberculosis  the  stupor  Is  less 
profound  ;  hypera3sthesia  of  the  chest  is  acute  (Bouchut) ;  ophthalmoscopic 
examination  sometimes  reveals  tubercles  in  the  choroid  (Bouchut);  the  stetho- 
fcicopic  signs  are  more  marked  at  the  apex  of  the  lungs,  and  the  sputum  l^ 


L 


206  TEXT-BOOK  OF  MEDICINE 

sometimes  mixed  with  red  blood ;  the  patient  has  attacks  of  dyspnoea, 
and  the  temperature  cm-ve  presents  some  differences.  While  the  febrile 
cycle  of  enteric  fever  is  made  up  of  three  periods,  in  which  the  temperature 
successively  ascends,  remains  stationary,  and  descends,  the  temperature  in 
acute  tuberculosis  is  much  higher  at  night  than  in  the  morning,  and  scarcely 
deviates  from  this  type  during  the  whole  disease.  Sero-diagnosis  (VVidal) 
will  remove  all  doubts  between  enteric  fever  and  acute  tuberculosis, 

5.  The  cerebral  form  may  show  itself  suddenly  by  loss  of  consciousness, 
followed  by  coma  and  symptoms  of  meningitis  ;  these  symptoms  recall  the 
description  of  acute  hydrocephalus,  and,  indeed,  abundant  effusion  is  found 
post  mortem  m  the  ventricles.  The  cerebral  symptoms  do  not  supervene 
as  a  simple  episode,  as  is  seen  in  the  other  varieties  of  acute  and  chronic 
tuberculization  ;  here  they  draw  all  the  attention  to  themselves. 

6.  Unusual  Forms. — There  are  cases  which  are,  indeed,  more  rare  and 
insidious  than  the  precedmg  ones,  in  which  tuberculosis  shows  itself  by 
such  imusual  symptoms  that  the  nature  of  the  disease  is  not  recognized 
at  first.  Colin  has  published  the  history  of  a  patient  in  whom  the 
miliary  tubercles  primarily  appeared  in  the  kidneys,  and  the  disease  was  at 
first  taken  for  acute  nephritis.  In  a  case  of  Laveran  the  tuberculosis 
first  invaded  the  articular  synovial  membrane,  and  for  the  first  few  days 
the  disease  was  looked  upon  as  acute  rheumatism. 

7.  In  some  cases  the  tubercular  lesions  are  little  marked,  but  the  viru- 
lence of  the  bacillus  is  exaggerated,  and  the  disease  truly  deserves  the  name 
acute  tubercular  infectious  fever.  The  case  looks  like  typhoid  fever, 
but  there  is  no  stupor,  and  the  fever  may  improve  under  the  influence  of 
antipyrin. 

Diagnosis — Prognosis. — I  have  indicated  the  difficulties  in  diagnosis 
with  regard  to  each  of  the  forms  which  acute  granular  tuberculosis  may 
assume.  A  search  for  bacilli  in  the  sputum  should  never  be  neglected. 
It  is  the  most  valuable  method,  and  in  many  cases  has  cleared  up  a  doubtful 
diagnosis. 

Acute  tuberculosis  and  acute  generalized  tuberculization  are  nearly 
always  fatal,  and,  indeed,  some  forms  carry  the  patient  off  in  a  few  days. 
There  are  exceptions  to  this  rule.  Sometimes  the  tubercular  granulations 
occur  m  intermittent  crops ;  the  disease  is  not  very  acute,  and  lasts  several 
months.  In  other  cases  the  acute  attack  gives  place  to  a  chronic  state, 
and  acute  tuberculosis  becomes  ordinary  pulmonary  phthisis.  In  some 
cases,  when  the  tubercles  have  not  been  confluent,  they  pass  into  the 
fibrous  state ;  the  disease  becomes  chronic,  and  may  then  be  almost  harm- 
less, if  the  patient  is  not  affected  with  other  acute  or  chronic  manifestations 
of  tubercular  infection. 

Acute  tuberculosis  especially  attacks  young  people  and  soldiers,  and 


DISEASES  OF  THE  LUNG  207 

the  military  medical  officers  have  insisted  on  its  quasi-epidemic  character. 
It  is  not  rare  in  very  young  children,  up  to  the  age  of  fifteen  or  eighteen 
months,  and  although  in  them  it  is  nearly  always  generalized,  the  absence 
of  local  symptoms  renders  the  diagnosis  very  difficult  (Parrot). 

The  treatment  of  acute  tuberculosis  varies,  according  to  the  form 
that  the  disease  assumes  :  tannin,  in  daily  doses  of  15  grains,  and  iodide 
of  soda,  in  daily  doses  of  from  120  to  240  grams  (Lepine),  appear  to  have 
given  good  results. 

XVII.  FALSE  TUBERCULOSIS  OF  THE  LUNG. 

The  tubercle,  which  is  a  mode  of  reaction  of  the  tissues  against  patho- 
genic agents,  is  not  in  any  way  specific  to  Koch's  bacillary  tuberculosis. 
It  may  be  met  with  in  different  affections,  characterized  histologically  by 
tubercles  ;  these  are  cases  of  pseudo-tuberculosis. 

The  causes  of  pseudo-tuberculosis  are  multiple.  I  would  mention  certain 
animal  parasites — the  Strongylus  vasorum,  whose  eggs  produce  in  the  dog 
a  tubercular  reaction  in  the  pancreas  (Laulanie) ;  the  Ollulanus  tricuspis,  and 
the  Pseudalius  ovis  fuhnonalis,  one  of  which  produces  pneumonia  in  the 
cat  and  the  other  m  the  sheep.  At  bther  times  bacterial  parasites  are  seen 
— for  example,  the  bacilli  of  Maiassez  and  Vignal's  zoogloeic  tuberculosis  ; 
also  tubercles  are  produced  by  fungi,  such  as  Favus  cladothrix  (Sabraces  and 
Dubreuilh),  Eppinger's  streptothrix  (Picot,  Riviere,  and  Sabraces),  and  the 
aspergilli,  which  include  Asfergillus  subfuscus  (Olsen  and  Gade),  Asper- 
gillus nidulans  (Lindt),  As-pergillus  flavescens,  and,  above  all,  Aspergillus 
jumigatus.  Pseudo-tuberculosis  is  especially  due  to  the  latter  fungus,  and 
as  it  is  the  only  one  that  has  been  observed  in  anything  like  a  complete 
manner  in  man,  it  is  the  only  one  we  shall  describe  here,  under  the  name  of 
aspergillary  pseudo-tuberculosis. 

Aspergillary  Pseudo-Tuberculosis. 

In  man  aspergillary  pseudo-tuberculosis  (pulmonary  aspergillosis)  has 
been  met  with  chiefiy  in  pigeon-feeders  and  hair-combers.  I  have  seen  it 
several  times  in  my  wards  at  the  Necker  Hospital.* 

Bacteriology. — The  Aspergillus  jumigatus,  which  belongs  to  the  order 
of  xVscomycctes  and  to  the  family  of  the  Perisporiacea?,  is  composed,  in  the 
adult  state,  of  a  mycelium  made  up  of  short  alternating  liyphae,  whicli  are 
slightly  dilated  at  their  extremities,  and  give  off  sterile,  sc[)tate,  and  colour- 
less branches,  and  colourless  or  slightly  colom-ed  fruit-bearing  ones.  These 
latter  support  the  spores,  which  rest  on  the  receptacle  or  spore-bearing  head, 

*  Diculafoy,  Chantemesso  ct  Widal,  "  Uno  rseudo-tubcic-ulujic  .Myti.i.si(luo " 
{Congress  do  Berlin,  1889). 


208  TEXT-BOOK  OF  MEDICINE 

from  which  they  emanate  by  the  strangulation  of  small  cells  having  the 
form  of  quills,  and  called  basidia. 

The  spores  of  the  Aspergillus  fumigatus  are  green  or  brownish,  accordiiig 
to  the  media.  Their  maximum  development  takes  place  at  98°  F.— that  is, 
at  a  temperature  nearly  the  same  as  that  of  the  human  body.  These  spores 
grow  very  well  on  Raulin's  liquid,  on  beer  wort,  and  Sabouraud's  maltose  ; 
their  colour  is  brown  on  the  former  and  green  on  the  latter  culture  medium. 
In  certain  cases  they  may  take  on  a  yellowish  colour.  Gelatine  is  liquefied 
by  Aspergillus  fumigatus. 

In  animals  the  pathogenic  action  of  this  fungus  is  well  marked.  Pigeons 
die  three  or  four  days  after  inoculation  of  the  spores  in  the  axillary  vein  ; 
rabbits  die  in  six  or  eight  days,  and  guinea-pigs  in  four  or  five  days,  after 
injection  into  the  veins  of  the  ear.  The  ape  is  less  sensitive  ;  and  this  patho- 
genic action,  which  is  nil  in  the  sheep,  is  present  in  the  case  of  dogs  and  cats 
(Saxer).  Inhalation  into  the  trachea  kills  pigeons  in  from  twelve  days  to  a 
fortnight.  The  ingestion  of  spores  produces  exceptionally  in  the  rabbit 
tubercular  lesions  of  the  intestine,  which  may  go  on  to  perforation  (Renon). 
Spontaneous  aspergillosis  is  fairly  frequent  in  birds  ;  it  may  invade  the 
eggs  during  incubation,  and  transmit  the  disease  to  the  chick  (Leucet). 
It^s  fairly  rare  in  Mammifera?,  where  it  takes  the  form  either  of  chronic 
phthisis  or  of  superacute  hgemorrhagic  septicaemia  (Leucet).  The  spores 
of  the  Aspergillus  fumigatus  are  present  in  the  air,  -upon  trees,  in  the  most 
superficial  layers  of  the  soil,  and  are  also  found  in  the  nasal  mucosa  and  the 
saliva  of  persons  who  are  healthy,  or  who  are  suffering  from  the  most  diverse 
affections.     The  surface  of  seeds  is,  however,  theu-  chosen  haunt  (Renon). 

The  resistance  of  the  spores  is  considerable,  and  their  vitality  is  enormous. 
They  still  reproduce  themselves  after  two  or  three  years'  sojourn  in  an  old 
culture,  but  their  virulence  is,  in  consequence,  found  to  be  attenuated.  Their 
vitality  is  weakened  by  a  more  or  less  prolonged  sojourn  in  organic  mem- 
branes (Renon).  Heat  kUls  them,  and  they  then  become  harmless  to 
animals  ;  but  the  animal  is  none  the  less  susceptible  to  the  injection  of  viru- 
lent spores,  and  appears  to  succumb  the  more  quickly,  as  the  degree  of  heat 
necessary  for  the  sterilization  of  the  primarily  injected  spores  has  been  high. 
By  a  progressive  inoculation  with  virulent  spores,  rabbits  can  be  made  to 
stand  considerable  doses,  that  would  rapidly  kill  the  control  animals. 

The  Aspergillus  fumigatus  does  not  produce  toxines.  Neither  culture 
fluids  nor  substances  extracted  from  the  mycelium  possess  any  vaccinal 
powers  (Kotliar,  Renon).  In  the  rabbit  the  spores  traverse  the  placenta, 
and  are  directly  transmitted  from  the  mother  to  the  foetus. 

^Etiology— Pathogenesis.— It  is  interesting  to  consider  how  pigeon- 
feeders  may  take  the  disease.  Infected  pigeons  present  on  the  floor  of  the 
mouth  a  small  tumour,  or  chancre,  which  may  cause  a  mouth-to-mouth 


DISEASES  OF  THE  LUNG  209 

contamination.  It  is  probable  that  more  usually  pigeon  and  feeder  find 
the  common  cause  of  their  disease  in  the  spores  of  the  AspergUlus  fumigatus 
which  are  present  on  the  grains  of  millet  and  vetch. 

Hair-combers  may  also  contract  aspergillary  tuberculosis.  They  are 
infected  from  the  flour  which  they  rub  on  the  hair  to  remove  the  grease  This 
flour  contams  many  spores,  while  the  undressed  hairs  collected  every  mornino 
in  the  dirt-boxes  by  the  rag-pickers  of  Paris  scarcely  contain  any  of  them*' 
Jiirds  livmg  m  this  dusty  atmosphere  succumb  in  a  fortnight  to  three  weeks  • 
pigeons  that  are  made  to  inhale  this  dust  die  of  aspergillary  tuberculosis 

In  some  cases  aspergillosis  finds  in  man  a  soil  perfectly  prepared  by 
previous  mflammation  of  the  broncho-pulmonary  system.  The  affection 
IS  then  secondary ;  its  progress  is  slow,  and  almost  alwavs  masked  by  the 
symptoms  of  the  primary  disease  ;  it  is  not  recognized,  as  a  rule,  until  the 
autopsy.  In  other  cases  aspergillary  pseudo-tuberculosis  is  a  primary  or 
autonomous  affection  that  is  identical  with  the  disease  seen  in  animals  and 
It  IS  this  form  that  I  have  especially  in  view  in  this  chapter.  The  French 
conception  of  primary  aspergillosis  (Dieulafoy,  Chantemesse  and  Widal 
lotam,  Renon,  Gaucher  and  Sergent),  after  having  been  actively  attacked 
in  Germany,  ls  now  completely  admitted  ;  it  is  indisputable,  for  it  corresponds 
exactly  with  anatomical,  experimental,  and  clinical  facts  (Renon)  Cases 
have  been  multiplied  during  the  last  few  years,  and,  according  to  Saxer 
primary  aspergillosis  is  much  more  frequent  than  is  usually  supposed 

The  only  difference  that  stiU  separates  the  French  from  the  German 
school  consLsts  in  the  term  "  pseudo-tuberculosLs,"  which  is  applied  in 
France  to  the  primary  aspergillary  ulcerative  process  in  the  lun.^  If  we 
remember  that  this  affection,  which  destroys  the  lung  tissue,  presents  all  the 
clinical  signs  of  tuberculosis,  we  see  that  we  are  very  nearly  in  agreement, 
and  that  in  every  case  the  idea  of  aspergillosis  as  a  primary  disease  receives 
a  striking  confirmation. 

Symptoms.-Asporgillary  pseudo-tuberculosis  presents  various  forms 
Ihe  disease  may  begin  with  slight  or  with  abundant  haemoptysis  followed 
m  general  by  other  attacks  at  intervals  of  several  months,  or  of  one  or  two 
years. 

At  the  same  time,  fatigue,  loss  of  strength,  with  dyspepsia  and  anorexia 
appear.  The  cough  is  dry,  and  recurs  in  fits.  The  expectoration,  at  first 
fro  liy  becomes  greenish  and  purulent,  and  the  sputum  is  often  streaked 
with  blood.  The  signs  of  pulmonary  tuberculosis  in  its  first  stage  are  found 
--namely,  slight  induration  at  one  apex,  with  harsh  breathing  and  some- 
times prolonged  expiration.  A  rise  of  temperature  to  102°  F.,  with  or  without 
niglit  sweats,  may  be  noted;  sometimes,  also,  pleurisy,  with  or  without 
eftusion,  may  occur.  In  some  patients  haemoptysis  is  rare,  and  the  signs 
"t  l>ronchitis  are  most   prominent.      The  cough   is  Licessant,  and  suffo- 

14 


210  TEXT-BOOK  OF  MEDICINE 

cation  i.  intense,  especially  during  the  night.  Indeed,  ;«->-  °|;>;*; 
asthma  "  (Benon)  are  seen ;  the  breathlessness  diminishes  durmg  the  day, 
bnt  3y  f  the  patient  makes  no  active  efforts.  The  .putum  is  greeni^. 
Z2nt  and  sometimes  nummular.  During  the  attaclcs  a  brmtd.  tempete, 
wMi  norh  g  sibilant  and  subcrepitant  rales,  is  heard  ;  between  the  attacks, 
r™ptom  of  puhnonary  induration  at  the  apex  of  the  lung  may  be  found. 
nrrruK  the  other  organs  are  healthy,  the  liver  and  spleen  bemg 

'■^Ihe'ci" -the  disease  is  not  always  progressive,  and  slight  improve 
ment  of  variable  duration  may  alternate  with  transient  ^W^^f^^,  ^^^ 
fe  not  as  in  ordinary  tuberculosis,  a  gradual  and  progressive  extensKin  of  the 
ons  After  a  period  of  transitory  cachexia,  the  patients  regain  tlieir  good 
condition,  and  sometimes  resemble  tubercular  patieii  s  ->}^f^l^l 
would  not  be  considered  sick  if  auscultation  were  not  performed  Retro 
Session  is  therefore  nearly  always  the  rule  -the  aspergiU,^  g-duaUy  d^ 
Ippears  from  the  expectoration,  and  a  definite  cure  may  be  caused  by 
fibrosis,  as  is  seen  in  the  case  of  animals.  j  ti,„  1„„<,<,  bv  Koch's 

The  most  formidable  complication  is  the  mvasion  of  the  lungs  by  K-och  s 
bacUlus,  which  gradually  takes  the  place  of  the  f™S- ■  t^^^;--  ^^^^ 
that  of  an  ordinary  pulmonary  tuberculosis,  accompanied  by  local  lesions, 

:  aiialt^ulalrUaneouftuberculosis.    Thisfibro-plast.^^^^^^^^^ 
asnerdUus   however,  helps  the  struggle  against  the  new  parasite    but  the 
cS   access  ma;  overshoot  the  mark,  and  m  one  case  Reiion  and  bergent 
h^ve  notTd  that  fibrosis  became,  in  its  turn,  the  chief  complication,  and 
the  patient  died  of  dilatation  of  the  heart,  with  asy.stole. 

The  duration  of  aspergillary  tuberculosis  is  very  long ;  it  has  lasted 
three  six  eight  years  and  more  in  the  cases  that  have  so  far  been  observed 

Th  iSfc  /««>«-  niay  not  harm  the  lung,  and  may  only  mvade 
the  bronchial  system.  The  result  is  a  peculiar  --''-»-  —^• 
which  was  essentially  chronic  in  the  two  known  case.  J^'^^^^™  ' 
composed  solely  of  mycelium  and  spores  were  situated  in  ^"^^  »  ««  ~ 
and  expelled  almost  every  month,  with  a  crisis  of  acute  dyspncea  (Obici, 

''"D^gTosUr-^^trLportant  to  make  an  early  diagnosis,  but  this  is  im- 
possMe'by  clinical  methods  alone.  We  should  think  of  the  asperg"  ; 
hi  a  patient  who  has  tubercular  lesions,  recognized  as  such  by  physical 
xam!:ation,  the  course  of  events  is  slow  and  the  general  heathremams  goo  ^ 
The  probability  will  become  much  greater  if  the  patient  be  exposed  in 
hfs  work  to  handlmg  gram  or  flour  (pigeon-feeders,  hair-combers   miller 

edimen.  etc.) ;  and  it  will  become  a  certainty  if  Koch's  bacillus  be  absent 
fromThe  sputim  and  the  mycelium  be  present.  The  diagnosis,  thereforp 
entirely  rests  on  bacteriological  exammation. 


DISEASES  OF  THE  LUNG  211 

In  searching  for  the  bacilli,  the  Ziehl-Kiihne  method  should  be  employed. 
If  the  result  ls  negative,  we  must  prove  the  absence  of  the  bacilli  by  inocula- 
tion of  a  guinea-pig  with  the  sputum.  If  thirty  or  forty  days  afterwards 
the  animal  presents  no  tubercular  lesion  (verified  bacteriologically)  at  the 
point  of  inoculation,  the  question  is  decided  :  it  is  not  a  case  of  Koch's 
tuberculosis. 

The  search  for  fragments  of  mycelium  in  the  sputum  should  be  made 
with  an  aqueous  solution  of  safTranin,  or,  better  still,  by  staining  with 
thionin.  If  the  search  is  negative,  recourse  may  be  had  to  cultures.  If 
it  is  positive,  the  same  procedure  should  be  employed,  to  make  certain  that 
the  fragments  are  really  those  of  the  aspergillary  mycelium.  The  fresh 
sputum,  collected  aseptically,  should  be  sown  in  tubes  of  sterilized  Raulin's 
liquid,  and  placed  in  an  oven  at  98°  F.  If  the  sputum  contains  spores  or 
mycelium,  we  shall,  by  the  second  day,  see  that  isolated  filaments,  which  are 
united  into  a  tuft  of  mycelium,  rise  up  from  the  sown  particle ;  the 
mycelium  will  rise  gradually,  and  take  from  three  to  six  days  to  reach  the 
surface.  Some  hours  later  it  will  form  a  whitish,  velvety,  and  absolutely 
characteristic  carpet,  which  twenty  hours  later  is  covered  with  greenish 
spores,  that  assume  a  smoky-black  colour  in  a  few  days.  We  must  then 
verify  the  pathogenic  action  of  the  fungus  thus  found  on  the  rabbit,  and 
absolutely  prove  the  Aspergillus  fumigatus,  since  the  two  other  species, 
Aspergillus  niger  and  Aspergillus  glaucus,  which  develop  under  these  con- 
ditions, are  non-pathogenic.  The  animal  will  succumb  in  a  few  days  to  a 
generalized  aspergillary  tuberculosis  of  all  the  viscera,  but  especially  of  the 
kidneys,  and  a  fragment  of  the  latter  organ,  sown  in  a  tube  of  Raulin's 
liquid,  will  in  five  or  six  days  reproduce  a  culture  of  the  Aspergillus  fumi- 
gatus. The  cycle  will  be  complete,  and  absolutely  no  room  will  be  left 
to  doubt  the  existence  of  the  fungus  in  the  sjiutum. 

We  can  thus  eliminate  asthma,  chronic  bronchitis,  and  Koch's  tuber- 
culosis. The  pseudo-tuberculosis  produced  by  the  Rhizomucor  parasiticus 
(Lucet  and  Constantin)  closely  resembles  aspergillosis  ;  minute  examination 
of  the  parasite  found  in  the  sputum  and  cultures  will  alone  prevent  error. 
Actinomycosis  of  the  apex  of  the  lung  is  often  accompanied  by  chocolate- 
coloured  expectoration,  which  consists  of  a  mixture  of  blood  and  pus  ;  the 
peculiar  grains  of  the  actinomyces  arc  found  in  it.  In  the  exceptional  cases 
of  puhuonary  mycosis,  due  to  Eppinger's  streptothrix,  the  form  of  the 
mycelium  in  the  sputum  is  different,  and  cultures  decide  the  question. 

Prognosis.— The  prognosis  of  aspergillary  pseudo-tuberculosis  is  rela- 
tively good  ;  this  does  not  obtain  in  pseudo-tuberculosis  complicated  by 
Koch's  bacillus.  The  remissions  arc  less  frequent  and  less  prolonged  ;  the 
puhuonary  signs  are  more  marked,  and  death  may  supervene  at  a  distant 
date. 

14-2 


212  TEXT-BOOK  OF  MEDICINE 

Pathological  Anatomy. — ^When  aspergillary  pseudo-tuberculosis  is 
secondary,  and  occurs  as  a  complication  of  chronic  bronchitis  or  of  previous 
pulmonary  tuberculosis,  it  is,  as  a  rule,  a  post-mortem  discovery  :  small 
velvety,  greenish,  or  brownish  tufts,  composed  of  adherent  mycelium,  are 
found.  The  cavity  contains  full-blown  spores.  Outside  this  infiltration 
of  the  walls  of  the  cavities  by  the  fungus  we  may  see  (Lichtheim,  Cohnheim, 
Fiirbinger)  tubercles  of  the  size  of  a  nut  or  of  a  millet-seed,  which,  under  the 
microscope,  show  an  abundant  mycelium  extending  from  the  tubercle  to  the 
alveoli. 

The  lesions  of  simple  and  primary  aspergillary  pseudo-tuberculosis  have 
been  studied  in  man  (Ribbert,  Boyce,  Saxer),  and  also  in  animals  (Dieulafoy, 
Chantemesse  and  Widal,  Ribbert,  Renon,  Obici,  Saxer).  Microscopically 
there  is  no  difference  between  the  tubercle  due  to  the  aspergillus  and  that  due 
to  Koch's  bacillus.  In  pigeons  the  lesions  affect  especially  the  lung  and 
the  liver  ;  in  rabbits  they  affect  the  kidneys  ;  and  pleurisy,  enteritis  with 
perforation  of  the  gut,  peritonitis,  cystitis,  and  osteitis  of  the  vertebrae, 
with  congestive  abscess,  simulating  Pott's  disease,  may  be  noted.  All  these 
lesions  are  tubercular  in  form.  The  mycelium  is  passed  in  the  urine,  when 
the  renal  changes  are  marked  (Renon). 

The  tubercles  vary  in  size  from  a  pin's  head  to  a  small  pea  ;  they  may 
undergo  vitreous  degeneration  and  calcification,  with  formation  of  true 
cavities  ;  at  other  times  we  find  a  tubercular  infiltration  en  nappe.  Asper- 
gillary tuberculosis  may  pass  into  a  fibrous  condition,  which  is  one  of  its 
active  modes  of  cure.  This  process  is  also  seen  in  man,  even  when  bacil- 
losis  is  present  as  a  complication.  At  the  autopsy  of  a  pigeon-feeder, 
affected  in  succession  by  these  two  maladies,  Renon  and  Sergent  noted 
marked  lesions  of  chronic  pneumonia  ;  the  fibrous  tissue  extended  from  the 
bronchi  to  the  pleura,  choking  the  lung  tissue  proper. 

"  The  histological  lesions  are  in  every  way  comparable  with  those  of 
bacillary  tuberculosis.  In  a  section  of  the  lung  we  see  a  large  number  of 
tubercular  nodules,  surrounded  at  their  periphery  by  giant  cells.  The 
growth  of  these  nodules  can  easily  be  followed.  The  young  ones  are  formed 
by  an  agglomeration  of  leucocytes  or  of  epithelial  cells  around  one  or  several 
branches  of  mycelium.  The  older  granulations  present  in  their  centra  a 
feltwork  of  mycelium,  the  interlacing  branches  of  which  stain  better  at  the 
periphery,  in  the  immediate  neighbourhood  of  the  giant  cells.  In  certain 
cases  the  tubercle  is  solely  represented  by  a  very  large  cell  with  multiple 
nuclei ;  while  the  protoplasm  contains  a  ramification  of  mycelium,  either 
alive  and  well  stained,  or  altered  in  structure:  moniliform,  unstained,  and 
partly  digested  by  phagocytes  "  (Dieulafoy,  Chantemesse  and  Widal).  In 
chronic  cases  we  sometimes  find  in  the  tubercle  tufts  of  abundant 
mycelium,  presenting  a  great  likeness  to  actinomycosis  (Laulanie,  Renoi 


DISEASES  OF  THE  LUNG  213 

Ribbert,  Boyce)  and  to  the  actinomycotic  forms  of  Koch's  bacilhis 
(Renon). 

Indeed,  according  to  the  German  school,  the  fungus  plays  the  chief  part  in 
the  production  of  the  histological  lasions  in  the  human  lung.  The  aspergillus 
is  said  to  provoke  foci  of  necrosis,  which,  by  elimination  of  their  con- 
tents, cause  cavities.  This  process  is  said  to  be  specific  (Saxer).  We  see, 
however,  that  two  at  first  irreconcilable  opinions  are  almost  brought  into 
harmony,  although  the  primary  pathogenic  action  of  the  parasite  has 
remained  a  subject  of  active  discussion. 

Treatment. — ^The  treatment  is  symptomatic  and  general.  Haemor- 
rhage must  be  treated  by  the  means  given  under  Pulmonary  Tuberculosis. 
Bronchitis  may  be  alleviated  with  creosote  and  terpene,  and  tincture  of 
lobelia,  with  iodide  of  potash,  which  has  given  fail-  results  in  animals,  should 
be  employed  for  the  attacks  of  suffocation  (Rer.on).  The  general  condition 
should  be  maintained  by  superalimentation  and  by  large  doses  of  cod-liver 
oil  (.3  to  5  ounces  daily),  and  residence  in  the  country,  at  the  seaside,  or  in 
a  climate  at  high  altitude  should  be  advised. 


XVIII.  CANCER  OF  THE  LUNG. 

etiology. — Cancer  of  the  lung  may  be  primary  or  secondary ;  the 
former  is  rare,  the  latter  common. 

The  growth  is  frequently  secondary  to  cancer  of  the  breast,  which  extends 
to  the  parietal  pleura,  when  the  subpleural  lymphatics  carry  cancer  cells  to 
the  lung.  Tlie  mechanism  is  the  same  in  the  propagation  of  cancers  from 
tlie  mediastinum  to  the  lung. 

Cancer  of  the  lung  is  sometimes  secondary  to  that  of  tlie  abdominal 
organs — glands,  stomach,  intestines,  liver,  and  ovary.  The  spread  of  cancer 
from  these  organs  to  the  lung  takes  place  in  different  ways :  by  venous 
emboli,  following  the  course  of  the  portal  vein,  vena  cava,  right  heart,  and 
pulmonary  artery  ;  by  way  of  the  lymphatics,  the  cancer  reaching  the 
peritoneum  over  the  diaphragm  and  passing  through  this  muscle  by  means 
of  the  lymphatic  communication  existing  between  the  peritoneum  and  the 
pleura,  and  invading  the  visceral  pleura  and  lung.  When  cancer  is  consecu- 
tive to  that  of  the  limbs  or  of  tlie  head,  the  propagation  takes  place  by  the 
venous  (■Jianiicls. 

Pathological  Anatomy. — Cancer  of  the  lung  may  be  lobar  or  diffuse. 
The  lobar  varirty  forms  a  bulky  mass,  which  may  involve  or  comjjress  the 
neighbouring  organs  (tracjiea,  oesophagus,  arteries,  and  veins);  in  tlir 
diffuse  form  th(!  growth  is  (lissimiinated  in  the  form  of  nodules  in  the  deep 
layers,  or  on  the  surface  of  the  organ. 


214  TEXT-BOOK  OF  MEDICINE 

Lobar  cancer  is  usually  primary  and  unilateral.  Diffuse  or  noaular 
cancer  is  nearly  always  secondary,  and  affects  both  lungs  ;  the  cancerous 
nodules  may  be  superficial  (sub pleural)  or  deep  (intrapulmonary).  They 
are  of  all  sizes  ;  some  are  no  larger  than  a  pin's  head,  and  the  condition  is 
called  miliary  carcinosis,  from  its  resemblance  to  tuberculosis  ;  other  nodules 
are  as  large  as  a  pea  or  a  walnut. 

Primary  cancer  nearly  always  assumes  the  encephaloid  form.  Secon- 
dary cancer  is  a  reproduction  of  the  parent  growth,  which  may  be  scirrhous, 
melanotic,  colloid,  or  adenomatous  (Marfan).  The  cancerous  mass  may 
finally  become  softened ;  in  some  cases  it  forms  a  bloody  pulp,  the  elimination 
of  which  may  give  rise  to  a  cavity. 

Microscopic  examination  in  primary  cancer  shows  the  alveoli  blocked  by 
spherical  or  polygonal  cells,  with  large  ovoid  nuclei.  The  alveolar  walls 
are  usually  normal.  "  There  is  no  stroma  of  new  formation  in  cancer  of  the 
lung,  and  it  is  the  fibrous  framework  of  this  organ  which  takes  its  place." 
The  epithelial  origin  has  been  definitely  shown  by  Malassez.  Cancer  arises 
in  the  epithelium  ;  it  is  uncertain  whether  the  bronchial  or  glandular  epi- 
thelium may  not  give  rise  to  it. 

All  the  structures  in  the  mediastinum  may  be  invaded  by  cancer  of  the 
lung.  The  lymphatic  vessels  and  the  corresponding  glands  (cervical  and 
axillary  glands),  especially  the  bronchial  ones,  may  show  simple  inflamma- 
tion or  cancerous  change.  The  pleura  is  usually  i'nvolved  in  cancer  of  the 
lung ;  the  result  is  pleurisy,  with  effusion,  which  is  very  often  haemorrhagic 
(see  Haemorrhagic  Pleurisy). 

Description. — In  a  description  of  cancer  of  the  lung  it  is  necessary  to 
distinguish  the  symptoms  which  properly  belong  to  it  from  those  which 
depend  on  invasion  of  the  mediastinum  and  of  the  pleura  ;  this  distincstion, 
however,  is  very  difficult,  for  cancer  rarely  remains  confined  to  the  lung 
without  affecting  the  pleura  or  the  glands  of  the  mediastinum. 

The  symptoms  proper  to  cancer  of  the  lung  are  somewhat  limited.  The 
patient  complains  of  pain  (pain  in  the  side,  which  may  or  may  not  be  radi- 
ating) of  increasing  intensity ;  the  pahi  may  be  brachial,  cervical,  or  inter- 
costal, and  accompanied  by  zona.  Cough  is  a  usual  symptom.  Dyspnoea 
may  be  slight,  severe,  continuous,  or  paroxysmal,  with  or  without  stridor, 
depending  on  the  multiplicity  of  its  causes.  Compression  of  the  trachea 
and  the  bronchi,  compression  of  the  vagus  and  recurrent  nerves,  lesions  of 
thejpleura,  and  pleural  effusion,  may  all  cause  dyspnoea. 

Haemoptysis  is  fairly  frequent,  and  some  authors  have  given  as  charac- 
teristic the  currant- jelly-like  expectoration  which  contains  cancer  elements 
and  elastic  fibres  from  the  lung.  I  have  lately  seen  a  typical  case  of  tliis 
expectoration,  with  Dr.  Marcano,  in  cancer  of  the  lung,  secondary  to  that  of 
the  breast.     According  as  the  cancer  is  lobar  or  diffuse,  the  dulhiess  yields 


DISEASES  OF  THE  LUNG  215 

more  or  less  precise  information  ;  auscultation  may  sometimes  show  tubular 
breathing  and  bronchophony. 

When  the  bronchial  glands  are  invaded  by  cancer,  the  symptom-complex, 
which  we  shall  study  under  Tumours  of  the  Mediastinum,  is  found.  I  shall 
here  simply  mention  two  of  these  symptoms  :  paroxysmal  or  intermittent 
dyspnoea  (compression  of  the  vagus  and  phrenic  nerve)  and  cough,  which 
is  often  analogous  to  the  fits  of  whooping-cough. 

The  cancerous  mass  may  also  cause  compression  of  one  recurrent  nerve 
(dyspncea  and  spasm  of  the  glottis),  of  the  oesophagus  (dysphagia),  or 
of  the  venous  channels  (oedema  of  the  face  and  neck  and  supplementary 
circulation). 

It  sometimes  happens  that  acute,  subacute,  or  latent  pleurisy  masks 
the  development  of  cancer  of  the  lung  ;  the  patient  only  complains  when 
dyspnoea,  due  to  effusion  or  to  other  causes,  has  become  severe.  Pleurisy  is 
discovered ;  thoracentesis  ls  performed,  and  fluid,  which  is  most  frequently 
blood-stained,  is  drawn  of?  ;  and  yet,  in  spite  of  the  operation,  pain,  cough, 
and  dyspnoea  continue.  I  have  seen  several  cases — one,  among  others, 
with  Dr.  Auburtin.  The  patient  had  a  considerable  pleural  effusion.  I 
evacuated  seven  pints  of  blood-stained  fluid  in  four  sittings.  The  im- 
provement was  of  short  duration,^  and,  though  the  effusion  did  not 
recur,  the  cancer  continued  its  progress.  In  one  of  the  following 
sections  we  shall  see  the  importance '  of  haemorrhagic  pleurisy  in 
cancer. 

After  a  duration  of  from  one  month  to  two  years,  cancer  ends  in  death. 
Death  which  supervenes  from  increasing  dyspnoea  and  asphyxia  is  terribly 
painful ;  injections  of  morphia  are  in  such  cases  the  only  palliative.  Rapid 
or  even  sudden  death  has  often  been  noted.  In  other  cases  the  patient 
dies  in  a  state  of  asystole,  with  general  oedema,  cyanosis,  and  coma.  Some- 
times hectic  fever  supervenes  and  ends  the  scene. 

The  diagnosis  of  cancer  of  the  lung  presents  serious  difficulties,  especially 
when  it  is  primary  and  runs  an  acute  course.  We  are  so  used  to  the  slow 
progress  of  cancer,  to  the  gradual  breaking-up  of  the  individual,  and  to  the 
characteristic  colour  of  the  skin,  that  the  diagnosis  is  often  at  fault  when 
cancer  runs  an  acute  course.  This  acute  course  is  not  rare  in  cancer  of  the 
lung.  An  individual  in  good  health  shows  symptoms  which  might  quite 
well  be  put  down  to  acute  phthisis.  He  dies  in  a  few  weeks,  and  cancer  of 
the  lung  is  found  post  mortem. 

In  doubtful  cases  we  must  never  omit  to  look  for  cancer  in  other  organs — 
e.g.,  cancerous  nodules  under  the  skin,  cancer  of  the  liver,  rectum,  testis,  or 
uterus.  A  previous  operation  or  the  presence  of  a  scar  (breast)  may  give  a 
clue.  I  have  twice  seen  cancer  of  the  lung  in  patients  wiio  liad  undergone 
operation — the  one  for  disease  of  the  left  testis,  the  other  for  an  osteo- 


216  TEXT-BOOK  OF  MEDICINE 

sarcoma  of  the  knee.*  It  is  also  necessary  to  make  sure  of  the  condition  of 
the  corresponding  axillary  or  cervical  glands  ;  this  evidence  of  cancer, 
although  inconstant,  is  none  the  less  valuable  when  it  exists. 

XIX.  BRONCHO-PULMONARY  LITHIASIS. 

Pathological  Anatomy  and  Pathology. — "  Lung  stones,"  or  broncho- 
pulmonary lithiasis,  has  been  well  described  by  Poulalion.  From  the  histo- 
logical point  of  view,  they  may  be  divided  into  three  categories — cartilagi- 
nous or  cartilaginiform,  bony,  and  calcareous  bodies.  We  must  also  differ- 
entiate the  growths  and  the  changes  which  take  place  in  the  thickness  of 
the  broncho-pleuro-pulmonary  tissues,  and  constitute  parenchymatous, 
cartilaginous,  bony,  or  calcareous  concretions,  from  those  which  occur  in 
the  Ulterior  of  normal  or  accidental  cavities  in  the  respiratory  system,  and 
are  always  calcareous  in  nature,  constituting  calculi,  properly  speaking 
(broncholiths). 

1.  The  cartilaginous  or  cartilaginiform  growths  are  made  up  of  carti- 
laginous or  other  dense  fibroid  tissue  ;  they  may  be  situated  in  the  walls  of 
the  bronchi,  in  the  pleura,  or  in  the  lung  tissue.  They  have  the  appear- 
ance of  cartilage,  and  are  resistant,  elastic,  whitish,  opaline,  and  of  a  bluish 
sheen. 

2.  Bony  growths  are  characterized  by  the  existence  of  osteoblasts  and 
the  presence  of  newly-formed  Haversian  canals.  These  bony  calculi  arise 
in  ossified  bronchial  cartilages  (bronchial  dilatation,  pulmonary  phthisis),  in 
ossifications  of  the  tracheo-bronchial  mucosa,  in  ossifications  of  the  pleura, 
developed  in  the  fibrous  shell  of  old  pleurisies. 

3.  Calcareous  growths  result  from  calcification  of  the  different  tissues 
in  the  respiratory  system,  by  incrustation  with  particles  of  tribasic  phos- 
phate of  lime  and  carbonate  of  lime.  Among  the  lesions  of  the  lung  which 
may  undergo  calcareous  transformation  we  must  notice,  m  the  first  place, 
the  caseous  tubercle,  then  infarcts,  broncho-pneumonic  nodules,  miliary 
abscesses,  pseudo-tubercles  of  actinomycosis  or  of  the  aspergillus,  and, 
lastly,  cysts  and  tumours  of  the  lung. 

The  lung  may  only  contain  some  isolated,  calcareous  concretions,  as  is 
the  case  in  the  caseous  nodules  of  ordinary  tuberculosis  which  is  in  process  of 
cicatrization  and  cure.  At  other  times,  on  the  contrary,  the  concretions 
are  in  considerable  number,  and  the  lung  tissue  is,  as  it  were,  riddled  by 
them  ;  this  condition  is  called  calcareous  granulosis  of  the  lung  (Poulalion). 

The  parenchymatous  concretions  may  become  stationary  and  remain 
latent,  but  in  other  cases  they  may  undergo  a  process  of  enucleation  which 

*  This  i:)atient,  whom  I  saw  with  Dechambre,  was  suffering  from  cancer  of  the  upper 
left  lobe,  which  presented  the  appearance  of  encysted  pleurisy. 


DISEASES  OF  THE  LUNG  217 

causes  their  migration  into  the  tissues,  and  generally  ends  by  their  passing 
into  the  air-passages. 

Intracavitary  calculi  present  the  most  marked  analogy  with  biliary 
and  urinary  calculi ;  they  may,  like  the  latter,  have  as  their  nucleus  of 
origin  foreign  bodies  from  wathout,  or  parenchymatous  concretions  which 
have  been  set  free  ;  they  are  formed  in  the  bronchial  channels,  or  in  cavities 
accidentally  developed. 

Symptoms. — In  some  cases  broncho -pulmonary  lithiasis,  especially  in 
its  parenchymatous  forms,  may  be  latent,  and  only  be  discovered  post 
mortem.  As  a  rule,  the  presence  of  calculi  in  the  respiratory  passages  pro- 
duces troubles  similar  to  those  which  occur  in  the  biliary  or  in  the  urinary 
tracts.  True  crises  of  bronchial  and  pulmonary  colic  occur.  Sometimes 
the  expulsion  of  the  concretion  takes  place  without  the  patient  perceiving 
it,  and  he  expectorates  the  calculus  while  coughing  ;  at  other  times,  on  the 
contrary,  as  happened  to  a  patient  in  my  wards,  the  expulsion  is  preceded  by 
heaviness,  dyspnoea,  pain,  constriction,  anguisli,  and  a  feeling  of  tearing, 
either  in  the  sternal  region  or  at  the  sides  of  the  chest.  Thene  pains  are 
almost  always  followed  by  obstinate,  jerky  cough,  during  which  the  patient 
suddenly  experiences  a  sharp,  tearing  sensation  in  the  larynx,  and  increase 
of  the  dyspnoea,  followed  immediately  by  the  expulsion  of  a  hard  body, 
which  may  strike  against  the  back  of  the  incisor  teeth.  The  expectoration 
of  the  calculas  being  accomplished,  the  bronchial  COlic  ends,  and  the 
cough  and  pain  frequently  yield  at  the  same  time.  Sometimes  it  is  only  a 
case  of  abortive  bronchial  colic  ;  the  patient,  while  coughing,  experiences 
a  painful  sensation  or  feeling  of  a  foreign  body  rising  in  the  trachea,  and 
then  passing  back  again  into  the  bronchi  and  lung.  The  duration  of  the 
crisis  is  very  variable.  It  may  last  a  few  moments,  or  even  some  hours — as 
many  as  forty-eight  (Poulalion).  The  number  and  size  of  the  calculi  brought 
up  are  also  variable  ;  as  many  as  400  have  been  counted,  and  may  be  as 
large  as  a  ])in's  head,  a  millet-seed,  or  a  nut. 

Tlie  expectoration  of  calculi  is  often  accompanied  by  Imemoptysis,  which, 
tliough  generally  slight,  is  sometimes  fulminant ;  the  bleeding  may  precede  the 
expectoration  of  the  calculus  by  some  days,  but  as  a  rule  accompanies  it. 

We  may  see  fever  due  to  neighbouring  inflammation,  or  to  the  action  of 
the  calculus  on  the  altered  mucosa,  with  consecutive  absorption  of  septic 
products.  PLxamination  of  the  chest  before,  during,  or  after  the  crisis 
most  often  yields  but  trifling  information  ;  bronchitic  rales  are  heard,  and 
it  is  only  in  obstruction  of  a  large  bronchus  by  a  concretion  that  we  can 
recognize  behjw  the  obstacle  more  or  less  extensive  absence  of  breath- 
sounds. 

Br()ncho-])ulnionary  lithiasis  may  ofcur  in  the  course  of  tnborculosis, 
and  favour  the  development  of  the  latter  trouhle. 


218  TEXT-BOOK  OF  MEDICINE 

In  other  cases  the  chronic  course  of  lithiasis  simulates  phthisis,  although 
absolutely  no  tuberculosis  is  present ;  this  is  known  as  pulmonary  pseudo- 
phthisis  of  calcareous  origin  (Poulalion).  During  a  more  or  less  lengthy 
period  the  patient  suffers  from  cough,  which  is  at  first  dry,  but  later  is  accom- 
panied by  mucous  or  muco-purulent  sputum.  These  symptoms  become 
worse  ;  signs  of  induration,  of  pulmonary  congestion,  or  of  localized  bron- 
chitis, aiad  even  those  of  small  cavities,  are  often  found.  The  general  con- 
dition becomes  bad  ;  wasting  and  night-sweats  appear.  Haemoptysis  is 
common.  The  attention,  however,  is  chiefly  attracted  to  the  dyspnoea  and 
the  pain ;  both  come  on  in  more  or  less  intense  attacks,  until  in  a  more 
violent  fit  of  coughing  than  usual  the  patient  brings  up  the  calculus,  with 
or  without  haemoptysis.  The  symptoms  now  show  marked  improvement, 
when  only  one  calculus  exists ;  but  the  relief  is  temporary  when  there  are 
several  calculi,  and  their  expulsion  is  always  preceded  by  a  period  of  aggrava- 
tion.    In  this  form  Koch's  bacilli  are  never  found  in  the  sputum. 

Cure  is  the  rule  when  there  are  no  complications.  As  complications,  I 
may  note  acute  bronchitis,  which  generally  ends  favourably ;  pleuro- 
pneumonia, which  is  often  fatal ;  abscess  of  the  lung,  which  sometimes  opens 
up  the  bronchi,  or  ends  in  perforation  of  the  pleura  and  pyopneumothorax. 
Sudden  death  from  obstruction  of  a  large  bronchus  by  a  calculus  has  been 
noted  (Tice). 

Diagnosis. — The  diagnosis  is  almost  always  impossible  before  expulsion 
of  the  calculus.  Cough,  dyspnoea,  and  pain  in  the  chest  are  quite  insufficient 
signs,  and  the  rejection  of  the  calculus  must  be  waited  for.  We  must  then 
ascertain  whether  the  patient  is  tubercular  or  not,  and  whether  the  con- 
cretion is  of  intraparenchymatous  or  intracavitary  origin.  Examination 
of  the  sputum  for  bacilli  and  inoculation  of  the  guinea-pig  will  help  to 
decide  the  first  point ;  as  regards  the  second,  histological  examination  of  the 
cut  section  will  establish  it. 

The  differential  diagnosis  must  be  made  from  fragments  of  bone  that 
are  coughed  up,  but  do  not  come  from  the  respiratory  system ;  from 
portions  of  the  vertebrae  in  Pott's  disease  (Chenieux) ;  from  a  sequestrum 
from  the  larynx  ;  calcareous  concretions  formed  in  the  ventricles  of  the  larynr 
(Pravaz) ;  concretions  from  the  crypts  of  the  tonsils ;  rhinoliths  which  have 
fallen  into  the  pharynx ;  and,  lastly,  foreign  bodies  which  have  reached  the 
lung  from  without. 

The  prognosis  of  calculous  pseudo-phthisis  is  not  grave  when  the  patient 
brings  up  the  foreign  body ;  yet  apart  from  the  complications  mentioned 
above,  the  prognosis  is  much  affected  by  the  weakened  condition  of  the  lung 
and  the  possible  development  of  tuberculosis. 

Treatment  can  only  be  symptomatic ;  surgical  intervention  appear^ 
hardly  possible,  because  precise  indications  are  wanting  as  to  the  seat  of  the 


DISEASES  OF  THE  LUNG  219 

calculus.  If  calcareous  change  in  tubercles  is  favourable  to  their  cure  we 
should  assist  this  calcification  by  the  use  of  soluble  phosphates  and  by 
nourishment  which  contains  much  vegetable  matter. 


XX.  HYDATID  CYSTS  OF  THE  LUNG  AND  OF  THE 

PLEURA. 

Pathological  Anatomy. — In  frequency  hydatid  cysts  of  the  lung  come 
next  to  those  of  the  liver — that  is  to  say,  we  see  them  fairly  often.  As  I 
have  described  in  detail  (see  Liver)  the  life  history  of  the  hydatid,  I  shall 
here  notice  only  the  characters  peculiar  to  hydatid  of  the  lung. 

The  cyst  usually  affects  the  right  base.  It  is  sometimes  associated  with 
a  cyst  in  the  liver.  The  pulmonary  cyst  is  unilocular,  the  alveolar  cyst 
being  extremely  rare.  In  order  to  reach  the  lung,  the  embryo  follows 
various  routes.  It  may  enter  the  respiratory  tract  by  aspiration  of  dust ; 
it  may  be  ingested  with  food  and  drink,  pass  from  the  intestine  into  the 
portal  veins,  traverse  the  liver,  the  subhepatic  veins,  the  vena  cava,  and  the 
heart,  to  be  arrested  in  the  lung.  The  embryo  may  perhaps  enter  the 
ha?morrhoidal  veins,  pass  tlirough  the  pudic  and  the  internal  iliac 
veins,  reach  the  inferior  vena  cava,  without  passing  into  the  liver 
(Chachereau),  and  travel  through  the  heart  into  the  lung.  In  the  case 
of  coexistence  of  hydatid  of  the  liver  and  of  the  lung,  it  may  be  asked  if 
the  embryo  has  not  migrated  directly  from  the  one  organ  to  the  other. 

The  adventitious  covering  of  hydatid  cysts  of  the  lung  is  very  thin  ; 
it  may  be  completely  absent,  and  this  fact  will  explain  why  the  cyst  so 
readily  opens  into  the  bronchi.  Hydatid  cysts  of  the  pleura  are  rare,  unless 
the  pleura  has  been  invaded  secondarily  by  a  pulmonary  cyst. 

Description. — As  the  lung  is  less  tolerant  than  the  liver,  the  early 
growtli  of  the  pulmonary  cyst  is  rarely  quite  latent.  In  the  liver,  cysts  may 
be  present  for  a  long  while  and  may  attain  large  proportions  without  pro- 
ducing symptoms  or  results ;  enlargement  of  the  right  hypochondrium  is 
sometimes  the  first  sign  of  the  hydatid  cyst.  In  the  lung,  on  the  other  hand, 
it  is  exceptional  for  the  hydatid  to  remain  quiet  long  ;  indeed,  its  presence 
may  be  revealed  early  by  important  symptoms,  of  which  haemoptysis  is  the 
most  striking. 

Period  of  Onset. — Dry,  jerky  cough  may  be  the  only  symptom  for 
weeks.  It  is  the  result  of  a  reflex,  and  simulates  the  cough  of  tuberculosis, 
with  this  difference,  however — that  the  cough  in  tuberculosis  is  almost 
always  followed  by  some  ex})ectorati()n. 

The  pain,  which  is  rarely  sharp  at  this  stage,  may  simulate  pleuritic 
pain  or  intercostal  neuralgia  ;  in  some  cases  it  is  obstinate,  and  radiates  into 
the  neck,  the  shoulder,  and  the  epigastrium. 


220  TEXT-BOOK  OF  MEDICINE 

Dyspnoea  is  present  at  an  advanced  stage  of  the  malady,  and  in  com- 
plications ;  although  it  is  rare  during  the  early  growth  of  the  hydatid,  it  has 
been  noted  in  some  cases. 

Haemoptysis,  from  its  importance  and  its  frequency,  deserves  careful  atten- 
tion, and,  while  it  may  be  either  slight  or  severe,  and  more  or  less  repeated, 
plays  a  large  part  in  the  history  of  pulmonary  hydatids.  Early  haemoptysis, 
arising  at  the  onset  of  the  malady — before  any  other  symptom,  indeed — and 
late  haemoptysis,  coincident  with  the  opening  of  the  cyst,  are  both  seen. 

Early  haemoptysis  comes  on  as  a  precursory  sign  in  this  disease,  as  in 
many  pulmonary  affections.  It  is,  indeed,  remarkable  that  the  first  cry 
of  revolt  on  the  part  of  the  lung  against  the  invader  is  perhaps  a  means 
of  defence.  Since  phagocytosis  is  insufficient  to  meet  the  attack,  the  vessels 
take  part,  and  it  may  be  said  that  the  lung  seeks  to  get  rid  of  its  adversary 
by  the  ejaculation  of  blood  ;  it  sometimes  succeeds,  and  the  haemoptysis, 
having  no  ill  results,  is  then  termed  "  essential." 

I  have  named  this  early  haemoptysis  "  defensive."  It  is  very  frequent 
in  pulmonary  tuberculosis ;  tubercular  haemoptysis  may,  indeed,  arise  in 
the  course  of  apparently  excellent  health,  when  no  suspicion  of  tuberculosis 
exists.  Parents  who  have  suffered  from  haemoptysis  may  beget  tubercular 
children,  although  the  former  may  have  had  no  other  sign  of  tuberculosis 
than  the  haemoptysis,  which  has  left  no  traces. 

We  also  find  early  haemoptysis  in  false  pulmonary  tuberculosis  ;  I  have 
seen  it  many  times  in  pigeon-feeders  affected  with  aspergillary  tuberculosis 
{vide  Chapter  IV.,  section  xvii.). 

Early  haemoptysis  is  also  seen  in  patients  with  broncho-pulmonary 
concretions,  who  are  suspected  of  tuberculosis,  until  they  bring  up  the 
concretions  during  an  attack  of  bronchial  colic.  Hydatid  cysts  of  the  lung 
especially  provoke  early  haemoptysis,  as  will  be  seen  from  the  following 
examples,  taken  from  my  clinical  lecture  on  the  subject  :*- 

A  case  sent  to  me  by  Dr.  Leroy : 

On  May  22,  1898,  the  first  haemoptysis  came  on,  without  appreciable  cause,  and  a 
so-called  pleuritic  pain  appeared  on  the  right  side.  Four  months  later  fresh  haemoptysis 
(about  a  pint  of  bright  frothy  blood)  suddenly  took  place  ;  obstinate  cough  supervened, 
and  the  patient  was  convinced  that  he  had  tuberculosis.  He  was  treated  without 
success,  for  his  strength  gradually  decreased.  At  intervals  pain  reappeared  on  the 
right  side  ;  appetite  diminished,  and  six  months  later  he  had  lost  32  pounds  in  weight. 

Next  year  the  same  symptoms  were  present :  frequent  fits  of  coughing,  and  further 
spitting  of  blood.  Four  large  hsemoptyses  were  recorded.  On  each  occasion  the 
haemoptysis  was  treated  with  ergotin,  Rabel -water,  and  applications  of  ice,  with  absolute 
rest  in  bed.  Each  bleeding  left  the  patient  still  more  feeble  ;  though  he  had  no  fever, 
he  coughed  continually.  The  situation  became  worse,  and  the  diagnosis  of  haemoptoic 
tuberculosis  appeared  no  longer  doubtful. 

*  Dieulafoy,  "  Les  Hemoptysies  des  Kystes  Hydatiques  du  Poumon  "  {Clinique 
Medicale  de  r Hotel -Dieu,  Paris,  1905),  16'"'^levon. 


I 


DISEASES  OF  THE  LUNG  221 

A  decisive  incident,  however,  revealed  the  true  nature  of  the  affection.  On  Novem- 
ber 12,  1899,  the  cough  became  more  violent  than  ever,  and  he  coughed  up  much  blood- 
stained sputum  and  a  large  piece  of  hydatid  membrane.  The  thoracic  pain,  the  cough, 
the  numerous  haemorrhages,  were  due,  not  to  tuberculosis,  but  to  a  hydatid  cyst  of  the 
lung,  which  had  previously  given  no  definite  sign. 

The  expulsion  of  hydatid  membranes  and  the  attacks  of  haemoptysis  recurred  on 
several  occasions.  The  .expulsion  of  hydatid  membranes  was  almost  always  heralded, 
twenty-four  hours  in  advance,  by  fits  of  coughing  and  by  more  or  less  abundant  haemop- 
tysis. On  the  other  hand,  some  of  the  haemorrhages  were  not  followed  by  expulsion 
of  hydatid  membrane.  From  March  24,  1900,  to  the  beginning  of  April,  1901,  thirteen 
large  hajmorrhages  were  counted,  without  expulsion  of  pus  or  of  membrane.  They  con- 
tinued during  May,  but  it  was  not  till  August  25  that  pus  and  large  membranes  were 
brought  up.  During  the  last  four  months  of  1901  the  hcPmcrrhages  recurred,  and  were 
always  followed  by  the  coughing  up  of  hydatid  membranes,  with  or  without  purulent 
sputum.  In  1902  haemoptysis,  membranes  coughed  up  ;  from  May  22,  1898,  to  April  12, 
1902,  haemorrhage  on  sixty  different  occasions,  and  membranes  coughed  up  on  forty- 
three.     He  is  now  cured. 

Case  published  by  Laveran  : 

A  soldier,  twenty-six  years  of  age,  was  in  excellent  health  up  to  the  end  of  October. 
He  practised  fencing  a  great  deal,  and  in  the  latter  part  of  October,  during  an  assault-at- 
arms,  he  suddenly  felt  sharp  pain  in  the  chest,  and  brought  up  about  a  tumblerful  of 
bright  red  blood.  After  a  few  days  he  resumed  his  duties,  but  soon  felt  pain  on  both  sides 
of  the  chest,  and  had  fresh  hajmorrhage.  On  December  5  he  was  sent  to  a  military 
hospital,  where  phthisis  was  diagnosed,  and  he  was  invalided  out.  Next  April  the 
cause  of  these  haemorrhages  was  discovered :  the  patient  coughed  up  pus  containing 
hydatid  membranes,  and  thus  got  rid  of  his  hydatid  cyst  seven  months  after  the  first 
spitting  of  blood. 

A  medical  student  has  published  his  own  case : 

After  an  attack  of  pleurisy  the  patient  had  slight  haemoptysis,  in  April.  The  sputum 
was  frothy  and  tinged  with  bright  blood,  while  signs  of  congestion  and  crepitant  rales, 
were  found  at  the  right  apex.  During  May  the  patient  was  treated  with  quinine, 
creasote,  etc.  Fever  app(;ared,  and  he  lost  his  appetite.  On  May  25,  fresh  haemoptysis. 
Finally,  after  a  series  of  troubles,  thought  to  be  tubercular,  in  January  1.3  of  the  next 
year,  he  found  a  piece  of  hydatid  membrane,  2  inches  square,  in  the  sputum. 

Watelet  relates  the  following  case  : 

A  man  of  forty  was  taken  ill  with  haemoptysis  and  wasting  ;  rales  in  tlic  left  lung  ; 
tuberculosis  suspected.  F'our  months  later  fresh  haemoptysis,  foetid  sputujn,  and  expul- 
sion of  enormous  hydatid  membrane. 

Landouzy  writes  : 

A  woman  had  five  ha-morrhages  three  months  before  the  rupture  of  the  pulmonary 
cyst.  The  blood  was  red  and  frothy  ;  the  quantity  about  half  a  tumblerful  on  each  occa- 
sion.    She  had  been  considered  tubercular. 

Fenger  and  Hollister  speak  of  a  patient  who  had  attacks  of  haemoptysis 
for  twelve  years.  Later  he  brought  up  the  cyst ;  pncumotomy  became 
necessary,  and  he  recovered  com})letely. 

In  a  case  of  hydatid  of  the  lung  reported  by  Delgrange  haemoptysis, 
which  was  sometimes  triHing,  sometimes  very  profuse,  persisted  for  five 
months. 


222  TEXT-BOOK  OF  MEDICINE 

In  his  admirable  lecture  on  hydatids  of  the  lung  Trousseau  has  been 
careful  to  say  that  hsemoptysis  has  been  noted  in  almost  every  case,  and, 
among  other  examples,  quotes  Mercier's  case  : 

A  man  was  subject  to  haemoptysis  for  several  years,  but  showed  no  other  signs  of 
tuberculosis  ;  he  was  suddenly  seized  with  acute  pain  in  the  right  side  ;  examination  of 
the  chest  revealed  hydropneumothorax.  Post  mortem  hydatid  of  the  lung  was  foiuid  ; 
it  had  caused  perforation  of  the  pleura  and  ulceration  of  a  bronchus. 

A  gentleman  from  the  Argentine  Republic,  thinking  himself  affected  with  pulmonary 
tuberculosis,  consulted  me  at  the  beginning  of  1902.  He  complained  of  obstinate  cough 
for  two  months  and  frequent  haemoptysis.  No  sputum.  On  auscultation,  I  dis- 
covered no  trace  of  tuberculosis,  neither  rales  nor  dullness  being  present.  Examination 
of  the  sputum  failed  us,  because  the  patient  brought  up  none.  The  appetite  was  bad, 
and  the  man  was  wasting.  I  left  the  diagnosis  open.  After  an  interval  of  some 
weeks  I  saw  the  patient  a  second  and  third  time,  and  the  most  minute  investigation 
revealed  nothing.     The  haemoptysis  continued. 

One  day  the  patient  brought  me  a  bottle  containing  a  cloudy  liquid,  with  a  quantity 
of  hydatid  shreds,  which  he  had  brought  up  during  the  night,  after  terrible  fits  of  cough- 
ing and  of  breathlessness,  which  almost  amounted  to  suffocation.  The  diagnosis  was 
clear,  and  I  took  the  offending  body  to  the  H6tel-Dieu,  telling  my  pupils  the  history 
of  this  patient. 

Hearn,  in  his  work,  which  comprises  144  cases  of  hydatid  of  the  lung, 
gives  prominence  to  the  frequency  of  haemoptysis.  "  In  less  than  a  fifth 
of  my  cases,"  says  he,  "  there  is  no  mention  of  it." 

In  Iceland,  where  hydatid  disease  is  so  frequent,  Finsen  says  that  it  is 
almost  possible  to  diagnose  pulmonary  echinococcus  from  spitting  of  blood. 

Vegar  and  Cranwell,  in  their  monograph  on  hydatid  cysts  in  the  Argentine 
Republic,  say  that  haemoptysis  constitutes  one  of  the  most  important 
symptoms  in  cysts  of  the  lung. 

Widal  has  reported  a  case  of  hydatid  cyst  of  the  lung  in  which  daily 
haemoptysis  without  fever  and  expectoration  remained  the  chief  symptom 
for  four  months. 

To  sum  up,  haemoptysis,  whether  early  or  anterior  to  the  rupture  of  the 
cyst,  presents  different  forms.  In  some  cases  haemoptysis  is  reduced  to  a 
minimum.  We  see  bloody,  brownish,  or  reddish  sputum  of  a  gooseberry 
or  currant  colour.  This  sputum  is  coughed  up,  and  may  recur  several  times 
in  the  day  for  weeks  or  for  months,  with  or  without  periods  of  arrest.  Some- 
times bright  red  blood  is  brought  up  at  more  or  less  definite  intervals  for 
months  or  even  years. 

On  examining  the  cases,  we  see  that  haemoptysis  may  precede  the  other 
signs.  I  think  that  the  embryo  may,  from  the  moment  of  its  fixation  in 
the  lung,  cause  haemoptysis,  and  I  believe  that  haemoptysis  may  be  repeated 
when  the  hydatid  cyst  is  only  as  big  as  a  pin's  head,  a  small  pea,  or  a  nut, 
and  may  go  on  during  the  growth  of  the  cyst  before  its  rupture.  Such  is 
the  early  haemoptysis.     It  is  evident  that  we  must  recognize  it. 

The  above  details  will,  I  think,  suffice  as  regards    early  haemoptysis] 


DISEASES  OF  THE  LUNG  223 

which  accompanies  the  growth  in  the  lung ;  subsequently  we  shall  have  to 
study  the  late  haemoptysis  which  accompanies  rupture  of  the  cyst. 

Let  us  now  consider  pleurisy — a  very  rare  complication,  it  is  true,  but 
one  which  may  nevertheless  supervene  from  the  first. 

It  is  important  to  remember  that  pleurisy  may  supervene  at  the  onset 
of  a  pulmonary  hydatid.  I  do  not  speak,  of  course,  of  hydatid  of  the  pleura, 
which  is  extremely  rare,  as  we  shall  see  later  ;  I  allude  to  those  cases  of 
pleurisy  which  develop  in  the  ordinary  way  from  the  onset  of  the  pulmonary 
cyst.  I  do  not  know  its  exact  pathogeny,  but  it  is  certain  that  pleurisy 
may  develop  in  hydatid  of  the  lung,  as  in  that  of  the  liver — e.g.  : 

A  hospital  attendant,  who  had  been  treated  for  a  month  for  pleurisy,  which  was 
cured,  coughed  up  four  months  later  foetid  sputum  and  hydatid  membranes. 

A  medical  student,  Marconnet,  was  taken  ill  "mith  pleurisy,  which  preceded  the  other 
symptoms  of  hydatid.  "  The  numerous  attacks  of  pleurisy,"  says  Marconnet,  "  from 
which  I  suffered  during  my  disease  were  assuredly  due  to  the  formation  of  the  cyst. 
They  were,  moreover,  so  strange  that  they  puzzled  my  doctors.  The  effusions  dis- 
appeared as  if  by  magic.  If  it  be  admitted  that  my  first  pleurisy  may  have  been 
primary,  and  that  it  was  not  the  result,  but  the  cause,  of  localizing  the  hexacanthus, 
how  can  the  pleurisies  wliich  were  consecutive  to  it  be  explained  ?  Is  it  not  more 
rational  to  consider  that  they  were  all  caused  by  the  parasite  ?" 

Another  medical  student,  Chachereau,  who  also  reported  his  own  case,  suffered  at 
the  age  of  twenty-three  from  pleurisy,  which  was  the  first  symptom  to  appear.  At  the 
end  of  1872  he  suffered  from  left  pleurisy,  with  much  effusion.  Dr.  Leonard!  recognized 
the  gra%nty  of  his  condition,  and  thought  of  puncture.  The  pleurisy  showed  a  most 
insidious  course.  The  effusion  was  absorbed  rapidly,  and  the  other  symptoms  of  hydatid 
made  their  appearance  much  later. 

From  the  first,  hydatid  of  the  lung  may  excite  general  symptoms.  Loss 
of  strength,  anorexia,  and  wasting  have  been  noted  in  a  large  number  of 
cases. 

In  short,  it  is  seen  that,  in  its  first  period,  hydatid  of  the  lung  shows 
its  presence  by  symptoms  which  simulate  pulmonary  tuberculosis  to  such 
an  extent  as  to  be  mistaken  for  it.  A  patient  comes  to  us  with  haemop- 
tysis, and  says  that  for  some  time  past  he  has  been  coughing  and  wasting. 
It  is  quite  natural  to  suppose  the  onset  of  tuberculosis.  However,  he  does 
not  bring  up  sputum,  and  the  rales  are  not  clearly  localized  to  the  apex 
of  the  lung,  while  the  search  for  bacilli  in  the  blood  couglied  up  is  negative. 
This  is  quite  true,  and  yet,  in  the  face  of  repeated  hamoptyses,  cough, 
anorexia,  wasting,  and  attacks  of  pleurisy,  we  cannot  eliminate  the  idea  of 
early  tuberculosis.  Perusal  of  the  reported  cases  shows  that  the  mistake 
has  almost  always  been  made.  In  such  cases  the  sero-diagnosis  of  tuber- 
culosis must  not  be  neglected,  for  a  negative  sero-diagnosis  is  of  great  value. 
Radingraj)liy  may  sometimes  be  of  use. 

Evolution  of  the  Cyst. — We  have  studied  the  onset  of  hydatid  of  the 
lung  ;  let  us  now  follow  the  other  pliases  of  its  growth.  If  the  growing  cyst 
reaches  the  size  of  the  foetal  or  adult  head,  and  spreads  towards  the  walls 


224  TEXT-BOOK  OF  MEDICINE 

of  the  thorax,  they  may  become  arched.  According  to  the  localization  of 
the  cyst,  the  arching  occupies  the  lower,  lateral,  or  upper  part  of  the  chest. 
It  simulates  in  different  cases  intrathoracic  tumour  or  encysted  pleurisy. 
Sometimes  the  cyst,  if  it  be  very  large,  may  simulate  general  pleurisy, 
Examples  of  these  different  varieties  are  as  follows  : 

Moutard-Martin  says  :  "  In  a  patient  who  had  akeady  had  several  attacks  of  ha?mop- 
tysis,  arching  of  the  lateral  and  inferior  part  of  the  thorax  appeared  on  the  left  side. 
This  arching  rose  as  high  as  the  seventh  intercostal  space.  Over  this  area  dullness  was 
complete,  tactile  vibrations  were  abolished,  and  the  normal  vesicular  murmur  was 
replaced  by  tubular  breathing.  With  all  reserve,  it  was  thought  to  be  a  case  of  encysted 
pleurisy.  Thoracentesis  was  performed,  and  it  was  found  that  a  hydatid  cyst  of  the 
lung  had  been  pimctured." 

"  A  patient,"  says  Danlos,  "  presented  arching  of  the  lower  lateral  and  posterior 
part  of  the  thorax  on  the  right  side.  This  arching  reached  as  high  as  the  fourth  inter- 
costal space.  At  this  level  the  intercostal  spaces  bulged  outwards.  Percussion  gave 
complete  dullness,  and  auscultation  showed  abolition  of  the  vesicular  murmur.  The 
patient  had  a  hydatid  cyst  of  the  lung." 

In  a  case  which  was  reported  by  Debove  all  the  signs  of  encysted  jjleural  effusion  on 
the  left  side  were  found — namely,  abolition  of  the  thoracic  vibrations,  dullness  on  per- 
cussion, absence  of  vesicular  murmur,  and  displacement  of  the  heart.  The  case  was 
one  of  hydatid  of  the  lung. 

Landouzy  writes :  "  The  patient,  who  had  had  violent  haemoptysis,  showed  dijata- 
cion  of  the  chest  on  the  left  side,  ■v^dth  bulging  below  the  clavicle.  Dullness  on  percus- 
sion, abolition  of  thoracic  vibrations,  tubular  breathing,  and  marked  deviation  of  the 
heart  were  found.  Puncture  confirmed  the  diagnosis,  and  6  pints  of  liquid  were  drawn 
oil  from  a  hydatid  cyst  of  the  lung." 

Large  cysts  may,  then,  produce  bulging  of  the  thorax,  displace  the  heart, 
and  simulate  encysted  or  extensive  effusion.  In  some  cases  they  produce 
other  symptoms,  of  which  the  most  important  are  pain,  dyspnoea,  myosis 
3n  the  same  side  as  the  cyst  (Widal),  and  pressure  signs,  such  as  oedema  of 
the  lower  and  upper  limbs. 

Diagnosis. — In  the  early  stage  hydatid  cyst  of  the  lung,  especially  if  it 
be  deeply  situated,  escapes  our  methods  of  investigation.  It  produces  no 
dullness,  no  deformity,  and  no  bulging  of  the  thorax.  Some  rales,  due  to 
the  pulmonary  congestion  around  the  cyst,  may  be  heard,  but  they  do  not 
help  us  in  diagnosis.  Radiography  may  furnish  some  information.  Haemop- 
tysis must  be  taken  into  careful  consideration.  If,  in  an  individual  suffering 
from  repeated  haemoptysis,  there  is  no  reason  to  suspect  tuberculosis,  asper- 
gillosis, calculosis,  or  bronchiectasis,  hydatid  cyst  of  the  lung  must  be 
especially  thought  of.  The  diagnosis  will  be  almost  certain  if  the  haemop- 
tysis is  accompanied  by  urticaria,  as  in  Chachereau's  case. 

The  diagnosis  of  hydatid  cysts,  when  they  produce  deformity  or  bulging 
of  the  chest,  is  also  very  difficult.  To  facilitate  the  discussion,  let  us  divide 
them  into  two  categories.  In  some  cases  the  bulging  is  so  clearly  limited 
that  the  cyst  forms  a  tumour.  If  the  bulging  occurs  at  the  tense  and  antero- 
lateral part  of  the  chest,  hydatid  cyst  of  the  liver  is  thought  of ;  if  it  deforms 


DISEASES  OF  THE  LUNG  225 

the  upper  region  of  the  thorax,  aneurysm  or  tumour  of  the  mediastinum 
Nvill  first  enter  our  minds  ;  if  it  is  posterior  and  lateral,  the  idea  of  an  inter- 
lobar pleurisy  presents  itself  ;  if  the  thoracic  deformity  occupies  the  postero- 
inferior  part  of  the  chest,  basal  effusion  is  diagnosed.  In  other  cases 
the  cyst  does  not  form  a  tumour,  but  by  its  large  extent  simulates  pleurisy 
of  the  great  pleural  cavity,  and  presents  most  of  its  signs  and  symptoms, 
such  as  dilatation  of  the  thorax,  absolute  dullness,  abolition  of  the  vibra- 
tions, tubular  breathing,  and  deviation  of  the  heart — in  fact,  everything 
tends  to  produce  mistakes.  Aspiratory  puncture  would  remove  all  doubts. 
This  is  true,  but  we  shall  see  later  the  mischief  which  may  result  from 
puncture.  In  making  a  decision,  we  must  inquire  carefully  into  the  symp- 
toms which  have  marked  the  onset  of  the  disease  and  have  accompanied  its 
progress.     Haemoptysis  occupies  the  chief  place. 

Rupture  of  the  Cyst.— All  hydatid  cysts  of  the  lung  do  not  grow  towards 
the  walls  of  the  thorax,  neither  do  they  acquire  a  large  size.  Many  cases 
are  not  large  enough  to  betray  themselves  by  any  bulging  of  the  chest ;  but, 
whatever  be  the  size  of  the  cyst,  be  it  large-  or  small,  complications  will 
certainly  appear.  They  comprise  inflammation  of  the  neighbouring  regions, 
infection  and  suppuration  in  the  cyst,  and  its  rupture  into  the  bronchi  or 
into  the  pleura. 

In  many  cases  rupture  of  the  cyst  is  preceded  or  accompanied  by  broncho- 
pulmonary lesions,  which  we  must  recognize.  Pulmonary  congestion, 
broncho-pneumonia,  and  pleuro-pneumonia  have  been  observed  either 
during  the  growth  of  the  cyst  or  at  the  moment  of  its  infection  (Walske, 
Lorieux).  This  side  of  the  question  has  been  neglected  by  some  writers  on 
hydatid  of  the  lung.  I  shall  sum  it  up  by  describing  a  case  under  my  care 
at  the  Necker  Hospital  : 

One  of  my  attendants,  wlio  had  had  htrmoptysis  several  months  before,  was  taken 
ill  with  fever,  cough,  pain  in  the  chest,  and  blood-stained  sputum.  On  examining  the 
patient,  we  found  subcrepitant  mucous  riiles  and  faint  tubular  breathing  over  the 
middle  third  of  the  chest  behind  on  the  right  side.  This  condition  simulated  a  bastard 
pneumonia,  or  pulmonary  infarct.  For  several  days  these  signs  did  not  change,  with 
the  exception  of  some  friction  sounds  which  blended  with  the  diffuse  rales. 

The  expectoration  continued  to  be  abundant,  viscid,  and  hicmoptoic  ;  but  then  it 
changed  in  character,  becoming  muco-purulcnt,  and  one  day  the  patient  coughed  up 
several  shreds  of  hydatid  membranes,  which  cleared  up  the  diagnosis.  The  fever  fell. 
The  liydatid  cyst  had  suj)purated,  and  tlu;  neigliljouring  lung  tissue  had  I'ecomo  aiTcct-ed 
by  a  bastard  pneumonia. 

These  pneumonic  attacks  (lesions  of  tli(!  jmcumocoi'cus)  may  appear  at 
different  periods  in  the  evolution  of  the  cyst.  They  arc  as  important  as 
the  attacks  of  pleurisy  mentioniMl  at  the  hcsginiiing  of  this  artich?. 

As  long  as  the  (;yst  docs  not  su[)[)urat(;  ru[)ture  docs  not  occur.  Kxctq)- 
tious  to  this  rule  arc  extremely  rare  (Marconnet's  case).     The  cyst  may 

15 


226  TEXT-BOOK  OF  MEDICINE 

open  into  the  bronchi  (vomica),  as  most  often  happens,  into  the  pleura,  or 
into  the  pleura  and  the  bronchi  at  the  same  time  (pyopneumothorax). 
Let  us  study  these  different  modes  of  rupture. 

Rupture  into  the  bronchi  is  sometimes  preceded  by  a  febrile  stage, 
with  bronchitis,  pulmonary  congestion,  incessant  cough,  and  purulent,  blood- 
stained, or  foetid  expectoration.  At  this  time  the  cyst  is  fissured,  but 
not  yet  freely  open.  If  the  cyst  is  small,  or  if  the  communication  with 
the  bronchus  is  of  small  size,  the  opening  of  the  cyst  does  not  quite  take 
the  characters  of  a  vomica.  The  patient,  after  fits  of  coughing,  brings  up 
homogeneous,  purulent,  sputum,  Kke  currant  jelly.  Sometimes  the  expec- 
toration is  genuinely  blood-stained,  and  booklets,  shreds,  or  hydatid  vesicles, 
that  prove  the  case,  are  found  in  the  blood  or  in  the  expectoration,  which 
is  sometimes  foetid. 

If  the  cyst  ls  large,  and  the  communication  with  the  bronchus  is  well 
established,  the  patient  is  seized  with  terrible  fits  of  coughing,  a  feeling  of 
tearing,  and  suffocation  bordering  on  asphyxia,  which  is  caused  by  the 
liquid  and  the  membranes  that  block  the  ah-tubes.  He  brings  up,  as  if 
by  vomica,  a  large  quantity  of  fluid,  which  is  clear  and  transparent,  like 
spring-water  if  the  cyst  is  not  suppurating  (Marconnet's  case),  but  muddy, 
sero- purulent,  blood-stained,  and  of  nauseous  odour  and  taste,  if  the 
ruptured  cyst  has  suppurated.  In  the  fluid  of  the  vomica  hydatid  vesicles 
are  sometimes  found,  from  the  size  of  a  pin's  head  to  that  of  a  walnut,  but 
more  often  membranous  shreds  of  various  sizes  are  seen. 

The  first  vomica  is  generally  the  largest,  but  it  is  rarely  the  only  one. 
We  sometimes  meet  with  a  series  of  vomicge  which  are  repeated  for  days, 
weeks,  and  months.  In  the  space  of  a  year  Chachereau  had  fifteen  vomicae, 
or  at  least  hydatids  were  expelled  fifteen  times.  As  a  rule,  I  repeat,  the 
first  vomica  is  the  most  severe,  and  the  others  are  rather  a  purulent  ex- 
pectoration with  shreds  of  membrane.  The  breath  and  the  expectoration 
are  often  foetid.  So  long  as  the  hydatids  are  not  all  brought  up,  the  purulent 
expectoration  does  not  cease. 

In  many  cases  rupture  of  the  cyst  is  announced  or  accompanied  by  a 
more  obstinate  and  abundant  haemoptysis  than  the  early  attacks  seen  ni 
the  first  period  of  its  growth.  Chachereau  had  fifteen  in  eighteen  months. 
They  were  trifling  before  the  rupture  of  the  cyst,  abundant  at  the  moment 
of  rupture,  and  persisted  for  five  months  after  the  last  vomica.  Marconnet 
had  slight  hemoptysis  before  rupture  of  the  cyst,  but  almost  fatal  haemor- 
rhage at  the  moment  of  rupture.  In  Habershon's  case  haemoptysis  caused 
the  death  of  the  patient,  and  at  the  autopsy  the  pulmonary  vein  was  foun4 
cut  tlu-ough,  causing  the  haemorrhage.  _  V 

Urticaria  fairly  often  accompanies  rupture  of  the  pulmonary  hydatid, 
like  that  of  hydatids  in  every  region.     Arnault  has  cited  a  case  of  genera ' 


DISEASES  OF  THE  LUNG  227 

urticaria  after  rupture  of  the  cyst  into  the  bronchi.  Chachereau  had  his 
first  attack  of  urticaria  some  days  before  the  cyst  opened  into  the  bronchi, 
and  had  ten  attacks  in  succession,  which  were  sometimes  so  severe  that 
sleep  became  impossible.  Delageniere  quotes  the  case  of  a  woman  who 
was  seized  with  urticaria  after  the  cyst  perforated  the  pleura.  Urticaria 
is,  therefore,  a  symptom  which  fairly  often  accompanies  rupture  of  hydatid 
cyst  of  the  lung. 

New  sigas  appear  after  rupture  of  the  cyst  into  the  bronchi.  On  auscul- 
tation, multiple  rales  and,  at  times,  cavernous  breathing  are  heard.  As 
secondary  infection  often  occurs  in  the  cyst,  fever  is  not  rare,  and  with  it 
the  usual  train  of  symptoms— viz.,  sweating,  anorexia,  wasting — appears. 
When  we  see  these  wasted,  anaemic  patients,  who  spit  up  pus  and  blood  and 
have  clubbed  fingers  (Trousseau),  we  would  not  be  able  to  eliminate  the 
idea  of  phthisis  if  bacteriological  examination  did  not  rectify  the  diagnosis. 

The  diagnosis  of  the  hydatid  vomica  is  quite  simple  when  membranes 
and  shreds  are  found  in  the  voided  matter.  In  default  of  hydatid  mem- 
branes that  present  a  characteristic  shape,  it  is  necessary  to  search  care- 
fully for  booklets,  because  the  presence  of  a  single  booklet  makes  a  doubtful 
diagnosis  certain.  In  many  cases  the  vomica  does  not  appear  with  charac- 
teristic symptoms,  and  we  then  lack  a  clue  to  the  diagnosis.  Most  patients 
think  they  are  suffering  from  bronchitis,  and  say  that  for  a  week,  a  fort- 
night, or  longer,  they  have  been  coughing  up  muco-purulent  or  blood-stained 
sputum.  They  do  not  mention  the  shreds  of  hydatid,  which  may  have 
passed  unnoticed.  These  patients  are  examined,  and  in  one  we  find  signs 
of  bronchiectasis  ;  in  a  second,  those  of  chronic  bronchitis,  with  bronchor- 
rh(jea  ;  in  a  third,  sigas  of  pulmonary  cavity,  Avith  repeated  haemoptysis  ; 
in  a  fourth,  signs  recalling  the  vomica  which  follows  encysted  interlobar 
pleurisy. 

So  far  it  in  sometimes  difficult  to  make  a  diagnosis.  Urticaria,  when  it 
exists,  is  a  point  of  great  value  ;  but  the  histological  examination  of  the 
expectorated  matter  must  never  be  neglected,  for  the  presence  of  hydatid 
membrane  and  booklets  can  alone  give  positive  information. 

Rupture  of  the  cyst  into  the  bronchi  is  sometimes  a  mode  of  cure,  but 
often  the  pulmonary  fistula,  which  is  a  centre  of  infection,  becomes  an 
inexhaustible  source  of  purulent  expectoration  and  haemoptysis.  The 
patient  continues  to  cough  up  membranes  and  much  purulent  foetid  sputum. 
Fever  supervenes,  with  its  train  of  septic  symptoms,  including  diarrhoea, 
loss  of  appetite,  wasting,  sweats.  We  sec  next  true  hydatid  phthisis  pro- 
duced by  secondary  infections.  Tuberculosis  may  also  develop  as  a  secon- 
dary infection  in  the  cdursi;  of  hydatid  of  tlie  lung. 

Rupture  into  the  Pleura. — Lot  us  consider  rupture  of  the  cyst  into 
the  pleura. 

15—2 


228  TEXT-BOOK  OF  MEDICINE 

I  must  first,  however,  discuss  an  interesting  question  :  Can  the  hydatid 
cyst  develop  primarily  in  ths  pleural  cavity  ?  Primary  hydatid  cysts  of 
the  pleura  are  extremely  rare.  Laennec,  Cruveilhier,  Davaine,  and  Trous- 
seau scarcely  admit  the  possibility  of  the  primary  development  of  a  hydatid 
cyst  in  the  pleural  cavity.  Davaine,  in  twenty-five  cases  of  thoracic  hydatid, 
only  once  found  a  primary  hydatid  of  the  pleura.  Dupuytren  and  Joffroy 
reported  a  case  of  pleural  hydatid  ;  careful  consideration,  says  Trousseau, 
shows  that  it  was  a  cyst  of  the  lung  which  opened  into  the  pleura,  because 
the  patient  had  had  haemoptysis.  Vigla,  in  his  work  on  hydatids  of  the 
thoracic  cavity,  quotes  only  one  case  of  pleural  hydatid,  and  it  is  a  very 
doubtful  case,  as  it  lacks  post-mortem  verification.  Maydl  published 
in  1891  a  memoir  upon  echinococci  of  the  pleura ;  after  having  analyzed 
in  detail  each  of  the  cases  contained  in  this  work,  I  find  that  there  is  no  case 
of  primary  hydatid  of  the  pleura,  but  only  of  hydatids  secondary  to  those 
of  the  lung  or  of  the  liver.  Further,  frequent  as  primary  hydatid  is  in  the 
parenchyma  of  organs,  it  is  exceptional  in  serous  cavities.  The  hydatid  is 
found  in  the  liver  and  the  subperitoneal  tissues,  but  very  seldom  in  the 
peritoneum.  The  hydatid  is  found  in  the  brain,  but  very  seldom  in  the 
meningeal  cavity  ;  in  the  heart,  but  very  seldom  in  the  pericardium ;  in  the 
lung,  but  very  seldom  in  the  pleura.  Cysts  of  the  serous  and  of  the  pleural 
cavities  have  in  most  cases  penetrated  these  cavities  by  effraction.  A  cyst 
of  the  lung  may  work  through  the  thickened  pleura,  and  thus  simulate  a 
cyst  of  that  tissue  (Trousseau). 

From  these  facts  we  must  conclude  that  hydatid  of  the  pleura  is  nearly 
always  secondary  to  one  that  starts  in  a  neighbouring  organ  and  per- 
forates the  pleural  cavity.  The  thickened  pleura  often  opposes  this  inva- 
sion, and  when  perforation  takes  place  it  may  consist  of  a  simple  slit  or  a 
large  tear  in  the  pleura. 

In  some  cases  the  invasion  of  the  pleura  may  be  insidious,  but  more  often 
it  is  accompanied  by  dyspna3a  and  pain.  We  find  signs  of  dry  pleurisy 
(rub)  or  of  pleural  effusion.     The  following  case  is  typical : 

A  boy,  of  tubercular  appearance,  was  suddenly  seized  with  stabbing  pain  in  the 
right  lung.  On  auscultation,  friction  sounds  were  heard.  The  whole  right  side  of  the 
chest  became  enlarged,  and  was  absolutely  motionless  during  respiration.  The  dullness 
was  absolute.  Post  mortem,  the  right  pleura  was  found  to  be  ruptured,  and  filled  with 
sero-purulent  fluid  and  membranes  from  a  huge  hydatid  of  the  lung,  which  had  burst 
into  the  pleural  cavity. 

In  other  cases,  which  are  the  most  frequent,  the  cyst  of  the  lung  shows 
two  perforations,  which  communicate  with  the  pleura  on  the  one  hand  and 
with  the  bronchi  on  the  other.  I  have  carefully  analyzed  these  cases,  and 
have  found  that  perforation  almost  always  takes  place  first  into  the  bronchus, 
while  the  other  perforation  occurs  a  little  later.     The  perforation  into  the 


DISEASES  OF  THE  LUNG  229 

bronchus  is  generally  a  small  fissure.  It  does  not  produce  tlio  large  vomica 
with  acute  symptoms,  and  the  patient  appears  to  have  only  foetid  bron- 
chitis or  broncho-pneumonia  with  gangrene.  He  brings  up  purulent,  foetid, 
blood-stained  sputum.  Perforation  of  the  pleura  now  occurs,  and  pneumo- 
thorax appears.  If  the  perforation  of  the  pleura  takes  place  before  that 
of  the  bronchi,  and  the  lung  is  adherent  to  the  pleura,  the  symptoms  of 
pneumothorax  may  not  be  violent ;  in  other  cases  the  pneumothorax  is 
accompanied  by  terrible  pain,  acute  dyspnoea,  and  threatening  asphyxia. 
The  subjoined  cases  give  a  clear  idea  of  these  different  modes  of  per- 
foration : 

In  a  case  reported  by  Bucquoy,  perforation  of  the  pleura  preceded  that  of  the 
bronchi.  The  patient  had  a  hydatid  cyst  of  the  right  lung.  Very  abundant  effusion 
into  the  right  pleura  (opening  of  the  pulmonary  cyst  into  the  pleura)  apjicai'ed.  Later, 
signs  of  pneumothorax  (opening  of  the  cystic  ca^^ty  into  the  bronchi)  supervened, 
and  the  patient  brought  up  much  foetid  purulent  fluid  by  repeated  vomica?.  The  situa- 
tion became  very  serious.  Thoracotomy  was  performed,  and  the  incision  gave  exit 
to  infectious,  purulent  fluid,  and  to  a  hydatid  cyst  as  large  as  an  orange. 

Danlos  relates  a  case  in  which  the  perforation  of  the  bronchi  preceded  that  of  the 
pleura.  The  onset  of  the  pneumothorax  was  dramatic,  and  followed  by  death.  In 
a  man  aged  forty-five  years  deformity  and  bulging  were  present  at  the  lower  lateral 
and  posterior  part  of  the  right  side  of  the  phest.  Hydatid  cyst  of  the  lung  was  diag- 
nosed. The  patient  was  seized  with  fits  of  coughing,  and  brought  up  purulent  and 
ffjetid  sputum  (small  opening  of  the  cyst  into  the  bronchus).  Ten  days  later  he  felt 
terrible  pain  on  the  right  side,  with  dyspncea.  On  auscultation,  amphoric  breathing 
was  heard  (perforation  of  the  pleura  and  pneumothorax).  The  jiatient  died,  and  the 
autopsy  revealed  a  huge  hydatid  cyst  at  the  base  of  the  right  hmg,  causing  the  above 
complications. 

In  a  oa.se  given  by  Fouquier  the  pneumothorax  came  on  suddenly.  The  patient 
died,  and  the  autopsy  showed  a  hydatid  cyst  of  the  lower  right  lobe  of  the  lung,  com- 
municating on  the  one  hand  with  two  bronchi,  and  on  the  other  with  the  pleural  cavity 
by  a  rounded  opening  with  raised  edges,  into  which  the  end  of  the  index-flnger  could 
easily  be  introduced. 

Summary. — The  diagnosis  of  hydatid  of  the  lung  is  very  difficult  before 
perforation  of  the  cyst  and  vomica.  Haemoptysis,  pleurisy,  and  attacks  of 
pneumonia  do  not  clear  up  the  diagnosis.  Bulging  of  the  chest,  dull- 
ness wliich  is  clearly  defined,  and  previous  or  simultaneous  hremoptysis 
not  due  to  tuberculosis,  are  valuable  signs  in  diagnosis.  We  know  that 
great  precautions  are  needed  in  exploratory  punctures,  which  are,  how- 
ever, tlie  only  means  of  clinclting  the  diagnosis  before  tlie  rupture  of 
the  cyst. 

When  a  patient  has  cough,  is  wasting,  and  has  repeated  hfemoptyses  and 
phniral  complications,  we  think  first  of  pulmonary  tul)erculosis.  Examina- 
tion for  Imcilli  is  negative,  and  the  diagnosis  remains  in  doubt.  The  patient 
later  brings  up  hydatid  vesicles  or  membranes,  and  the  diagnosis  becomes 
certain. 

In  some  cases,  however,  even  after  purulent  fluid  lias  been  rejected 


230  TEXT-BOOK  OP  MEDICINE 

through  the  bronchi,  diagnosis  is  very  difficult,  because  the  membranous 
shreds  may  escape  the  patient's  notice,  and  tlie  lesion  would  pass  unper- 
ceived  if  we  did  not  find  vestiges  of  membranes  or  booklets  on  microscopic 
examination.  Lastly,  in  other  cases  the  disease,  at  a  given  moment, 
assumes  the  appearances  of  broncho-pneumonia,  as  in  my  hospital  atten- 
dant, and  a  hydatid  of  the  lung  would  not  be  recognized  if  membranes 
and  booklets  were  not  found  in  the  expectoration. 

The  same  remarks  apply  to  the  passage  of  the  hydatid  into  the  pleural 
cavity  and  to  the  question  of  pyopneumothorax. 

As  I  have  discussed  the  diagnosis  in  regard  to  the  different  complica- 
tions which  may  arise  in  the  course  of  hydatid  of  the  lung,  further  reference 
is  superfluous. 

Prognosis. — In  this  chapter  I  have  reviewed  the  complications  of  hydatid 
of  the  lung,  and  we  have  seen  its  gravity.  In  exceptionally  fortunate  cases, 
the  cyst  may  be  cured  spontaneously — that  is  to  say,  it  may  undergo  necro- 
biosis, which  is  equivalent  to  cure.  In  some  cases  rupture  of  the  cyst  into 
the  bronchi  results  in  cure,  but  before  recovery  is  definite  the  patient  runs 
the  risk  of  most  grave  complications — viz.,  at  the  moment  of  rupture 
haemoptysis,  vomicae,  and  pyopneumothorax  ;  and  later  secondary  infec- 
tions, hectic  fever,  and  tuberculosis. 

Treatment. — As  medical  treatment  has  no  effect  on  hydatid  of  the  lung, 
surgical  intervention  must  be  resorted  to. 

Certain  authors  have  recommended  expectant  treatment,  but  this 
method  has  scarcely  given  good  results,  as  the  following  statistics  prove  : 
Hearn,  in  128  cases  of  pulmonary  hydatid,  left  to  run  their  own  course, 
counts  82  deaths — a  death-rate  of  64  per  cent.  Madelung,  in  19  untreated 
cases,  records  6  deaths. 

Thomas  Daviss  records  31  deaths  in  133  cases  of  pulmonary  hydatid 
which  opened  into  the  bronchi.  Such  figures  are  not  encouraging,  and 
explain  the  necessity  for  surgical  intervention. 

Aspiratory  puncture  is  insufficient  and  frequently  dangerous  in  hydatid 
cysts  of  the  lung.  Mirallie  has  collected  43  cases  in  which  simple  puncture 
was  performed ;  1 1  cures,  22  deaths,  and  10  negative  results  are  recorded. 
Punctures  are  frequently  followed  by  sudden  or  by  rapid  death.  Thus,  in 
the  22  fatal  cases  noted  above,  we  find  that  they  may  be  divided  as  follows  : 
In  1  case  the  patient  died  after  a  blank  puncture  ;  in  10  cases  death  was 
sudden — death  came  on  in  one  minute  (Acland,  Philippe,  etc.),  in  five 
minutes  (Holden),  in  seven  minutes  (Bristowe),  in  half  an  hour  (Lansdale 
and  Holden),  in  two  hours  (Hector  Mackenzie),  in  nine  hours  (Cornil  and 
Gibier),  in  thirteen  hours  (Duffey).  In  almost  all  these  cases  the  accident 
was  accompanied  by  some  attacks  of  coughing,  with  cyanosis  and  asphyxia, 
coldness  of  the  extremities,  and  sometimes  rejection  of  blood  and  fluid. 


DISEASES  OF  THE  LUXG  231 

Puncture,  therefore,  must  be  abandoned ;  it  is  dangerous  even  for  purposes 
of  exploration. 

Pneumotomy  is  tlie  best  method,  and  is  absolutely  indicated.     It  gives 
such  good  results  that  the  recoveries  amount  to  90  per  cent. 


XXI.  SYPHILIS  OF  THE  LUNG. 

Discussion. — Syphilis  of  the  lung  is  of  the  highest  importance.  Too 
many  mistakes  in  diagnosis  occur  from  want  of  care  in  looking  for  this  malady. 
It  endangers  the  patient's  life  ;  but,  on  the  other  hand,  it  gives  us  an  opening 
to  score  a  therapeutic  success,  for  we  can  sometimes  restore  health  in  a 
few  weeks  or  in  a  few  months  to  people  who  appear  to  be  in  the  last  stage 
of  phthisis. 

The  chief  manifestations  in  the  lung  include  broncho-pneumonia  of 
tubercular  aspect,  cavities  simulating  phthisis,  gangrene,  fibrosis  of  the 
lung,  and  dilatation  of  the  bronchi,  without  counting  mediastinal  adeno- 
pathies and  pleurisy.  Before  we  undertake  the  clinical  study  of  these 
syphilitic  lesions,  we  must  consider  an  important  point :  At  what  date  may 
syphilis  attack  the  lung  ?  Is  it  soon  or  long  after  infection  ?  This  division 
into  early  and  late  lesions  is  clearly  marked  in  such  organs  as  the  brain, 
the  spinal  cord,  the  kidneys,  etc.  Take,  for  example,  cerebral  syphilis. 
Its  lesions  are  sometimes  late  and  at  other  times  early.  The  late  lesions, 
such  as  obliterating  or  dilating  arteritis,  and  gummatous  lesions  of  the  bones, 
meninges,  or  brain  (general  paralysis),  appear  many  years  after  infection. 
We  also  see  early  cerebral  syphilis  which  is  almost  exclusively  confined  to 
the  arteries  of  the  circle  of  Willis.  It  may,  some  months  after  infection, 
give  rise  to  endarteritis  obliterans,  with  cerebral  softening  and  hemiplegia, 
and  to  arteritis  ectasians,  with  rupture  of  an  aneurysm,  meningeal  haemor- 
rhage and  death  from  apoplexy. 

This  distinction  between  early  and  late  lesions  is  nowhere  more  marked 
than  in  the  kidneys.  The  tertiary  disease  usually  takes  the  form  of  chronic 
nephritis,  with  or  without  gummatous,  sclero-gummatous,  and  amyloid 
lesions,  while  early  renal  syphilis  appears  some  months  after  the  chancre, 
and  causes  acute  or  hyperacute  nephritis,  which  Is  sometimes  most  dan- 
gerous. 

It  was  formerly  thought  that  syphilis  only  attacked  the  organs  in  the 
so-called  tertiary  stage.  This  view  Ls  incorrect.  Some  organs  are  aff(M'tod 
by  syphilis  at  a  very  early  stage,  and  the  lesions,  though  early,  are  far  from 
being  benign.     They  are  quite  as  serious  as  the  lesions  of  the  tertiary  stage. 

I  will,  therefore,  put  the  question  afresh  :  Do  we  find  in  the  lung  early 
syphilis,  that  appears  within  the  first  few  months  after  infection,  and  late 


232  TEXT-BOOK  OF  MEDICINE 

syphilis,  that  appears  only  after  a  long  interval  ?  The  answer  is  categorical. 
Syphilitic  lesions  of  the  lung  are,  practically  speaking,  never  early.  I 
would  ask  you  to  remember  that  I  am  speaking  of  the  lung,  and  not  of  the 
bronchi.  Bronchitis  may  be  one  of  the  earliest  manifestations  of  syphilis. 
Many  people,  when  once  infected,  take  cold  with  the  greatest  ease.  They 
suffer  from  laryngitis  or  tracheo -bronchitis  ;  they  cough  and  expectorate. 
On  auscultation,  sibilant  and  mucous  rales  are  heard,  and  the  trouble  is 
put  down  to  influenza  or  to  an  ordinary  cold,  and  not  to  recent  syphilis. 
Tracheo-bronchitis  may  recur  several  times,  even  during  the  early  years  of 
Infection,  and  sometimes  arouses  unjustifiable  suspicions  of  tuberculosis. 
These  so-called  attacks  of  bronchitis  lead  us  to  send  patients  to  take  a  cure 
at  Mont-Dore,  Cauterets,  Eaux-Bonnes,  and  Luchon,  when  we  should  have 
begun  by  prescribing  mercury.  Laryngo-tracheo-bronchitis  is,  then,  one  of 
the  early  manifestations  of  syphilis.  Lesions  in  the  lungs,  on  the  other 
hand,  occur  late,  and  not  one  of  the  other  visceral  determinations,  as 
Mauriac  rightly  remarks,  develops  at  a  later  period.  This  rule  appears  to 
me  absolute,  and,  save  for  some  exceptional  cases,  it  may  be  said  that 
syphilis  of  the  lung  only  appears  in  the  advanced  tertiary  stage. 

After  these  explanations,  let  us  enter  upon  our  subject.  Syphilis  of  the 
lung,  as  of  other  organs,  presents  various  forms — gumma  (circumscribed 
syphiloma),  diffuse  syphiloma,  and  fibrosis.  These  different  forms  may  be 
isolated  or  associated.  For  the  clear  arrangement  of  this  question  I  propose 
the  classification  which  I  have  followed  in  my  clinical  lectures  at  the  Hotel- 
Dieu.* 

Syphilis  of  the  lung  may  show  the  following  forms  : 

First  Type. — Pulmonary  syphiloma,  with  acute  febrile  course,  simu- 
lating acute  tuberculosis  or  tubercular  broncho-pneumonia. 

Second  Type.  —  Pulmonary  syphiloma  of  slow  course,  simulating 
ordinary  chronic  tuberculosis  and  phthisis  in  the  stage  of  cavity. 

Third  Type. — Broncho-pulmonary  syphiloma,  with  fibrosis  or  sclero- 
gummatous  lesions,  simulating  chronic  pneumonia  and  cirrhosis  of  the  lung, 
with  or  without  bronchial  dilatation,  pleurisy,  and  tracheo -bronchial 
adenopathy. 

Fourth  Type. — Syphilitic  gangrene  of  the  lung. 

Fifth  Type.  —  Syphilitic  pneumopathy,  complicated  by  pulmonary 
tuberculosis. 

Sixth  Type. — Hereditary  pulmonary  syphilis. 

*  Dieulafoy,  "  Syphilis  du  Poumon  et  de  la  Plevre  "  {CUnique  Medicale  de  V Hotel- 
Dieu,  1898,  lemons  18  et  19). 


DISEASES  OF  THE  LUNG  233 

1.  Pulmonary  Syphilis,  with  Acute  Course,  simulating  Acute 

Tuberculosis. 

In  some  cases — which  are  rare,  it  is  true — syphilis  of  the  lung  shows  an 
almost  faithful  picture  of  acute  tubercular  broncho-pneumonia — i.e.,  fairly- 
sudden  onset,  acute  fever,  incessant  cough,  violent  dyspnoea,  muco-purulent 
expectoration,  rapid  wasting  and  profuse  sweats,  dullness  on  percussion, 
rales  and  tubular  breathing  on  auscultation.  The  above  symptoms  may 
be  common  to  syphilitic  and  to  acute  or  subac-ute  tubercular  broncho- 
pneumonia. The  following  example  was  seen  by  Giraudeau  in  Hayem's 
wards  : 

Patient,  thirty-five  years  old.  She  had  cough,  and  for  a  week  fever  was  continuous. 
Temperature  up  to  104°  F.  On  admission,  dull  zone,  with  tubular  breathing  and  sub- 
crepitant  rales  over  the  middle  part  of  the  left  lung.  Nothing  elsewhere.  Right  lung 
healthy.  Frequent  cough  and  profuse  expectoration.  During  the  next  few  days, 
rapid  formation  of  a  cavity.  The  breathing  soon  became  tubular,  and  the  expectora- 
tion muco-purulent.  Later,  in  addition  to  tubular  breathing,  large  mucous  rales 
appeared,  wasting  was  considerable,  and  night-sweats  occurred.  On  February  21 — 
that  is  to  say,  in  twenty  days — a  cavity  had  formed  in  the  lung.  Cavernous  breathing, 
pectoriloquy,  and  bronchophony  were  audible  over  the  greater  part  of  the  middle  lobe. 
Gurgling  was  present ;  the  sputum  was  ruunmular,  and  streaked  with  blood.  The 
patient  appeared  to  be  suffering  from  acute  phthisis. 

On  February  28  vaginal  examination  revealed  in  the  right  cul-de-sac  a  rounded 
ulcer,  which  was  as  big  as  a  sixpence,  punched  out,  and  covered  by  a  greyish,  adherent 
layer.  This  gummatous  ulcer  showed  the  need  for  specific  treatment.  The  lung 
trouble  was  then  thought  to  be  specific  in  nature,  and  Gibert's  syrup  given  in  doses  of 
two  tablespoonfuls  daily.  After  some  weeks,  the  situation  improved,  the  appetite 
came  back,  the  nummular  sputum,  sweats,  and  fever  disappeared.  The  cavernous 
breathing  and  gurgling  were  replaced  by  rough  breathing.  The  cavity  had  cicatrized. 
As  the  treatment  had  caused  stomatitis,  it  was  st02:)pcd.  Ninety  grains  of  iodide  of 
potash  were  prescribed  daily,  and  when  the  patient  left  the  hospital  she  had  regained 
her  healthy  look,  and  the  gummatous  ulcer  in  the  vagina  was  undergoing  cicatrization. 
A  littl(!  while  after,  this  woman  came  back  for  treatment,  not  for  the  lung,  which  was 
healthy,  but  for  ost(!op(!riostitis  of  the  frontal  bone,  which  yielded  to  sj)eeific  treat- 
ment. It  was,  therefore,  undeniable  that  this  woman  had  been  attacked  in  a  short 
time  with  vaginal  gumma,  sy})hilis  of  the  lung,  and  frontal  ostefjporiostitis.  .hidgitig 
by  the  rapid  and  excej)tionally  serious  course  of  the  l<'si(in  in  the  lung,  she  was  doomed 
to  die.     She  was  saved  by  specific  treatment. 

I  have  seen  a  similar  case. 

I  att<'nded  a  ])a(ient  supposed  t^  bo  suffering  from  influenza.  He  coughed,  had 
slight  fever,  and  cfmii)lain<'d  of  j)ain  in  the  chest,  esjieciaiiy  at  the  apex  of  tlu'  left  lung, 
where  I  found  tubular  breathing  and  rules,  due  to  ]))ilmoiiary  congestion.  This  man, 
who  was  up  to  then  in  robust  health,  asked  for  a  blister,  which  i  ijrcscribed,  as  well  as 
n  draught  containing  kermes.  During  the  next  few  days  the  situation  became  worse. 
TIk-  cough  was  incessant,  and  at  niglit  the  dyspncea  was  unusually  sc^vere.  The  spiitmn 
soon  became  muco-jiurulent  and  nummular.  The  early  rales  changed  to  guiniiiig.  ilis 
strengtii  failed,  and  I  thought  of  acut<'  lul)ereular  pneumonia. 

The  jjrognosis  wius  very  grave.  Incidentally,  the  jiatient  told  uw.  that  his  left  t<>ati3 
iiad   been   affected   for  some  days.      I   found   it  enlarged   and   painful.     Orchitis   wiw 


234  TEXT-BOOK  OF  MEDICINE 

present,  but  not  epididymitis.  As  he  had  no  discharge,  I  thought  at  once  of  tertiary 
syphilis.  I  questioned  the  patient,  who  rephed  that  he  had  had  a  cliancre  ten  months 
before.  This  revelation  threw  Hght  on  the  subject.  Was  it  not  possible  that  syphilis 
was  at  once  the  cause  of  the  lesion  in  the  Ixmg  and  in  the  testis  ?  I  prescribed  iodide 
of  potash  in  large  doses,  and  also  asked  the  advice  of  Foumier.  He  considered  the 
orchitis  and  the  lung  trouble  to  be  syphilitic,  and  advised  inunction  of  mercury  in 
addition  to  the  iodide  of  potash.  The  picture  changed  so  rapidly  that  after  a  few 
nights  the  dyspnoea  disappeared.  A  fortnight  later  the  fever  had  subsided,  the  general 
condition  was  excellent,  tubular  breathing  and  gurgling  had  disappeared,  and  the  only 
local  sign  remaining  at  the  apex  of  the  right  lung  was  slight  dullness  with  some  rales, 
which  finally  disappeared.  The  lesion  of  the  testis  was  also  cured.  The  case  was 
undoubtedly  acute  phagedsenic  syphiloma,  which  rapidly  caused  breaking-down  of  the 
apex,  and  was  clearly  arrested  in  its  course  by  specific  treatment.  I  have  never  lost 
sight  of  this  man,  and  I  have  treated  him  since  that  time  for  a  syphilitic  whitlow,  but 
there  has  never  been  any  further  question  of  pulmonary  lesions. 

In  my  clinical  lectures,  several  cases  of  this  acute  and  subacute  broncho- 
pneumonic  syphiloma  with  fever  will  be  found.  In  nearly  all  these  cases  it 
has  simulated  acute  tubercular  broncho-pneumonia  :  onset  fairly  sudden, 
acute  fever  and  dyspnoea,  muco-purulent  expectoration,  rapid  wasting,  pro- 
fuse sweats,  with  dullness,  rales,  tubular  breathing,  and  gurgling,  are  the 
signs  common  to  acute  broncho -pneumonic  syphiloma  and  to  acute  or  to 
subacute  tubercular  broncho-pneumonia. 

It  has  been  said  that  syphilitic  pneumopathy  may  occur  without  fever, 
wasting,  or  any  sign  of  hectic.  This  is  true  in  a  certain  number  of  cases  of 
slow  course,  which  we  shall  study  later,  but  not  of  the  acute  forms,  in  which 
the  diagnosis  is  extremely  difficult.  If  we  carefully  think  over  the  acute 
cases,  we  shall  agree  that  patients  who  suffer  from  fever,  accompanied  by 
signs  of  pulmonary  softening,  purulent  sputum,  and  night-sweats,  and  pass 
into  rapid  consumption  within  a  few  weeks,  clinically  resemble  those  who 
are  suffering  from  acute  phthisis. 

In  them,  it  is  true,  dyspnoea  is  often  severe  and  out  of  proportion  to  the 
lesion,  but  this  symptom  is  not  sufficient  to  decide  the  diagnosis.  The 
physical  signs — rales,  tubular  breathing,  gurgling — are  those  of  acute 
phthisis.  It  has  been  said  that  the  localization  of  the  lesions  may  reveal 
the  true  nature,  because  the  syphilitic  lesion  is  often  situated  in  the  middle 
part  of  the  lung,  and  especially  on  the  right  side.  This  special  topography 
is,  indeed,  worth  remembering  :  it  may  lead  us  to  think  of  syphilis ;  still 
it  is  not  constant,  for  in  a  case  of  Raymond,  and  also  in  one  of  my  cases, 
the  lesion  was  at  the  apex  of  the  lung,  which  is  the  usual  seat  of  tuber- 
culosis. 

Acute  syphiloma  and  acute  tubercular  broncho-pneumonia  have,  there- 
fore, very  many  points  of  resemblance,  and  hence  it  is  only  possible  to 
make  a  diagnosis  of  pulmonary  syphilis  if  the  patient  present  other  syphilitic 
lesions,  such  as  osteitis  or  painful  periostitis,  ulcerating  gumma,  specific 
eruption,  or  syphilitic  testis.     If  we  find  some  such  stigmata  of  syphilis  as 


DISEASES  OF  THE  LUNG  235 

an  exostosis  of  the  tibia,  frontal  periostitis,  the  presence  of  scars,  and  the 
repeated  absence  of  Koch's  bacilhis  from  the  sputum,  we  can  give  a  diag- 
nosis of  acute  syphilitic  pneumopathy.  In  short,  if  pathognomonic  symptoms 
of  acute  pneumonic  syphiloma  do  not  exist,  it  is  at  least  necessary  to  collect 
all  the  information  which  may  give  a  clue  to  the  diagnosis.  In  one  of  my 
patients  at  the  Hotel-Dieu  pneumonic  syphiloma  was  diagnosed,  thanks 
to  tertiary  syphilis  of  the  shoulder  and  the  back.  In  the  patient  whom  I 
saw  with  Fournier  syphilis  of  the  testis  revealed  the  nature  of  the  pul- 
monary lesion.  In  Giraudeau's  patient  an  ulcerated  gumma  of  the  vagina 
led  him  to  discern  acute  s}T)hilis  of  the  lung. 

What  is  the  cause  of  acute  syphiloma  of  the  lung  ?  The  syphiloma  may 
be  circumscribed  (syphilitic  gumma)  or  diffuse  (broncho-pneumonic  syphi- 
loma). Gummata  of  the  lung  may  be  as  large  as  a  lentil  or  an  egg.  They 
are  more  or  less  numerous,  and  may  be  situated  on  the  surface  oithe  lung, 
under  the  pleura,  or  in  the  deep  parts  of  the  organ.  They  are  indurated 
anct  greyish  in  an  early  stage  of  their  growth,  but  finally  soften  and  become 
converted  into  a  yellowish  pulp,  which  may  pass  into  a  bronchus,  and  leave 
in  Its  place  a  gummatous  cavity,  with  fihrous  walls.  When  cure  sets  in, 
the  walls  of  the  cavity  become  covered  with  granulations,  the  cavity  con- 
tracts, and  is  replaced  by  scar  tissue. 

Diffuse  syphiloma  of  the  lung  assumes  a  special  form,  and  causes  a 
kmd  of  sypliilitic  broncho-pneumonia,  which  may  be  acute,  subacute,  or 
clironic.  The  acute  form,  which  has  been  discussed  in  the  examples  quoted 
above,  is  somewhat  rare.  Microscopic  examination  has  given  the  following 
r.'^ults :  ^ 

"  Microscopic  examination,"  says  Remy,  "  shows  that  the  tumour  is 
composed  of  a  number  of  nodules  of  broncho-pneumonia  in  various  stages 
(catarrhal,  fibrinous,  and  caseous).  There  is  no  well-marked  general  cap- 
sule formed  by  a  zone  of  fibrous  tissue,  as  in  the  case  of  gummata.  At  some 
pomte,  however,  this  capsule  is  seen,  but  it  is  formed  by  the  septum  of  the 
lobule,  and  not  by  newly-formed  tissue.  No  central  artery  is  found.  The 
lesions  are  rather  grouped  around  the  l^ronchi,  as  in  broncho-pneumonia. 
The  lesion  as  a  whole  consists  in  several  masses  of  caseous  appearance,  which 
are  surrounded  by  more  active  zones.  The  caseous  mass  is  composed  of 
pulmonary  alveoli,  filled  with  cells,  whicli  have  lost  their  shape  and  appear 
to  be  undergoing  fatty  degeneration.  The  envelope  of  the  caseous  mass  is 
sometimes  formed  by  a  thickened  interlobular  septum,  at  other  times  by 
alveoli  which  are  filled  with  leucocytes,  and  present  thickened  walls.  Further- 
more, we  find  in  the  thickness  of  the  broiu-lii,  vessels  or  interlobular  septa, 
masses  of  young  cells  which  reveal  an  inflammatory  condition." 

Syphilitic  broncho-pneumonia  has  ho.o.n  studied  in  the  f<ntus  and  in  tiio 
new-born    by  Balzar  and   Grandhomme.     They  have  found  lesions    like 


236  TEXT-BOOK  OF  MEDICINE 

those  of  ordinary  broncho-pneumonia.  The  vascular  and  interstitial  lesions, 
however,  appeared  to  be  most  marked,  but  epithelial  desquamation  and 
slight  exudation  were  also  noted.  Whether  diffuse  pulmonary  syphilis 
begins  as  a  broncho-pneumonia  of  bastard  form, with  parenchymatous  in- 
filtration involving  the  bronchus  and  the  alveolus,  or  whether  the  process 
chiefly  affects  the  arterioles,  it  is  none  the  less  true  that  the  diffuse  syphiloma 
may  run  a  rapid  or  a  slow  course.  In  the  former  case  the  lesion  results  in 
dissolution  of  the  invaded  tissues.  Tertiary  syphilis,  then,  causes  a  kind 
of  phagedsenism  of  the  lung,  similar  to  that  of  the  velum  palati  or  of  the 
pharynx.     These  cases  simulate  acute  tubercular  broncho-pneumonia. 

2.  Pulmonary  Syphiloma,  simulating  Ordinary  Chronic 
Tuberculosis. 

We  must  now  consider  the  slow  form  of  pulmonary  syphilis  which  simu- 
lates chronic  tuberculosis,  with  or  without  cavities.  The  following  examples 
are  typical : 

In  November,  1878,  Fonmier  had  a  woman  under  his  care  at  the  Loiircine 
Hospital  for  an  enormous  phagedaenic  ulcer,  which  involved  a  large  part  of  the  foot.  He 
ordered  inimctions  of  mercury  and  iodide  of  potash.  The  patient  was  cachectic,  and 
looked  phthisical,  so  that  she  was  thought  at  first  to  have  pulmonary  tuberculosis. 

"  This  presumption,  deduced  from  the  external  api^earance,"  says  Fournier, 
"  found  support  in  that  the  patient  comj^lauied  that  she  had  coughed  for  several 
months,  brought  up  abundant  green  sputum,  and  suffered  from  fever,  profuse  night- 
sweats,  etc.  Physical  examination  of  the  chest  seemed  to  confirm  this  view,  and 
revealed  somewhat  extensive  dullness  in  front  of  and  behind  the  apex  of  the  left  lung. 
The  rest  of  the  lung  appeared  free.  At  the  same  spot  rough,  cavernous  breathing, 
cavernous  rales,  and  sjDlashing  sounds  were  heard.  In  short,  the  general  condition,  the 
local  symptoms,  and  the  physical  signs  corresponded  to  those  of  jDulmonary  phthisis." 

Although  the  idea  of  pulmonary  syphihs  entered  Fournier's  mind,  this  eminent 
authority  felt  obUged  to  hold  to  the  most  probable  diagnosis — that  of  pulmonary 
phthisis  (Koch"s  bacillus  was  not  yet  discovered).  The  later  course  did  not  agree 
with  Fournier's  opinion.  The  patient,  "  whose  days  appeared  numbered,"  suddenly 
began  to  improve  under  specific  treatment,  and  her  strength  returned,  so  that  when 
she  left  the  hospital,  after  a  stay  of  four  months,  she  was  fat  and  well.  The  local 
lesions  and  the  functional  troubles  improved  at  the  same  time  as  the  general  condition. 
The  dyspnoea  and  the  pain  in  the  side  disappeared,  while  the  auscultatory  sounds  were 
reduced  to  slight  crackling  or  to  disseminated  subcrepitant  rales.  When  Foumier 
saw  the  patient  again  several  months  later,  careful  auscultation  failed  to  show  the  least 
traces  of  the  lesion. 

Panas  has  published  a  similar  case  : 

"  A  woman,  thirty-two  years  of  age,  consulted  me,"  says  Panas,  "  for  a  lesion 
of  the  left  eye,  and  for  disease  of  the  lung.  She  told  me  that  the  former  began  as  a 
little  whitish  point  at  the  inner  edge  of  the  cornea.  This  tumour,  which  was  a  little 
larger  than  a  pin's  head,  grew  rapidly.  The  eye  became  red,  and  in  a  fortnight  vision 
was  lost.  We  found  the  eye  much  enlarged.  The  cornea  was  hypervascular,  opaque, 
and  scarcely  distinguishable  from  the  conjunctiva.  A  yellowash  swelling,  like  a  tubercle, 
appeared  near  the  inner  border.       The  ciliary  body  projected  like  a  blackish  mushroom 


DISEASES  OF  THE  LUNG  237 

through  a  perforation  in  the  sclerotic.  Perception  of  liglit  was  abolished.  On  examina- 
tion of  the  chest,  the  left  lung  was  healthy,  but  the  right  one  was  dull  in  its  upper 
third,  and  auscultation  revealed  both  behind  and  in  front  large  mucous  rales  and 
gurgling,  indicative  of  tuberculosis  nearing  the  end  of  its  second  stage,  and  going  on  to 
cavity.  Add  to  this  slight  hajmoptysis,  continual  cough,  with  scanty  expectoration 
and  a  loss  of  weight  of  40  pounds.  In  spite  of  this  wasting,  the  patient  appeared  healthy, 
and  had  a  good  appetite.  There  was  no  reason  to  ehminate  phthisis,  but  I  was  put 
un  my  guard  by  the  existence  of  a  corona  Veneris  upon  the  forehead.  She  had  had 
syphilis  seven  years  before.  The  chancre  had  passed  unnoticed,  but  two  miscarriages, 
two  children  dying  in  infancy,  and  then  a  general  enaption,  which  had  left  enormous 
scars  all  over  the  body,  together  with  the  syphilide  on  the  forehead,  made  the  diagnosis 
quite  clear.  We  therefore  hoped  that  the  ocular  and  pulmonary  lesions  were  both 
syphilitic. 

"  I  gave  evcrj'^  second  day  an  injection  of  peptonate  of  mercury  (representing  nearly 
-J-  grain  of  the  active  principle).  After  the  second  injection  the  improvement  was 
remarkable,  and  the  progress  was  evident  with  each  fresh  injection.  In  the  eye,  which 
was  a  red  stajihylomatous  shell,  the  sclex-otic,  the  cornea,  and  the  iris  gradually  became 
distinct,  and  the  eye  regained  its  proper  shape.  At  the  same  time,  the  lung  rapidly 
improved.     Dullness  and  rales  diminished,  and  then  disappeared." 

In  my  wards  at  the  Hotel-Dieu  we  have  had  quite  as  conclusive  cases. 

Some  years  ago  I  saw  a  case  of  this  kind.  I  was  called  to  see  a  young  man  condemned 
as  phthisical.  We  had  to  decide  if  he  were  fit  to  leave  for  the  South,  in  order  to  reside 
there  during  his  few  remaining  months.  I  saw  him,  and  as  soon  as  I  entered  his  room 
he  recognized  me,  while  I  remembered  that  he  had  consulted  me  the  year  liefore  for  a 
large  ulcerative  syphihde  of  the  arm,  elbow,  and  forearm.  He  had  apphcd  ointments 
and  blisters  without  the  least  success.  Specific  treatment  (inunction  of  mercury  and 
iodide  of  potash)  rapidly  cured  this  tertiary  ulceration,  which  was  of  nearly  a  year's 
duration.  I  now  found  that  be  looked  like  a  case  of  advanced  phthisis.  He  told  me 
that  he  had  had  a  "  neglected  cold  "  eight  months  before.  He  had  begim  to  cough 
and  to  spit,  and  had  often  brought  up  a  little  blood.  He  next  lost  his  appetite,  night- 
sweats  appeared,  the  expectoration  became  muco-purulent,  and  the  customary  drugs 
for  phthisis  had  effected  no  result. 

On  auscultation,  I  heard  cavernous  breathing  and  gurglmg  at  the  lower  angle  of 
the  right  scapula.  This  site,  which  is  an  unusual  one  for  a  tubercular  cavity,  made 
me  reflect ;  and,  warned  by  the  tertiary  ulceration  which  I  had  cured  the  j)reeeding  year, 
I  suspected  syphilis  of  the  lung,  and  ordered  iniuiction  of  mercury  and  iodide  of  potash 
the  dose  of  which  was  raised  to  1(30  grains  daily.  In  a  few  weeks  the  change  was  com- 
plete. The  patient  recovered,  and  the  physical  signs  disappeared.  The  cavity  in  the 
lung  filled  up,  the  expectoration  diminished,  and  the  daily  progress  was  evident. 

The  preceding  cases  give  an  idea  of  pulmonary  syphiloma  of  slow  course 
simulating  ordinary  chronic  tuberculosis.  This  form  has  an  insidious 
onset,  and  fever  is  priictically  al)sent.  At  hrst  it  simulates  bronchitis,  pul- 
monary congestion,  or  ill-defined  broncho-pneumonia.  The  appetite  remains 
good,  the  patient  does  not  waste,  the  cough  is  frc({ucnt,  and  the  expectora- 
tion has  no  special  characters.  Later,  we  find  other  symptoms,  su(;h  as 
pain,  dyspnoea,  which  may  be  severe  and  is  worse  at  night,  purulent  ex- 
pectoration, night -sweats,  loss  of  appetite,  ajid  wasting.  Later  still,  hectic 
fever,  gmgling,  and  bronchial  or  cavernous  breathing  appear,  according  to 
the  degree  of  the  lesion  (hiduration,  softening,  cavity).     Gunmiatous  ex- 


238  TEXT-BOOK  OF  MEDICINE 

pectoration  and  syphilitic  vomica  have  been  spoken  of,  but  I  think  they 
are  exceptional.  Haemoptysis  is  rare  and  small  in  amount.  The  patient 
only  brings  up  some  blood-stained  sputum  in  most  cases,  yet  in  a  case  of 
Lancereaux  much  blood  was  expectorated,  and  one  of  my  patients  brought 
up  two  tumblerfuls  of  blood. 

Chronic  syphiloma,  like  the  acute  form,  often  occupies  the  middle  part 
of  the  right  lung  outside  the  hilum.  The  sounds  on  auscultation  are  most 
marked  either  at  the  spine  of  the  scapula  or  in  front  in  the  third  and  fourth 
intercostal  spaces.  To  this  rule  there  are  numerous  exceptions  (Fournier 
and  Giibler's  cases). 

Though  the  patient  with  pulmonary  syphilis  does  not  become  phthisical 
so  soon  as  with  tuberculosis,  and  though  his  health  may  remain  good  for 
some  time,  while  he  coughs  up  elastic  fibres  or  fragments  of  a  gumma, 
Bazin's  idea  that  the  syphilitic  patient  is  always  a  caverneux  bien  fortant 
must  not,  however,  be  exaggerated. 

Whatever  be  the  mode  of  onset  of  this  syphilitic  pneumopathy,  even 
when  the  patient  has  for  some  time  remained  in  good  health,  it  is  rare  for 
cure  to  supervene  without  treatment.  Sooner  or  later  fmictional  troubles 
appear,  the  sputum  becomes  nummular,  fever  commences,  night-sweats  are 
profuse,  wasting  makes  progress,  the  nails  are  curved,  and,  iu  default  of 
treatment,  the  patient  dies  in  consumption. 

What  are  the  causes  of  this  syphilitic  phthisis  ?  We  can  readily  under- 
stand how  gummata  in  the  lung  soften  and  leave  cavities.  We  know,  too, 
that  a  syphilitic  patient  may  become  cachectic  from  the  simultaneous 
develo23ment  of  specific  lesions  or  of  amyloid  degeneration  in  other  tissues 
(liver,  kidney,  spleen,  larynx) ;  but  how  can  pulmonary  syphilis  cause  a 
patient  to  become  phthisical  ?  There  is  nothing  m  the  course  of  tertiary 
syphilis  in  other  organs  to  determine  hectic  fever  and  consumption,  with 
night-sweats  and  clubbed  fingers.  Microbiological  discoveries  seem  to 
simplify  the  problem,  and  I  think  that  in  the  patient  with  pulmonary 
syphilis  hectic  fever  is  not  the  direct  result  of  syphilis,  but  of  secondary 
infections,  whose  origin  is  readily  grasped.  In  the  lung,  syphilis  causes 
ulcers  and  cavities  in  which  micro-organisms  swarm.  Some  of  these 
microbes  find  in  the  cavities  a  soil  favourable  to  infections  and  toxic  pro- 
ducts. 

The  diagnosis  of  chronic  pulmonary  syphiloma  is  surrounded  by  the 
greatest  diflficulties,  because  no  single  sign,  by  its  presence  or  by  its  absence, 
can  make  it  certain  that  the  mischief  is  syphilitic.  The  presence  of  Koch's 
bacillus  in  the  sputum  solves  the  difficulty,  but  tubercle  and  syphiloma 
may  occur  together  in  the  same  lung,  and  in  this  case  the  functional  troubles, 
the  physical  signs,  and  the  bacteriological  examination  all  conspire  to 
obscure  the  diagnosis. 


DISEASES  OF  THE  LUNG  239 

Unless  a  happy  chance  should  point  to  the  development  of  a  gumma,  an 
osteoperiostitis,  or  a  tertiary  eruption,  in  whatever  region  it  may  be,  or 
unless  characteristic  scars  were  present,  the  nature  of  the  pneumopathy 
would  often  pass  unnoticed.  In  one  of  my  patients  in  the  Saint-ClirLstophe 
Ward  tertiary  glossitis  put  us  on  the  track  of  the  diagnosis  ;  in  one  of  Giibler's 
patients  the  nature  of  the  pulmonary  lesion  was  suspected,  thanks  to  an 
exostosis  of  the  tibia.  In  the  so-called  phthisical  patient  to  whom  I  was 
called  the  tertiary  ulceration  of  the  arm  revealed  the  diagnosis  ;  the  corona 
Veneris  caused  Panas  to  think  that  his  patient's  cavity  was  of  syphilitic 
origin.  As  a  general  rule,  in  spite  of  the  marked  frequency  of  tuberculosis 
over  pulmonary  syphilis,  the  personal  and  family  history  should  always 
be  scrutinized,  and  if  some  stigmata  of  syphilis  be  fomid,  specific  treatment 
mast  be  instituted  without  delay. 

The  pulmonary  syphilis  that  I  have  just  described  is  due  to  the  cir- 
cumscribed gumma  and  to  the  diffuse  syphiloma.  In  acute  cases  events 
hasten  on,  and  the  patient  appears  to  be  suffering  from  acute  tubercular 
lesions.  In  cases  of  slow  course  the  lesions  gradually  lead  to  caseation, 
ulceration  of  the  lung  and  cavity.  They  simulate  ordinary  chronic  tuber- 
culosis. To  sum  up,  whether  it  be  a  question  of  circumscribed  gummatous 
syphiloma  (gummata)  or  of  diffuse  gummatous  infiltration  (false  broncho- 
pneumonia), we  see  a  process  which  has  a  tendency  to  ulceration,  whUe  its 
course  may  be  rapid  or  slow  with  all  intermediate  forms. 

3.  Pulmonary  Syphiloma,  with  Fibrosis  or  Sclero-Gummatous  Lesions. 

In  this  variety  the  lesion  consists  in  hyperplasia  of  the  connective  tissue 
wliich  forms  the  stroma  of  the  lung.  Fibro-plastic  tissue  is  thus  dissem- 
inated through  the  whole  parenchyma.  This  syphilitic  cirrhosis,  which 
clinically  assumes  the  form  of  chronic  broncho-pneumonia  in  most  cases, 
presents  the  following  anatomical  changes  :  We  find  in  a  lobe  of  the  lung 
a  reddish-grey,  hard  block,  which  creaks  under  the  knife,  contains  ampullary 
or  sacciform  dilatations  of  the  bronchi,  and  is  covered  by  very  thickened 
pleura,  while  intercostal  periostitis  may  be  also  present.  The  surface  of 
the  lung  may  be  furrowed  by  ridges,  that  radiate  like  the  cicatrices  seen 
in  a  syphilitic  liver.  We  sometimes  find  in  the  deep  tissues  large  bands  of 
fibrous  tissue  having  the  white  pearly  appearance  of  tendons.  The  lesion 
may  vary  much  in  kind.  It  may  be  purely  fibrous,  without  caseous 
nodules  or  evident  gummata  ;  it  may  be  sclero-gummatous,  in  which  case 
we  find  in  the  bronchi  or  in  the  peribronchial  or  p(;rilobular  fibrous  tissue 
gummata  which  are  sometimes  so  small  that  it  would  be  impossible  to  say 
at  first  sight  whether  they  are  tubercular  granulations  or  microscopic 
gummata.  The  lesion  may  resemble  the  syphilitic  i)ncum()[)atliy  of  the 
new-born,  which  we  shall  describe  under  the  name  of  white  pneumonia. 


240  TEXT-BOOK  OF  MEDICINE 

The  histogenesis  of  this  process  presents  some  interesting  points.  The 
lesion  begins  most  often  around  the  medium-sized  bronchi  at  the  hilum, 
from  whence  it  appears  to  radiate  into  the  lung  tissue.  The  new  tissue  thus 
forms  a  fibrous  or  sometimes  chondroid  muff  around  the  bronchi  or  around 
the  arterioles  which  accompany  them.  It  finally  surrounds  the  alveolus 
and  the  pulmonary  lobule,  so  that  in  distribution  it  is  a  form  of  broncho- 
pneumonia. The  connective  proliferation  causes  deformity  of  the  bron- 
chioles, which  may  be  dilated  or  stenosed.  The  alveoli  are  pressed  together, 
and  their  epithelium  is  often  in  a  state  of  fatty  degeneration. 

In  some  cases  the  broncho-pulmonary  lesions  are  accompanied  by  chronic 
pleurisy,  with  thickening  of  the  pleura  and  eflusion.  The  effusion  may 
indeed  be  the  chief  lesion,  as  we  shall  see  under  Syphilitic  Pleurisy. 

Syphilitic  cirrhosis  of  the  lung  is  difficult  to  diagnose.  Chronic  broncho- 
pneumonia is  easily  diagnosed,  according  to  certain  signs  presented  by  the 
patient  during  the  past  few  months  or  years  ;  later,  if  abundant  foetid  sputum 
appears,  with  gurgling  and  cavernous  breathing,  dilatation  of  the  bronchi  is 
readily  recognized.  The  diagnosis  is  facilitated,  furthermore,  by  the  pul- 
monary antecedents  and  the  absence  of  Koch's  bacillus  in  the  sputum.  A 
physician,  suspicious  of  the  signs  furnished  by  auscultation,  will  establish 
an  exact  anatomical  diagnosis  :  chronic  broncho-pneumonia,  fibroid  state 
of  the'  lung,  with  or  without  dilatation  of  the  bronchi.  What  escapes  him, 
however,  is  the  cause  of  this  condition.  He  finds  neither  measles  nor 
previous  whooping-cough  to  explain  it,  and  unless  he  discovers  a  specific 
lesion  of  the  larynx,  the  skin,  the  tibia,  etc.,  elsewhere,  or  the  presence  of 
syphilitic  scars,  the  true  nature  of  the  lung  trouble  will  pass  unnoticed. 
This  cirrhotic  broncho-pneumonia,  which  usually  runs  a  slow  course,  may, 
in  exceptional  cases,  be  acute.  It  is  susceptible  to  improvement  by  anti- 
syphilitic  treatment. 

The  sclerous  syphiloma  is  often  accompanied  by  dilatation  of  the 
bronchi,  both  in  the  hereditary  and  the  acquu-ed  disease  (Balzer,  Grand- 
homme,  and  Grawitz).  Sometimes  bronchiectasis  is  the  cliief  lesion. 
Several  cases  have  been  collected  by  Bourdieu.     For  example  : 

A  man,  fifty-eight  years  of  age,  who  contracted  syphilis  at  the  age  of  twenty-five, 
came  under  Lancereaux  for  limg  trouble,  characterized  by  incessant  cough  and 
abundant  expectoration.  He  had  coughed  for  ten  years,  and  brought  up  8  to  10  oimces 
of  purulent  sputum  in  the  twenty-four  hours.  Examination  of  the  chest  revealed  at 
the  bases  rather  than  at  the  apices  gurgling,  which,  with  the  other  signs,  led  to  the 
diagnosis  of  bronchial  dilatation.  As  albuminuria,  axlema  of  the  lower  limbs,  and 
dyspnoea  were  present,  the  existence  of  nephritis  was  allowed.  The  patient  died,  and 
the  autopsy  gave  the  folloA\ing  results  :  The  bronchi  showed  cylindrical  dilatation  ;  the 
walls  were  transformed  into  a  greyish,  resistant  tissue,  which  encroached  on  the  neigh- 
bouring parenchyma.  The  newly-formed  tissue,  which  replaced  the  wall  of  the  bronchus, 
was  infiltrated  by  miliary  gummata.  Several  of  these  were  calcified,  and  looked  like 
small  stones,  in  size  from  a  pin's  head  to  a  pea.    The  interbronchial  tissue  was  resistant 


DISEASES  OF  THE  LUNG  241 

and  traversed  by  bands  of  fibrous  tissue.  The  gummatous  lesion  in  the  bronchi  was 
more  marked  than  the  fibrosis  in  the  lung,  for  none  of  those  fibrous  masses  which  resist 
the  knife  and  correspond  to  the  description  of  syphilitic  intei'stitial  pneumonia  were 
found.  The  liver  was  syphilitic  and  of  the  "  tight-laced  "  form.  The  kidneys  showed 
amyloid  degeneration  of  syphilitic  origm.  Syphilis  had  destroyed  the  resistance  of 
the  bronchial  walls,  causing  bronchiectasis. 

Local  or  generalized  bronchiectasis  is  certainly  tlie  most  rare  of  all  the 
anatomical  forms  of  pulmonary  syphilosLs.  It  is  always  more  or  less  asso- 
ciated with  broncho-pneumonia,  fibrosis,  and  pleurisy.  The  symptoms  and 
the  course  of  syphilitic  bronchiectasis  differ  in  no  way  from  those  which 
accompany  bronchiectasis  in  general. 

Syphilitic  adenopathies  of  the  mediastinum  are  sometimes  associated 
with  syphiloma  of  the  lung.  They  exist  both  in  the  case  of  hereditary  and 
of  acquired  syphilis.  They  are  not  frequent,  but  may  acquire  supreme 
importance,  because  they  exert  pressure  upon  the  neighbouring  organs,  as 
in  the  following  case  : 

A.  G.  was  brought  by  her  mother  to  the  Saint-Andre  Hospital.  This  child,  aged  ten 
and  a  half  yeai-s,  had  suffered  for  three  months  from  palpitation  of  the  heart,  giddiness 
with  breathlessncss,  and  violent  headache  at  night.  Painful  fits  of  coughing  had  been 
present  for  nearly  three  months. 

We  learnt  that  the  mother  had  aborted.twice — at  seven  months  and  at  eight  and  a 
half  months.  Before  the  birth  of  A.  she  had  had  sore  throat,  lost  her  hair,  and  noticed 
spots  on  her  body  and  an  eruption  on  the  palm  of  her  hands.  The  husband  had  similar 
trouVjles  six  weeks  before.  Examination  of  the  child  :  Notched  teeth,  ulcerated  on 
their  anterior  surface.  On  both  sides  of  the  neck  was  a  chain  of  glands,  hard, 
and  not  matted  together.  Chest  thin  and  boat-shaped.  Supra-  and  subclavicular 
hollows  well  marked.  The  jugular  veins  were  dilated,  and  on  the  front  of  the  neck 
was  a  large  network  of  veins,  which  collapsed  during  rest,  but  swelled  under  the  influ- 
ence of  any  effort.  On  percussion,  a  band  of  dullness,  most  marked  over  the  right 
sternoclavicular  articulation  and  Ijehind  over  the  three  ujjper  dorsal  vertebra?,  was 
found.  Harsh,  almost  cavernous,  breathing,  with  some  moist  rules,  was  heard  over 
the  right  apex.  The  child  had  fits  of  coughing,  which  lasted  several  months,  and 
threatened  to  choke  her.  In  short,  the  symptoms  of  enlarged  glands  in  the  mediastinum 
were  found.  Profuse  muco- purulent  expectoration.  Given  the  diagnosis  of  hereditary 
syphilis,  the  following  prescription  Avas  ordered  :  locUde  of  potash,  150  grains  ;  per- 
chloride  of  mercury,  1  grain  ;  currant  syrup,  5  ounces.  Three  t«aspoonfuls  a  day. 
Chlorate  of  pota.ssium,  4.5  grains  daily. 

Under  specific  treatment  the  appetite  returned  in  the  first  week,  and  the  headache 
ceased  ;  the  heart  regained  its  normal  rhythm  ;  the  interscapular  dullness  disappeared, 
and  the  breathing  improved.  Similar  changes  in  the  chain  of  glands.  After  twenty- 
five  days'  treatment  there  was  hardly  any  dullness  over  the  right  stemo- clavicular 
articulation.  The  vesicular  murmur  reappeared  under  the  right  clavicle,  and  tlie 
cough  wa.s  less  paroxysmal,  while  the  sp.osms  of  suffocation  diminished  in  fre(iuency 
and  then  disapjieared.  'J'he  child  was  examined  five  months  later.  Heart  and  lungs 
presented  nothing  abnormal.  She  was  seen  next  year  on  several  occiusions,  and  remained 
in  good  health.  Tracheo-bronehial  adenopathy  of  syphilitic  origin  was  therefore 
inidcniable  in  this  cjxse. 

Hal/.cr  has  reported  (raeheo  bronchial  adenopathy  in  a  patient  witii  juiniiicd 
svpliilis.     The  patient  had,  among  other  symptoms,  stridor  and  sucking-in.     At  the 

16 


242  TEXT-BOOK  OF  MEDICINE 

autopsy  sclero-gummatous  adenopathy  of  the  tracheo-bronchial  glands  was    found, 
with  fibrous  syphiloma  involving  the  lung  and  pleura. 

In  a  case  published  by  Raymond  the  patient  had,  among  other  symptoms, 
stridor  and  sucking-in.  Syphilitic  adenitis  of  the  peritracheal  glands  was  found,  with 
narrowing  of  the  trachea  and  compression  of  the  right  recurrent  nerve. 

4.  Syphilitic  Gangrene  of  the  Lung. 

Syphilitic  gangrene  of  the  lung  exists.  "  In  such  a  case,"  says 
Mauriac,  "  the  expectoration  exhales  an  evil  odour,  and  may  even  have 
the  foetor  of  gangrene.  The  condition  is  not  common,  but  it  must  be 
noted.  It  is,  hideed,  surprising  that  it  is  so  rare,  for  many  conditions 
favourable  to  gangrene  are  present — e.g.,  necrobiosis  of  the  parenchyma, 
contact  of  the  air  with  the  products  of  pulmonary  disintegration,  and 
stagnation  of  sputum  in  the  dilated  bronchi  or  m  the  gummatous  cavities." 

The  followmg  case  (Feulard)  may  be  quoted  : 

A  man,  thirty -seven  years  of  age,  who  contracted  syphilis  when  twenty,  was  seized, 
after  some  days  of  malaise,  with  pain  in  the  side,  fever,  and  expectoration.  Ausculta- 
tion revealed  blowing  inspiration  and  rales,  localized  behind  to  the  middle  third  of  the 
right  lung.  The  expectoration  was  blackish,  and  of  an  alliaceous  odour.  Gangrene  of 
the  lung  was  diagnosed,  and  as  the  patient  was  syphilitic,  he  was  put  on  iodide  of 
potash.  At  first  improvement  occurred,  but  a  month  later  the  patient  brought  up 
fCEtid  sputum  containing  blood  and  pus  after  violent  fits  of  coughing.  Within  two 
months  a  cavity  formed  under  the  right  clavicle.  The  general  condition  and  the  signs 
on  auscultation  led  Duguet  to  diagnose  j^hthisis  in  the  cachectic  period.  As  examina- 
tion of  the  sputum,  made  by  Feulard  and  confirmed  by  Chantemesse,  revealed  no 
tubercle  bacilli,  he  was  again  put  on  iodide  of  potash  in  doses  of  150  grains  daily,  in 
case  the  pulmonary  lesion  was  perhaps  syphilitic.  After  this  treatment  improvement 
was  manifest,  yet  a  fresh  gangrenous  vomica  occurred  a  month  later.  Inunction  of 
mercury  was  also  employed,  and  complete  success  at  once  followed.  In  three  months 
the  cavity  had  filled  up,  and  six  years  after  Feulard  was  satisfied  that  the  cure  was 
maintained. 

In  the  course  of  this  chapter  I  have  cited  a  case  of  Dr.  Latty's — a  girl  eight  years 
old,  who  was  suffering  from  hereditary  syphilis,  taken  ill  with  symptoms  of  gangrene 
of  the  lung.  She  brought  up  gummatous  matter  in  the  sputum,  which  was  the  colour 
of  wine-lees,  and  terribly  foetid.  The  patient  recovered,  and  the  evacuation  of  the 
gummata  was  followed  by  enormous  retraction  of  one  side  of  the  chest. 

5.    Syphilitic  Pneumopathy,  associated  with  Pulmonary  Tuberculosis. 

Let  us  now  consider  the  possible  association  of  syphilis  and  tuberculosis 
m  the  lung.     This  condition  may  arise  in  two  ways.     Sometimes  tubercu 
losis  complicates  syphilis,  at  other  times  syphilis  complicates  tuberculosis. 

In  the  former  category  tuberculosis  appears  hi  a  syphilitic  patient.  It 
may  occur  early,  within  a  few  months  of  infection,  or  late,  some  years  after. 
The  appearance  of  tuberculosis  is  sometimes  so  early  that  it  coincides  with 
the  roseola  and  the  first  mucous  patches.  I  have  asked  myself  m  such  a 
case  whether  syphilis  did  not  hatch  the  latent  bacilh. 


DISEASES  OF  THE  LUNG  243 

I  have  seen  two  cases  of  this  kind,  one  of  them  with  Foiirnier.  In  a 
strong,  well-built  youth,  twenty  years  of  age,  hsemoptysis  and  early  signs 
of  pulmonary  tuberculosis  at  the  left  apex  appeared  two  months  after 
the  chancre.  Jacquinet,  in  hLs  thesis,  has  collected  eight  cases  of  early 
tuberculosis  during  the  secondary  stage.  The  patients  had  cutaneous  or 
mucous  syphilides,  and  the  syphilitic  infection  dated  only  a  few  months  or 
a  few  years  back.  "  In  these  cases  the  pulmonary  tuberculosis  ran  its 
course  in  a  few  months.  Statistics  would  seem  to  show  that  these  grave 
cases  of  tuberculosis  belong  to  the  period  in  which  syphilis  is  most  virulent." 
This  assertion  is  possible  ;  let  us  add  that  it  is  not  absolute. 

Tuberculosis  most  often  makes  its  appearance  during  the  tertiary  period 
of  syphilis.  In  the  section  on  Syphilis  of  the  Larynx  we  have  seen  that  an 
ulcerated  syphilide  of  the  larynx  may  determine  the  fixation  of  Koch's 
bacillus  ;  so,  too,  in  a  healthy  patient  exempt  from  any  tubercular  taint, 
tertiary  syphilis  of  the  lung  may  favour  the  fixation  of  the  bacillus  and  the 
growth  of  tubercles.  We  can  thus  explain  how,  after  a  long  and  fruitless 
search  for  Koch's  bacillus  in  the  sputum  of  patients  with  pulmonary  gum- 
mata,  it  may  finally  be  met  with.  If  in  the  same  lung  the  tubercle  miites, 
as  it  were,  with  the  syphiloma,  it  does  not  mean  that  a  hybrid,  anatomical 
condition  exists  in  the  shape  of  "  scrofulate  de  verole,^^  as  Ricord  said. 

The  syphilitic  and  tubercular  lesions  arise  and  develop  side  by  side, 
though  separately,  and  each  on  its  own  account.  The  anatomical  proof  of 
this  has  been  given  by  Potain,  during  an  autopsy  in  which  he  met  with 
disseminated  tubercles  around  a  mass  of  white  syphilitic  pneumonia.  This 
secondary  infection  of  a  syphilitic  lung  by  tuberculosis  permits  us  to  para- 
plirase  the  old  adage  of  Niemeyer  :  "  The  greatest  danger  for  a  syphilitic 
phthisical  patient  is  to  become  tubercular." 

According  to  Landouzy,  the  appearance  of  tuberculosis  in  a  patient 
with  old  syphilis  is  not  so  serious  as  its  appearance  during  recent  syphilis. 
"  The  course  of  events  appears  to  me  to  be  quite  different,"  says 
Landouzy,  "  in  a  patient  who  has  had  syphilis  for  some  twenty  years, 
and  is  attacked  by  tuberculosis.  Patients  showing  this  chronological  variety 
of  morbid  association  appear  to  me — in  a  tenth  of  the  cases,  at  least — to 
present  a  peculiar  tuberculosis  which  is,  from  the  pathological  point  of  view, 
rather  fibrous,  and  from  that  of  evolution,  slow,  apyretic,  and  localized. 
Referring  to  this  category  of  patients  who  are  suffering  from  old  syphilis 
and  recent  tuberculosis,  I  am  in  the  habit  of  saying  familiarly  that  they 
go  on  to  the  verolate  de  tuber culose.''^ 

Hereditary  syphilis  has  an  action  upon  the  development  of  tuberculosis, 
which  may  be  interpreted  in  various  ways,  but  which  is  indisputable. 
"  Clinical  observation,"  says  Fournier,  "  shows  that  hereditary  syphilis 
predisposes  to  various  diseases,  doubtless  by  reason  of  the  relative    im- 

16—2 


244  TEXT-BOOK  OF  MEDICINE 

poverishment  of  the  organism.  Hence  the  frequency  of  scr of ulo -tuber- 
cular affections  has  long  been  marked  in  children  born  of  syphilitic  stock. 
It  is  certain  that  the  syphilitic  soil  is  eminently  propitious  to  the  culture 
of  the  bacillus,  for  from  statistics  and  contemporaneous  observation  which 
have  quite  confirmed  the  results  of  our  predecessors  on  this  point,  it  is 
undeniable  that  patients  with  hereditary  syphilis  are  very  subject  to 
scrofulo-tuberculosis,  notably  to  affections  of  the  bones  (Pott's  disease, 
coxalgia,  etc.),  and  to  tubercular  lupus.  It  may  be  asked  why  the  syphilitic 
person  so  often  gives  birth  to  a  tubercular  child,  whether  it  results  from 
the  condition  of  cachexia,  which  is  not  constant,  or  from  the  transmission 
of  a  specific  agent,  which  favours  the  development  of  the  other.  We  know, 
too,  that  syphilis  is  one  of  the  constitutional  diseases  which  produces  most 
of  the  abortions,  of  the  strumous  diseases  of  the  glands,  and  of  degenerated 
scrofula— in  short,  most  of  those  puny,  rachitic,  and  weakly  subjects  who 
are  an  easy  prey  to  tuberculosis." 

6.  Hereditary  Syphilis  of  the  Lung. 

Let  us  return  to  the  important  question  of  hereditary  syphilis,  which 
may  affect  the  lung,  as  it  does  other  parts.  It  may  be  early  or  late.  Early 
syphilis  is  no  longer  seen.  It  is  met  with  in  still-born  children,  or  in  those 
who  have  lived  a  few  months,  and  has  only  a  pathological  mterest.  Depaul 
had  already  observed  among  the  cutaneous  and  visceral  changes  the  lesion 
of  the  lung  which  Virchow  described  later  under  the  name  of  pneumonia 
alba.  White  pneumonia,  described  by  Parrot  m  1877,  and  later  m 
1879  by  Cornil,  in  children  who  died  when  five,  six,  and  seven  months 
old,  is  peculiar  to  the  syphilitic  cachexia  of  the  new-born  in  the  same  way 
as  the  flint-like  liver  of  Giibler.  The  term  "  white  pneumonia  "  is  correct, 
because  the  tissue  is  white  or  greyish.  The  lesion  is  sometimes  disseminated 
in  a  lobular  form,  at  other  times  confluent  in  a  pseudo-lobar  one.  The 
hepatized  nodules  are  smooth,  hard,  and  dense,  creak  under  the  knife,  and 
sink  m  water.  The  histological  lesions  may  be  thus  summed  up  :  Thickening 
of  the  walls  of  the  bronchioles  and  of  the  alveoli,  lesions  of  epithelial  pneu- 
monia, with  desquamation  into  the  alveoli,  while  the  cells  themselves  have 
undergone  granulo-fatty  degeneration. 

Late  hereditary  syphilis  of  the  lung  is  not  so  well  known,  but  is  far  more 
interesting.  It  is  less  frequent  than  hereditary  syphilis  of  the  larynx,  for 
in  1886,  out  of  a  total  of  212  cases,  Fournier,  in  his  "  Syphilis  Hereditaii-e 
Tardive,"  could  collect  only  five  cases  of  hereditary  syphilitic  phthisis.  It 
may  appear  some  months  after  birth,  but  is  most  often  seen  from  the  sixth 
up  to  the  twentieth  year,  and  possibly  still  later.  It  is  therefore  in  most 
cases  a  disease  of  childhood  or  of  youth,  and  sometimes  also  of  mature  age. 


DISEASES  OF  THE  LUNG  245 

I  need  not  dwell  on  the  sclero -gummatous  lesions  of  late  hereditary 
syphilis.  They  are  identical  with  those  of  the  acquired  disease.  T  shall 
simply  quote  cases  which  prove  that  syphilitic  lesions  of  the  lung  may 
develop  in  children  born  of  syphilitic  parents. 

Fournier  speaks  of  a  child,  seven  years  of  age,  who  suffered  from 
hereditary  syphilis,  and  died  by  accident  of  an  acute  intercurrent  malady. 
Three  small  gummata,  which  had  given  rise  to  no  symptoms  during  life, 
were  found  post  mortem  in  the  lung. 

Lannelongue  and  Lancereaux  have  each  seen  a  similar  case.  The  dis- 
covery of  gummata  in  the  lung  in  these  cases  was  a  post-mortem  surprise. 

Fournier  has  reported  a  case  of  Dr.  Latty's  given  on  p.  242. 

I  have  observed  the  following  case  of  hereditary  syphilis  of  the  lung  : 

I  was  called  in  to  treat  a  little  girl  of  fourteen  or  fifteen  months,  whose  father  I 
had  previously  attended  for  syphilis.  She  suffered  in  succession  from  ocular  troubles, 
otitis,  and  periostitis  of  both  Avrists,  and  then  went  back  to  Russia.  Two  years  later 
the  father  came  back  to  Paris  to  bring  his  son  to  me,  who,  as  he  thought,  was  sure  to 
die.  He  showed  all  the  signs  of  cavity  in  one  lung,  and  had  every  appearance  of 
phthishs.  Knowing  the  father's  history,  I  diagnosed  hereditary  syphilis,  ordered 
specific  treatment,  and  gave  hopes  of  an  early  cure.  My  predictions  were  realized 
for  aft<'r  a  few  days  the  sweats  ceased,  the  appetite  returned,  the  physical  signs 
improved,  and  in  a  few  weeks  the  trouble  had  disappeared.  It  is  possible  that  a 
physician  who  was  ignorant  of  the  father's  history  would  have  treated  the  ca.se  as 
tuberculosis,  and  this  error  would  have  cost  the  boy  his  life. 

The  following  case  of  pulmonary  syphilis  was  reported  by  Legrand. 
Tlic  disease  was  hereditary,  as  the  reader  will  see  : 

A  man  was  admitted  into  the  Saint-Antoine  Hospital  with  cough,  ha-moptysis, 
and  the  usual  signs  of  phthisis.  We  were,  however,  in  doubt  from  the  strange  localiza- 
tion of  the  lesion  to  the  middle  part  of  the  lung,  the  absence  of  bacilli  in  the  sputum, 
and,  Uwtly,  by  the  presence  of  Hutchinson's  teeth.  On  inquiring  into  his  past  history,  we 
found  stigmata  of  syphilis,  the  chronological  connection  of  which  was  so  evident  as  to 
surprise  us.  This  man,  some  years  previously,  had  suffered  from  gummata  of  the 
tibia,  recognized  by  Dr.  Barbe  ;  the  astonishing  thing  wa,s  that  he  had  afterwards 
contracted  an  indurated  chancre  of  the  penis,  the  scar  of  which  wa.s  only  noticeable 
for  sixteen  months.  He  had  had  syphilis  on  two  occa.sions— first,  hereditary  (the  dental 
deformities  and  the  gummata  in  the  lower  limbs  proved  this) ;  and,  secondly,  acquired 
(the  hard  chancre  of  relatively  recent  date  proved  this).  Iodide  of  pota.sh  and  mercury 
were  administered,  and  soon  cured  tlK^  lung  trouble. 

I  <!(>  not  know  of  a  more  conclusive  case  than  the  following  (Dubousquet- 
Laborderie  and  Gaucher)  : 

A  little  girl,  eight  and  a  half  years  old,  was  wasted  and  cachectic.  She  coughed 
continually,  her  apjietite  wjus  gone,  her  tem|)erature  was  102 '  F.,  and  her  pulse  HO.  Her 
general  condition,  in  short,  wa,s  that  of  a  patient  in  the  last  stage  of  phthisis.  Cavemou.s 
breathing  and  gurgling  were  heard  in  the  right  supraspinous  fossa.  I^rge  mucous 
rales  were  scattered  throughout  the  whol(.  chest.  The  diagnosis  was  pulmonary  tuber- 
culosis in  the  third  stage.  Treatment  gav<!  no  results.  Fever,  cough,  and  wasting, 
and  signs  furnished  by  auscultation,  underwent  no  change,  llie  child  complained  .tf 
acute  pain  in  the  middle  of  the  sternum.      Pressure  was  very  painful,  and  tuU-rcuhir 


246  TEXT-BOOK  OF  MEDICINE 

osteitis  was  at  first  thought  of.  After  a  few  days  a  tumour  developed  in  the  painful 
region.  This  tumour  reached  the  size  of  a  small  orange,  and  fluctuated.  The  skin 
became  thin,  and  ulceration  commenced.  Puncture  gave  issue  to  a  puriform,  gela- 
tmous,  and  shreddy  fluid.  The  luiusual  course  of  this  tumour,  which  was  taken  at 
first  for  an  abscess,  and  the  nature  of  its  contents,  gave  the  idea  of  a  gumma,  more 
especially  as  the  child  presented  dental  changes  which  had  previously  been  considered 
rachitic. 

As  it  was  felt  that  the  lesion  might  be  syphilitic,  Gibert's  syrup  was  prescribed, 
^  drachm  morning  and  evening.  A  few  days  later  the  diagnosis  of  hereditary  syphilis 
was  confirmed,  because  the  father  came  to  Dr.  Dubousquet  for  syphilitic  onychia  of 
the  left  hand  and  thickening  of  the  periosteum  of  the  right  tibia.  Gibert's  syrup 
cured  both  these  lesions  in  a  fortnight.  The  girl  took  the  syrup  for  a  week,  and  was 
then  treated  with  mercurial  inunctions  and  iodide  of  potash  in  gradually  increasing 
doses  imtil  10  grains  were  taken  daily.  Improvement  was  soon  manifest.  The  strength 
came  back,  the  evening  fever  disappeared,  the  physical  signs  diminished  rapidly,  the 
cavity  filled  up,  and  at  the  end  of  a  month  only  faint  tubular  breathing  was  heard  at 
the  apex.  The  sternal  gumma,  after  suppurating  for  some  time,  became  covered  by 
granulations,  and  soon  healed.  In  about  two  months  the  child  was  completely  cured, 
and  was  in  good  health  ten  months  after  the  first  recognition  of  these  symptoms. 

In  cases  of  this  kind  we  are  given  a  clue  to  the  diagnosis  by  the  usual 
signs  of  hereditary  syphilis,  which  are  as  follows  : 

(1)  Dental  malformations,  indentation,  cup  -  like  excavations,  trans- 
verse striae,  small  size  of  the  incisor  teeth ;  (2)  ocular  lesions,  diffuse  inter- 
stitial keratitis  ;  (3)  aural  lesions  and  troubles,  deafness  ;  (4)  malformations 
of  the  tibia,  swelling  of  the  epiphysis,  bosses  on  the  shaft,  flattening  of  the 
crest  (Fournier). 

Treatment. — The  drugs  here,  as  in  other  cases  of  syphilis,  are  mercury 
and  iodide.  They  both  have  a  marvellous  action  upon  syphilis,  but  had 
I  to  choose  between  the  two,  I  should  give  the  preference  to  mercury. 
The  old  preparations  of  mercury,  the  proto-iodide,  van  Swieten's  liquor, 
and  mercurial  inunctions,  etc.,  are  of  service,  but  nothing,  in  my  opinion, 
is  so  valuable  as  an  injection  of  biniodide  of  mercury  in  aqueous  solution. 
Each  Pravaz's  syringeful  represents  yV  grain  of  the  active  principle.  Fifteen 
injections  are  given,  injecting  daily  from  ^V  to  |  grain  of  biniodide  of 
mercury. 

The  injections  are  then  replaced  by  iodide  of  potash  in  a  daily  dose  of 
30  to  75  grains,  according  to  the  tolerance  of  the  patient.  Ten  days  to  a 
fortnight  later  the  injections  are  again  given. 

The  results  obtained  vary  according  to  the  varieties  of  the  pulmonary 
syphilosis.  In  the  case  of  sclerous  broncho-pulmonary  syphiloma,  with 
fibrous  change  in  the  lung,  the  bronchi,  and  the  pleura,  improvement  is 
delayed,  and  complete  cure  is  rarely  obtained,  because  of  the  definite  change 
in  the  tissues.  If  the  syphiloma  of  the  lung  is  still  in  active  growth,  if 
there  is  a  circumscribed  gumma,  or  an  infiltrating  syphiloma,  with  acutej 
subacute,  or  chronic  broncho-pneumonia,  surprising  results  are  sometimej 


DISEASES  OF  THE  LUNG  247 

obtained.  The  proof  is  found  in  the  history  of  the  patients  given  in  this 
chapter,  or  in  my  clinical  lectures  at  the  Hotel-Dieu.  Two  patients  in  the 
Saint-Christophe  Ward  were  cured,  the  one  of  acute,  the  other  of  chronic, 
syphiloma  of  the  lung.  Giraudeau's  patient  (p.  233)  was  cured  in  a  few 
weeks.  Giibler's  patient,  with  cavity  and  symptoms  of  phthisis,  was  also 
cured  in  a  short  while.  The  patient  in  whom  Fournier  and  myself 
found  rapid  breaking-down  of  the  apex  of  the  right  lung  and  a  syphilitic 
testis  was  cured  in  a  few  weeks.  The  young  man  who  appeared  m  the  last 
stage  of  phthisis,  and  in  whom  I  found  an  enormous  cavity  in  the  right 
lung,  recovered  with  truly  marvellous  rapidity.  By  grouping  these  cases 
and  recognizmg  how  health  was  restored  to  cachectic  people  who  presented 
the  picture  of  acute  phthisis  or  of  advanced  pulmonary  tuberculosis,  we 
learn  the  imperative  necessity  of  making  a  correct  diagnosis  and  of  employ- 
ing proper  treatment. 

The  irrefutable  proof  that  all  these  patients,  saved  by  specific  treatment, 
really  had  syphilitic  lesions  of  the  lung,  is  that  they  were  cured  of  visible 
syphilitic  manifestations  which  occurred  in  the  other  parts  at  the  same 
time  as  the  lesion  in  the  lung.  The  patient  whom  I  saw  with  Fournier 
was  cured  simultaneously  of  syphiloma  of  the  lung  and  of  the  testis. 
Giraudeau's  patient  was  cured  successively  of  pulmonary  syphiloma, 
of  vaginal  gumma,  and  of  periostitis  of  the  forehead.  Giibler's  patient 
was  cured  of  pulmonary  syphiloma  and  of  a  tibial  exostosis.  Fournier's 
patient  was  successively  cured  of  a  phagedsenic  ulceration  of  the  foot  and 
of  a  syphilitic  cavity  of  the  lung. 

So  many  accumulated  proofs  cannot,  and  ought  not,  to  leave  any  doubt 
concerning  the  existence  of  pulmonary  syphiloma  and  the  efficacy  of  the 
treatment,  which  is  sometimes  surprising.  In  a  suspected  case  of  pul- 
monary tuberculosis  let  us  always  think  of  the  possibility  of  syphilis  ;  in 
dealing  with  a  patient  considered  as  a  case  of  incurable  phthisis  let  us  still 
think  of  syphilis ;  and  if  repeated  examinations  of  the  sputum  show  the 
a))sence  of  Koch's  bacillus,  let  us  have  immediate  recourse  to  specific  treat- 
ment— let  us  use  injections  of  biniodide  of  mercury.  It  is  the  touchstone, 
and  we  shall  perhaps  obtain  an  unexpected  cure. 


CHAPTER  V 
DISEASES  OF  THE  PLEURA 

I.  ACUTE  SERO-FIBRINOUS  PLEURISY— TUBERCULAR 
SERO-FIBRINOUS  PLEURISY 

Pleurisy  is  inflammation  of  the  pleura.  According  to  its  situation, 
pleurisy  may  be  partial,  diaphragmatic,  mediastinal,  or  interlobar  j 
according  to  the  nature  of  the  effusion,  it  may  be  sero-fibrinous,  haemor- 
rhagic,  or  purulent.  The  last  two  varieties  will  be  described  in  this 
chapter.  In  this  section  I  shall  consider  only  acute  sero-fibrinous  pleurisy 
of  the  great  pleural  cavity,  which,  I  may  say  in  advance,  is  nearly  always 
tubercular.  Acute  pleurisy,  formerly  called  genuine,  legitimate,  or  a  frigore, 
is  tubercular  in  most  cases. 

etiology.  —  Acute  pleurisy  is  seen  at  all  ages  ;  nevertheless,  it  is 
exceptional  in  very  young  children,  increases  in  frequency  about  the  age  of 
five  or  six  years,  and  reaches  its  maximum  in  the  adult,  while  it  becomes 
rarer  in  the  elderly.  Chill  has  long  been  considered  as  the  most  potent 
or  almost  the  only  cause  ;  this  form  has  been,  therefore,  called  "  pleurisy 
a  frigore."  And,  indeed,  it  appears  at  first  sight  that  chill,  in  its  different 
forms,  should  often  be  held  guilty.  It  may,  indeed,  be  a  provoking  agent, 
but  every  case  of  acute  pleurisy,  even  when  it  appears  to  be  primary,  is 
associated  with  an  infection  which  is  usually  tubercular.  This  important 
question  will  be  discussed  later. 

Pathological  Anatomy. — The  pleura,  the  false  membranes,  the  pleuritic 
fluid,  and  the  lung  demand  consideration. 

The  two  layers  of  the  pleura  are  congested  and  covered  by  fibrinous 
membranes  ;  the  serosa  is  infiltrated  with  leucocjrtes,  the  bloodvessels  are 
dilated,  the  lymphatics  are  packed  with  white  corpuscles,  and  the  most 
superficial  alveoli  are  the  seat  of  catarrhal  pneumonia.  Under  the  fibrinous 
layer  the  pleura  presents  granulations,  formed  of  embryonic  tissue  and  of 
young  vessels  ;  these  new  formations,  welded  to  those  of  the  opposite  layer, 
form  adhesions,  which  are  rare  in  the  acute,  but  common  in  the  chronic 
form  of  pleurLsy. 

248 


DISEASES  OF  THE  PLEURA  249 

The  false  membranes  are  more  or  less  spread  out  over  the  surface  of 
the  pleura  ;  they  are  easily  detached.  Their  surface  may  be  smooth  or 
mammillated.  Sometimes  they  extend  from  one  layer  to  the  other,  like 
bands,  and  often  float  in  the  pleural  fluid.  They  are  formed  of  fibrin, 
which  enmeshes  white  and  red  corpuscles  and  epithelial  cells. 

The  effusion  varies  in  amount ;  some  ounces  or  some  pints  are  found. 
The  fluid  is  fibrinous,  transparent,  and  citron-coloured,  and,  according  to 
my  observations,  only  commences  to  take  a  rosy  or  haemorrhagic  tint  when 
it  contains  5,000  to  6,000  red  corpuscles  per  cubic  millimetre.  On 
examining  the  fluid  at  the  moment  when  it  leaves  the  pleura  during  thora- 
centesis, I  have  always  counted  a  large  number  of  red  corpuscles  per  cubic 
millimetre.  It  may  be  said  of  this  pleurisy  that  it  is  histologically 
haemorrhagic.  When  the  fluid  is  left  in  a  beaker,  it  is  more  or  less  changed 
into  a  gelatiniform  mass,  according  to  the  amount  of  the  fibrin  present. 
If  we  pass  this  coagulated  liquid  through  linen  which  is  well  wrung  out, 
we  obtain  a  fibrinous  membrane,  which  owes  its  rosy  colour  to  the  red 
corpuscles  contained  in  its  meshes. 

The  fluid  has  a  density  of  1012  to  1022.  The  tension  of  the  fluid  in 
the  pleural  cavity  is  rarely  negative  ;  it  may  reach  or  exceed  4- 10  or  -i- 15. 
The  molecular  concentration  and  the  freezing-jjoint  of  these  liquids  are 
nearly  the  same  as  those  of  blood-serum.  •  Chloride  of  sodium  ingested  by 
the  patient  readily  passes  into  the  exudate,  and  appears  to  accumulate 
there,  by  favouring  the  increase  of  the  fluid  (Achard  and  Loeper). 

The  lung  subjacent  to  the  effusion  is  flattened,  congested,  and  airless. 
The  lesions  of  interstitial  pneumonia  and  carnification  of  the  lung  are  only 
seen  in  old  pleurisies. 

Bacteriology. — Examination  of  the  fluid  from  cases  of  sero-fibrinous 
pleurisy  proves  that  an  effusion,  which  is  tubercular  in  nature,  may  also 
contain  ordinary  pathogenic  microbes.  Thus,  in  these  cases — which,  how- 
ever, are  very  rare — the  existence  of  the  streptococcus  (Lacaze),  pneumo- 
coccus,  staphylococcus,  Bacterium  coli  (Le  Damany),  Eberth's  bacillus 
(Kelsch),  and  also  of  the  Micrococcus tetragenus,  has  been  proved.  Inocula- 
tion of  animals  may  prove  the  virulence  of  these  microbes,  without  allowing 
any  conclusion  to  be  drawn  as  to  the  prognosis  and  pathogenic  diagnosis 
of  the  j)leurisy.  These  bacterial  associations  do  not  a[)pear  to  influence 
the  course  of  tubercular  sero-fibrinous  pleurisy,  which  hardly  ever  becomes 
])uruletit,  although  the  effusion  may  contain  pyogenic  microbes.  These  cases 
are  so  rare  that  Nettcr,  Vaiilard,  and  Lemoine  admit  that  every  sero-fibrinous 
pleurisy  which  remains  sterile  should,  a  priori,  be  looked  upon  as  tuber- 
culous. We  must,  however,  make  an  exception  in  the  case  of  meta- 
pneumonic pleurisy,  in  which  the  ])neuniococcus  may  have  disapjicanMl 
at  the  time  of  puncture.     Prudden  wished  to  deduce  from  tiiis  fact  the 


250  TEXT-BOOK  OF  MEDICINE 

general  theory  that  microbes,  whatever  be  their  species,  might  play  an 
important  part  in  the  onset  of  pleurisy,  but  would  disappear  when  the 
effusion  was  clearly  formed.  A  different  opinion  has  been  upheld  by  Ferney 
in  France,  Lecoq  in  Austria,  and  Pansini  in  Italy. 

Pleural  Permeability.— The  study  of  the  permeability  of  the  pleura 
(Ramon,  Tourlet,  and  Castaigne)  aims  at  discovering  whether  the  absorbent 
power  of  the  serosa  varies  according  to  the  age  of  an  effusion,  and  whether 
it  differs  according  to  the  nature  of  the  effusion.  Renon  and  Latron  have 
just  carried  out  this  research  in  two  cases.  Widal  and  Ravaut  have  pro- 
posed the  use  of  salicylate  of  soda,  injected  in  doses  of  0'30  gramme,  first 
under  the  skin,  and  then  into  the  pleura.  Salicylic  acid  has  the  advantage 
that  it  can  be  estimated  with  great  precision  and  is  more  rapidly  eliminated 
in  the  urine  than  methylene  blue  or  iodide  of  potash.  The  two  injections 
(subcutaneous  and  intrapleural)  may  be  made  at  very  short  intervals.  It 
is  a  question,  in  short,  of  a  double  proof  by  pathological  physiology,  and 
further  study  will  be  interesting. 

Widal  and  Ravaut  have  drawn  the  following  conclusions  from  the 
examination  of  five  cases  :  In  a  case  of  primary  tubercular  pleurisy,  the 
permeability  of  the  pleura  was  diminished  ;  in  a  case  of  pneumonic  pleurisy 
it  was  altered  as  to  the  time,  but  not  as  to  the  quantity  of  salicylic  acid 
eliminated  ;  in  three  cases  of  pleurisy  of  mechanical  origin,  in  patients  with 
cardiac  lesions  or  with  Bright's  disease,  the  permeability  was  slightly  in- 
creased in  two,  while  it  was  diminished  in  the  third. 

In  the  next  section  we  shall  discuss  the  cyto-diagnosis  of  tubercular 
pleurisy. 

Symptoms. — How  does  acute  sero-fibrinous  pleurisy  begin  ?  The  disease 
may  begin  with  pain  and  fever,  or  may  be  latent.  Chills  and  fever  may 
open  the  scene.  The  patient  is  seized  with  dry,  painful  cough,  and  suffers 
on  one  side  of  the  chest,  most  often  in  the  region  of  the  nipple,*  from  a  more 
or  less  sharp  stabbing  pain  in  the  side,  which  is  made  worse  by  each 
attack  of  cough,  and,  indeed,  by  each  inspiration.  This  pain,  however, 
is  not  always  acute  ;  it  may  be  very  moderate  or  quite  absent. 

The  patient  has  difficulty  in  breathing,  so  that  the  respirations  are  short, 
jerky,  and  incomplete,  because  of  the  pain.  We  cannot,  however,  call  it 
true  dyspnoea.  The  pulmonary  congestion  which  so  often  accompanies 
pleurisy  may  also  cause  distress. 

At  this  period,  before  any  trace  of  effusion,  the  following  signs  are 
found  :  Percussion  yields  dullness,  without  special  character  and  precise 
limits ;  the   expansion  is   diminished  on  the  diseased  side,  and  ausculta- 

*  This  pain  in  the  side  is  not  always  at  the  level  of  the  nipple,  but  may  radiate  in 
various  directions.  According  to  the  most  widely  held  opinion,  it  is  due  to  neuritis  of 
the  intercostal  nerves.     See  Peter,  Clin.  Med.,  t.  i. 


DISEASES  OF  THE  PLEURA  251 

tion  reveals  either  true  friction  sounds  or  a  sound  somewhat  analogous  to 
a  fine  rale,  which  may  be  heard  at  the  back  of  the  chest  or  in  the  axilla, 
both  during  inspiration  and  expiration.  This  sound  is  more  moLst  and 
more  liquid  than  the  crepitant  rale  of  pneumonia,  and  is  also  much  more 
diffuse.  Opinions  differ  as  to  the  interpretation  of  this  sound.  Some  con- 
sider it  a  friction  sound,  others  a  rale,  due  to  the  cortical  pneumonia 
that  often  accompanies  pleurisy  (Trousseau) ;  and  Damoiseau  has  given 
it  the  name  of  "  friction  rale.'*     In  some  cases  it  is  wanting. 

The  initial  period  lasts  several  days,  and  its  approximate  limit  cannot 
be  fixed.  If  appreciable  exudation  does  not  supervene,  the  pleurisy  is  said 
to  be  dry ;  but  this  dry  form,  which  is  so  frequent  in  secondary  pleurisies, 
or  in  inflammation  of  the  chest,  is  quite  rare  in  acute  pleurisy.  Laennec 
doubts  it ;  Woillez  has  recognized  it  only  once  in  eighty-two  cases  ;  and  I 
have  very  rarely  met  with  it. 

Effusion,  then,  is  the  rule  in  acute  pleurisy,  but  it  appears  at  an  in- 
definite time,  usually  from  the  twelfth  to  the  fifteenth  day ;  I  have  even 
seen  a  case  on  the  seventeenth  day.  Let  us  suppose,  for  the  sake  of 
description,  that  the  disease  is  at  the  fifth  or  sixth  day,  while  the  effusion 
amounts  to  about  a  pint  and  a  half.  The  indefinite  signs  of  the  onset  have 
given  place  to  new  and  definite  ones.  The  diagnosis,  which  was  doubtful, 
is  now  certain.  The  pain  is  better,  and  therefore  the  patient  breathes  more 
freely.  On  percussion,  we  find  at  the  posterior  and  lower  part  of  the  chest 
dullness,  which  Piorry  called  "  fluid  dullness  ";  its  upper  limit  does  not  end 
suddenly,  but  gradually  shades  off  into  resonance.  Percussion  of  the 
clavicular  region  on  the  affected  side  gives  exaggerated  resonance  (called 
"  skodaic  "  by  Trousseau),  which  disappears  when  the  effusion  becomes 
very  abundant.  Palpation  shows  that  the  thoracic  vibrations  are  diminished 
or  abolished  behind  even  the  effusion,  and  measurements  taken  with  the 
cyrtometer  (Woillez)  reveal  the  enlargement  of  the  chest. 

Auscultation  above  the  effusion,  in  the  axilla,  or  at  the  antero-superior 
part  of  the  thorax,  may  reveal  friction  sounds  or  a  friction  rale  at  different 
points  ;  but  these  friction  sounds  are  no  longer  heard  over  the  area  occupied 
by  the  fluid,  because  the  two  layers  of  the  pleura  are  separated  from  one 
another. 

Auscultation  over  the  region  of  the  effusion  reveals  four  signs : 
(1)  Absence  of  vesicular  murmur  ;  (2)  presence  of  distant  tubular  breathing, 
which  is  sometimes  muffled,  at  other  times  clear  :  it  is  audible  only  during 
expiration,  and  principally  at  the  end  of  expiration ;  (3)  quavering  of  words, 
pronounced  in  a  high  voice  by  the  patient,  called  by  Laennec  "aegophony  "* 

*  iEgophony,  pectoriloquy,  and  bronchophony  aro  throe  physical  phcnonicii.-i  wiiic  Ii 
are  characterized  by  tlie  eclioing  of  the  voice ;  in  a>gophony  tl)o  voice  is  bleating,  while 
it  is  diffuse  in  bronchopliony,  and  clearly  articulate  in  pectoriloquy. 


252  TEXT-BOOK  OF  MEDICINE 

("the  bleating  of  a  goat") ;  and  (4)  aphonic  pectoriloquy*— that  is  to  say, 
the  clear  and  articulate  transmission  of  words  pronounced  by  the  patient 
in  a  Avhisper  (Bacelli,  Gueneau  de  Mussy).  These  signs  are  usually  most 
marked  at  the  lower  angle  of  the  scapula,  and  are  of  great  importance, 
but  yet  not  one  of  them  is  pathognomonic  of  pleural  effusion.  They  may 
lose  their  purity  and  become  disfigured  if  the  lung  be  congested  and  re- 
sistant beneath  the  effusion  (pleuro-congestion), 

I  shall  now  say  a  few  words  on  the  correct  method  of  percussion,  and 
the  means  used  in  determining  absence  or  diminution  of  the  vocal  fremitus. 
If  percussion  is  to  give  reliable  information,  it  must  not  be  performad 
forcibly,  as  is  too  often  done,  for  the  sound  then  obtained  destroys  in  a  grsat 
measure  the  delicate  shades  of  dullness,  or  of  impaired  resonance  which 
indicate  the  presence  or  the  absence  of  effusion.  Care  must  therefore  be 
taken  to  percuss  as  lightly  and  softly  as  possible,  in  order  to  give  a  true  result. 

I  may  make  a  similar  remark  as  regards  the  disappearance  of  the  vocal 
fremitus.  If  the  patient  be  made  to  count  in  a  high  voice,  the  vibrations 
are  transmitted — less  strongly,  it  is  true — on  the  side  of  the  effusion ;  but 
they  are  still  transmitted,  and  their  presence  may  give  rise  to  error.  If, 
on  the  contrary,  the  patient  be  made  to  count  in  a  slightly  raised  voice, 
the  vibrations  may  still  be  transmitted  to  the  healthy  side,  but  are  quite 
absent  over  the  effusion. 

As  the  effusion  increases  (2  to  3  pints),  certain  signs  are  modified  :  the 
aegophony  becomes  less  clear,  and  rather  bronchophonic  in  character  ;  the 
soft  tubular  breathing  on  expiration  takes  a  bronchial  tone,  and  is  also 
audible  during  inspiration  ;  auscultation  reveals  the  exaggerated  breathing, 
called  "  puerile,"  on  the  healthy  side  ;  and  the  effusion,  by  its  constant 
progress,  displaces  the  neighbouring  organs. 

The  displacement  of  organs  is  of  value  in  estimating  the  amount  of  the 
effusion.  It  has  much  less  value  in  effusions  on  the  right  side,  because 
the  liver  is  much  less  mobile  than  the  heart,  and  is  only  pushed  downwards 
when  the  fluid  amounts  to  at  least  3  pints.  On  the  other  hand,  in  effusions 
on  the  left  side,  displacement  of  the  heart  is  a  sign  on  which  I  cannot  lay 
too  much  stress.  The  displacement  of  the  heart  is  shown  by  inspection, 
palpation,  and  auscultation.  It  is  not  only  the  apex  of  the  heart  which  is 
displaced,  but  the  whole  heart  itself,  and  with  the  change  of  position  it  also 
alters  its  relations  to  the  chest-wall.  In  order  to  ascertain  the  displacement, 
we  must  look  for  the  maximum  point  of  the  impulse.  My  numerous  observa- 
tions lead  me  to  conclude,  aj^proximately,  that  this  maximum  point  reaches 
the  left  border  of  the  sternum  in  effusions  of  20  ounces  ;  it  reaches  the  right 
border  of  the  sternum  with  an  effusion  of  40  ounces ;  and  lies  between  the 

*  LatJnnec  had  already  jjointed  out  this  phenomenon,  and  Bacelh  has  given  the 
conclusions  which  may  be  drawn  from  aphonic  pectoriloquy  as  a  sign  of  pleiu"al  effusion. 


DISEASES  OF  THE  PLEURA  253 

sternum  and  riglit  nipple  with  an  effusion  of  60  ounces.  This  is  the  moment 
at  which  thoracentesis  must  be  performed. 

When  these  effusions  are  on  the  left  side,  dullness  replaces  the  normal 
tympanitic  sound  in  Traube's  space.  The  semilunar,  or  Traube's,  space,  is 
situated  at  the  left  base,  and  corresponds  in  part  to  the  pleuro-parieto- 
diaphragmatic  cul-de-sac.  Its  upper  limit  is  the  fifth  or  sixth  costal 
cartilage  in  front,  and  the  ninth  or  tenth  ribs  behind,  while  its  lower  limit 
is  the  edge  of  the  thorax.  At  its  middle  part — that  is  to  say,  in  the  nipple 
line — the  vertical  height  is  about  4  inches,  and  its  width  about  4-|  inches. 
The  costal  wall  and  its  pleura,  the  diaphragm  and  its  pleura,  the  colon  and 
the  stomach  correspond  anatomically  to  the  semilunar  zone  ;  the  lung 
only  touches  the  upper  limit  (Jaccoud).  In  the  normal  state  percussion 
cf  this  zone  gives  a  tympanitic  note  ;  on  the  other  hand,  m  a  large  left 
effusion  the  diaphragm  is  pushed  down,  and  dullness  replaces  resonance. 
It  is  true  that  normal  resonance  may  also  disappear,  at  least  in  its  upper 
part,  as  the  result  of  adhesions. 

When  the  effusion  is  very  large  (5  pints  and  more),  the  skodaic  note  in 
the  clavicular  region  disappears,  the  dullness  becomes  absolute  over  all  the 
affected  side,  the  displacement  of  organs  reaches  its  maximum,  the  whole 
mediastinum  is  pushed  back,  and  the  obstruction  in  the  pulmonary  cir- 
culation, without  doubt,  leads  to  pulmonary  thrombosis,  and  perhaps  to 
sudden  death,  which  sometimes  occurs  in  large  effusions.  On  auscultation, 
we  find  total  absence  of  all  normal  or  abnormal  sounds,  or  else  tubular 
breathing,  which  may  be  so  loud  as  to  resemble  cavernous  or  even  amphoric 
breathing  (Landouzy). 

Paresis  of  the  thoracic  muscles  on  the  affected  side  is  more  or  less  marked, 
but  constant.  It  is  accompanied  or  followed  by  muscular  atrophy,  which 
may  begin  with  the  onset  of  pleurisy  and  may  remain  after  it.  These 
muscular  atrophies  affect  the  intercostal  and  pectoral  muscles,  the  latis- 
simus  dorsi,  the  serratus  magnus,  etc.,  and  it  is  easy  to  appreciate  them, 
either  at  first  sight  or  by  the  respiratory  troubles  which  they  cause.  These 
muscular  changes  explain  in  part  the  modifications  in  the  respiratory  type, 
the  smaller  amplitude  of  the  chest  (on  the  affected  side),  its  relative  im- 
mobility on  inspection  and  palpation,  and  the  respiratory  restraint  which 
results.  They  also  enter  largely  into  the  external  deformities,  as  well  as 
into  those  of  the  skeleton  which  accompany  and  survive  pleurisy. 

Functional  Symptoms. — As  soon  as  the  fluid  reaches  a  certain  amount, 
the  [)atient  lies  on  the  affected  side,  in  order  to  give  free  play  to  the  healthy 
lung.  He  experiences  a  sensation  of  distress  or  of  heaviness,  but  dyspnoea 
Is  rarely  seen. 

Dys[)n(ra  is  not  a  usual  symptom  of  pleurisy  with  effusion.  'i'hc 
ellusion,  even  when  it  amounts  to  '6  i)ints,  causes  little  acceleration  of  the 


254  TEXT-BOOK  OF  MEDICINE 

respiration  rate.  I  do  not  speak,  of  course,  of  the  early  pain  in  the  side, 
which  is  often  accompanied  by  acute  dyspnoea,  and  I  make  exception  if 
congestion  of  the  lung  is  also  present.  In  all  other  cases  of  acute,  subacute, 
or  latent  pleurisy,  however,  dyspnoea  is  not  marked,  even  with  an  effusion 
of  3  pints  ;  and,  as  we  shall  see  in  a  moment,  when  discussing  the  indications 
for  thoracentesis,  we  should  be  quite  wrong  in  waiting  for  dyspnoea  to 
decide  the  prognosis  and  the  treatment  of  pleurisy. 

The  conclusion  from  this  absence  of  dyspnoea,  even  when  the  fluid  is 
considerable,  is  that  dyspnoea  indicates  the  presence  of  complications. 
When  the  respirations  in  pleural  effusion  exceed  thirty,  the  reason  is  either 
that  the  fluid  is  very  abundant,  amounting  to  about  5  pints,  or  that  com- 
plications are  present.  On  careful  search,  we  shall  find  that  the  pleurisy  is 
secondary,  and  has  appeared  in  the  course  of  Bright's  disease  or  cardiac 
mischief.  Other  inflammations,  such  as  double  pleurisy,  bronchitis, 
pneumonia,  pericarditis,  inflammation  of  the  chest,  or  congestion  of  the 
lung,  will  be  discovered. 

I  must  dwell  for  a  moment  on  congestion  of  the  lung,  which  so  fre- 
quently accompanies  pleurisy.  This  fact  has  been  emphasized  by  Potain. 
Congestion  of  a  part  of  the  lung  often  accompanies  pleurisy,  especially  in 
its  period  of  formation  ;  as  a  result,  the  signs  of  effusion  are  somewhat 
modified  by  those  due  to  the  affected  lung — segophony  is  not  pure,  but 
becomes  broncho-segophony ;  tubular  breathing,  instead  of  being  distant 
and  muffled,  becomes  more  harsh  ;  the  quality  of  the  dullness  and  the  shades 
of  the  thoracic  vibrations  are  modified.  When  we  are  not  familiar  with 
these  points,  we  may  miss  an  existing  effusion  and  refer  the  signs  to  conges- 
tion of  the  lung  ;  or,  on  the  other  hand,  we  may  fancy  the  fluid  to  be  abundant 
when  it  is  as  yet  scanty.     I  shall  consider  this  point  again,  under  Diagnosis. 

In  acute  pleurisy  the  fever  is  moderate  and  sometimes  absent :  the 
temperature  does  not  exceed  102°  F.,  as  a  rule ;  the  defervescence  may  be 
rapid  or  slow,  and  occurs  at  ill-defined  times,  in  some  cases  with  symptoms 
of  crisis. 

Course — Duration — Termination. — Pleurisy  is  a  disease  of  surprises. 
Its  course  is  insidious,  and  the  extreme  irregularity  of  its  habits  is  not 
the  least  important  point  in  its  history.* 

I  was  therefore  very  surprised,  at  the  Academic  de  Medecine,  to  hear 
that  pleurisy  is  a  cyclical  f  disease.  I  have  only  to  consult  our  case 
records  to  prove  that  pleurisy  is  quite  the  opposite  of  a  cyclical  malady. 
In  pleurisy  we  cannot  foresee  the  succession  of  symptoms,  the  temperature 
curve,  the  time  of  defervescence,  or  the  moment  when  the  effusion  appears 

*  Dieulafoy :  "  Des  Irregularites  de  la  Pleurisie  Aigue,"  Ga^tte  Hebdomad.,  1878, 
No.  3. 

•j-  Academie  de  Medecine,  April,  1892. 


DISEASES  OF  THE  PLEURA  255 

or  is  absorbed.  In  one  case  pain  and  fever  are  marked,  and  the  effusion 
appears  between  the  twelfth  and  the  fifteenth  day.  In  another  the  disease 
is  insidious,  and  effusion  exists  for  a  month  or  six  weeks,  when  the  patient 
comes  to  the  hospital  with  some  distress,  which  often  scarcely  merits  the 
name  of  dyspnoea.  I  have  several  times  seen  fever  persist,  although  the 
effusion  diminished.  Binet  gives  a  remarkable  example.*  In  many  cases 
fever  disappears  with  or  without  symptoms  of  crisis,  the  patient  considers 
himself  cured,  and  still  the  effusion  increases.  In  fact,  pleurisy  is  so  irregular 
in  its  course  that  it  pr^ents  a  different  appearance  in  each  patient.  It 
is  not  possible  to  say  whether  the  febrile  period  will  be  of  long  or  of  short 
duration,  whether  the  effusion  will  be  abundant  or  scanty  ;  at  what  time 
defervescence  will  occur,  and  whether  it  will  coincide  or  not  with  absor2)tion 
of  the  fluid  ;  whether  this  absorption  will  be  slow  or  quick  ;  and  whether,  in 
spite  of  the  fall  of  the  fever,  the  fluid  will  not  continue  to  increase.  Do  not 
these  clinical  considerations  justify  the  assertion  that  pleurisy  proceeds  in 
quite  a  different  way  to  cyclical  diseases  ?  We  cannot,  therefore,  speak 
of  a  cycle  in  pleurisy.  This  question  will  be  referred  to  under  the  Indica- 
tions for  Thoracentesis. 

If  the  effusion  is  slow  to  absorb,  the  insufficiency  of  the  haematosis  and 
the  lack  of  appetite  often  cause  weakness  and  anaemia.  In  exceedingly  rare 
cases  sero-fibrinous  pleurisy  has  ended  by  vomica.  When  pleurisy  ter- 
minates favourably,  the  fluid  is  absorbed ;  the  displaced  organs  recover  their 
former  position ;  the  lung  resumes  its  function ;  and  on  inspiration  and 
expiration  we  hear  a  grating  friction  sound,  or  hruit  de  cuir  neuf,  which 
indicates  absorption  of  the  fluid  and  presence  of  false  membranes  on  the 
layers  of  the  pleura.  This  redux  friction  may  be  heard  at  several  spots 
in  front  and  in  the  axilla.  It  is  sometimes  so  marked  that  it  may  be  felt 
on  palpation.  These  signs  remam  long  after  the  pleurisy.  Impaired 
resonance  and  weak  vesicular  murmur  often  persist  months  after  recovery. 

The  immediate  prognosis  is  not  grave.  We  must,  however,  not  forget 
that  large  effusions  may  determine  thrombosis  of  the  pulmonary  vessels  or 
cardiac  embolism,  and  induce  syncope,  rapid  asphyxia,  and  death.  This 
important  point  will  be  discussed  under  Thoracentesis.  Convalescence  is 
usually  protracted,  and  many  patients,  even  though  taken  ill  while  in 
excellent  health,  remain  weak,  and  for  several  months  carry  the  stamp  of 
their  disease. 

Pleurisy  at  times  leaves  false  membranes  and  adhesions,  which  affect 
the  functions  of  neighbouring  orgaiLS  (diaphragm,  lung,  and  pericardium), 
and  may  ultimately  give  rise  to  encysted  effusions.  Another  important  fact 
as  regards  prognosis  is  that  the  most  frank  pleurisy  Is  often  the  begimiing 
of  tuberculosis,  which  becomes  evident  months  or  years  later. 
♦  Archives  de  Midecine,  April,  188-4,  p.  4UG. 


256  TEXT-BOOK  OF  MEDICINE 

Diagnosis. — At  first,  before  efEusion  appears,  diagnosis  may  be  difficult. 
Pleurisy  should  not  be  confused  with  lobar  pneumonia,  for  the  latter  begins 
with  a  violent  rigor,  very  high  temperature,  intense  dyspnoea,  crepitant 
rales,  and  rusty  sputum.  The  diagnosis,  however,  may  be  difficult,  for  the 
friction  rale  of  pleurisy  somewhat  resembles  the  rale  of  pneumonia.  Inter- 
costal neuralgia  and  hepatic  colic  may  simulate  the  pleuritic  pain  in  the 
side,  but  they  differ  in  the  absence  of  fever  and  of  physical  signs.  Febrile 
pleurodynia  shows  more  analogy  with  pleurisy,  and  it  may  coincide  with 
a  partial  dry  pleurisy.  This  question  has  been  discussed  under  Inflammation 
of  the  Chest. 

Pulmonary  congestion,  massive  pneumonia,  and  spleno-pneumonia 
(Grancher)  have  several  signs  in  common  with  pleural  effusion.  In  the 
case  of  pulmonary  lesions,  however,  the  dullness  is  less  complete,  the  thoracic 
vibrations  are  less  affected,  the  neighbouring  organs  are  not  displaced,  and 
the  aphonic  pectoriloquy  is  less  clear.  In  spite  of  all  these  distinctive  signs, 
I  admit  that  an  early  diagnosis  is  difficult  in  some  cases. 

It  is  also  important  to  recognize  the  diseases  which  may  be  associated 
with  pleurisy — e.g.,  the  coexistence  of  pulmonary  congestion  and  pleurisy 
(pleuro-congestion),  for  the  presence  of  the  former  modifies  the  signs  of 
efEusion.  In  consequence  of  the  congestion,  the  distribution  of  the  fluid 
in  the  pleura  is  modified.  The  congested  lung  becomes  more  dense,  and 
does  not  allow  itself  to  be  flattened.  It  sinks  in  t)ie  fluid,  raising  the  level, 
so  that,  without  careful  examination,  the  effusion  would  appear  very  abun- 
dant, when  it  may  really  be  quite  scanty.  The  limits  of  the  dullness,  the 
nature  of  the  tubular  breathing,  the  characters  of  the  voice,  and  the  fre- 
quent presence  of  bronchial  rales  are  the  most  important  jioints. 

We  must  distinguish  between  effusion  due  to  pleurisy  and  that  due  to 
hydrothorax.  Hydrothorax  is  not  rare  in  the  course  of  acute  or  chronic 
nephritis,  and  sometimes  occupies  both  pleurae.  It  is  sometimes  associated 
with  oedema  of  the  extremities  and  of  the  lung.  This  is  chiefly  the  case  in 
acute  nephritis.  At  other  times  hydrothorax  is  an  isolated  manifestation 
of  chronic  nephritis,  just  as  oedema  of  the  larynx  or  of  the  lung  may  be. 
The  general  rule  is  :  hydrothorax  due  to  nephritis  causes  more  severe 
dyspnoea  than  pleuritic  effusion  does,  because  hydrothorax  in  Bright's 
disease  is  nearly  always  associated  with  oedema  of  the  lung  or  with  uraemic 
dyspnoea.  The  discovery  of  symptoms  of  "  Brightism "  and  of  albu- 
minuria will  complete  the  diagnosis. 

It  is  still  necessary  to  distinguish  effusion  due  to  pleurisy  from  hydro- 
thorax consecutive  to  heart  disease. 

The  diagnosis  of  effusions  into  the  pleura  presents  other  difficulties,  as 
we  shall  see.  For  example,  a  patient  suffers  from  dyspnoea.  He  is  examinedj 
and  on  one  side  of  the  chest  signs  of  a  large  effusion  are  found.     The  c 


DISEASES  OF  THE  PLEURA  257 

ness  is  complete,  or  nearly  so,  the  thoracic  vibrations  are  diminished,  and 
aegophony,  aphonic  pectoriloquy,  and  tubular  breathing,  or  even  cavernous 
and  amphoric  breathing,  are  heard.  A  patient  who  presents  these  signs, 
or  some  of  them,  may  have  pleurisy  with  effusion,  just  as  he  may  have  a 
cyst  in  the  liver,  the  spleen,  or  the  kidney,  which  has  pushed  up  the  diaphragm 
and  encroached  on  the  thoracic  cavity.  Another  patient  may  have  cancer 
of  the  lung,  or  malignant  hypertrophy  of  the  thoracic  glands,  etc.  Vergely 
has  clearly  shown  these  points  in  the  case  of  a  patient  who  presented  all 
the  signs  of  pleural  effusion  and  in  whom  an  adeno-carcinoma  was  found. 
yEgophony,  aphonic  pectoriloquy,  and  blowing  breathing  are  certainly  of 
great  value,  but  these  signs  may  exLst  without  any  large  effusion  in  the 
pleura.  False  membranes,  tumours,  flattening  of  the  bronchi,  and  con- 
densation of  the  Imig  tissue,  may  modify  the  normal  conditions  of  ausculta- 
tion to  an  extent  not  yet  well  defined,  and  may  sometimes  simulate 
pleural  effusion.  In  a  doubtful  case  the  surest  sign  of  pleural  effusion  on 
the  left  side  is  displacement  of  the  heart.  When  the  effusion  is  on  the 
right  side,  depression  of  the  liver  should  be  taken  into  consideration.  We 
shall  see,  when  we  study  hydatid  cysts  of  the  liver  and  of  the  spleen,  upon 
what  signs  a  diagnosis  must  be  based  if  these  cysts  simulate  pleural  effusion. 

When  pleurisy  has  been  recognized,  it  is  also  necessary  to  diagnose  its 
cause,  to  ascertain  whether  it  is  sero-fibrinous,  hsemorrhagic,  or  purulent, 
and  whether  it  is  associated  with  tuberculosis  which  is  latent  or  is  already 
at  work. 

We  cannot  say  without  exploration  whether  an  effusion  is  sero-fibrinous 
or  htcmorrhagic.  We  often  expect  to  draw  off  scrum,  and  are  surprised  to 
find  blood-stained  fluid. 

Clinical  Varieties. — Pleurisy  presents  numerous  clinical  varieties,  a  fact 
which  it  is  important  to  remember. 

1.  Latent  Pleurisy. — Acute  pleurisy  does  not  always  begin  witli  the 
acute  symptoms  mentioned  above.  The  pain  is  sometimes  trifling,  and  the 
symptoms  of  onset  are  so  slight  tliat  in  hospital  we  frequently  see  people 
wh(j  have  been  at  work  without  Ijcing  able  to  fix  the  start  of  their  illness. 
It  is  not  rare  to  see  latent  cases  in  which  fever,  pain,  and  dyspnoea  are 
absent,  while  the  effusion  reaches  considerable  proportions  unnoticed  by 
the  patient,  but  these  cases  may  be  accom[)anied  by  fever  of  the  inter- 
mittent ty})e.     It  usually  indicates  infective  changes  in  the  fluid. 

'2.  Rheumatic  pleurisy  may  be  dry,  or  accompanied  by  effusion  ;  it 
may  be  simple  or  double  ;  it  appears,  changes,  and  disappears  with  great 
mobility  (see  Rheumatism). 

In  many  cases  })leurisy  is  provoked  by  a  neighbouring  or  by  a  remote 
lesion  (hydutid  cyst  of  the  lung,  of  the  liver,  etc.). 

Treatment. —  In  acute  pleurisy  two  chief  elements — pain  and  clTusion 

17 


258  TEXT-BOOK  OF  MEDICINE 

— demand  relief.  For  pain,  we  employ  wet-cupping,  leeches,  injections  of 
morphia,  antipyrin ;  later,  if  the  effusion  makes  rapid  progress,  what 
line  of  treatment  must  be  followed  ?  Blisters  have  only  a  very  limited  use 
in  the  treatment  of  pleurisy.  Many  persons  have  three,  four,  and  five 
blisters,  and  are  exposed  to  the  risk  of  cystitis,  erysipelas,  or  of  a  crop  of 
boils,  without  gaining  the  least  benefit.  As  I  believe  that  blisters  have  no 
real  effect  on  the  effusion,  I  abstain  from  prescribing  them. 

I  think  that  other  medical  means,  such  as  bleeding,  purgatives,  diuretics, 
and  sudorifics,  have  quite  a  secondary  place  in  the  treatment  of  pleural 
effusions.  The  more  I  see,  the  more  I  recognize  that  these  means  are 
useless  and  sometimes  harmful.  We  may  therefore  discuss  the  value  of, 
and  the  opportunity  for,  surgical  intervention,  or  thoracentesis. 

Thoracentesis. — To  my  eminent  teacher.  Trousseau,  belongs  the  honour 
of  having  clearly  stated  the  indications  and  operative  technique  of  thora- 
centesis. In  spite  of  keen  opposition.  Trousseau  so  popularized  this  opera- 
tion, which  had  been  previously  neglected,  that  he  may  justly  be  con- 
sidered as  its  inventor.  He  only  punctured  the  chest  when  the  effusion 
threatened  the  patient's  life,  and  the  operation  was  performed  with  Rey- 
bard's  trocar. 

In  1869,  however,  when  I  designed  the  aspirator  and  applied  the  method 
of  aspiration  to  the  treatment  of  pleural  effusions,  the  technique  of  thora- 
centesis was  so  simplified  that  the  old  method  was  gradually  abandoned, 
and  it  must  be  admitted  the  new  one  was  soon  abused.  As  thoracentesis 
by  aspiration  has  been  universally  adopted,  I  shall  describe  my  published 
method. 

Indications. — On  the  question  of  thoracentesis,  the  first  point  for  dis- 
cussion is  that  of  the  indications.  Should  we  operate  in  spite  of  fever,  or 
wait  for  defervescence  ?  Should  we  employ  aspiration  in  moderate  effusions, 
or  reserve  it  for  large  ones  ?  How  far  should  we  consider  the  complications 
which  may  arise  ?  These  questions,  which  have  been  often  debated  and 
differently  decided,  are  reduced  to  the  following  proposition,  which  sums 
up  the  question  of  opportunity  :  Given  acute  pleurisy  with  effusion,  two 
cases  may  present  themselves — in  one  thoracentesis  is  urgent,  in  the 
other  it  is  debatable.  When  is  it  urgent,  and  when  is  it  debatable  ?  The 
discussion  should  proceed  on  these  lines. 

The  urgency  of  thoracentesis  must  be  based  only  upon  the  estimation 
of  the  quantity  of  fluid  effused.  The  presence  or  the  absence  of  fever 
or  of  dyspnoea  are  secondary  considerations.  We  must,  before  all,  con-j 
sider  the  amount  of  the  effusion.  We  cannot  rely  upon  dyspnoea,  for  it 
a  faulty  guide.  Large  effusions  are  sometimes  associated  with  slight  dis-j 
tress,  and  patients  may  have  three  or  four  j)ints  of  fluid  in  the  pleura,  anc 
still  be  able  to  walk  about. 


DISEASES  OF  THE  PLEURA  259 

Trousseau  says  that  a  nursing  woman,  who  carried  her  child,  walked 
from  Saint-Eustache  to  the  Keeker  Hospital  without  feelmg  much  fatigue. 
Six  pints  were  drawn  ofE  by  thoracentesis.  A  carman  of  whom  Andral 
speaks  went  on  driving  his  horses,  and  felt  but  slight  discomfort,  although 
he  had  a  very  large  effusion.  We  see,  says  Landouzy,  people  who  walk 
several  miles  to  hospital,  and  complain  of  stomach-ache,  or  of  attacks  of 
fever,  although  they  have  enormous  effusions.  I  have  often  seen  similar 
cases.  I  have  performed  thoracentesis  in  a  student  who  came  regularly  to 
the  hospital,  and  felt  very  little  distress,  in  spite  of  an  effusion  amomiting 
to  4  pints.  Dyspnoea  is  quite  deceptive.  If  we  wait  until  dyspnoea 
appears  before  evacuating  an  effusion,  we  shall  delay  until  the  patient's 
life  has  long  been  in  danger  from  the  quantity  of  the  effusion  before  our 
decision  has  been  made. 

With  still  more  reason,  thoracentesis  should  not  be  delayed  until  the 
patient  has  cyanosis  of  the  face  and  of  the  fingers,  as  some  authors  would 
advocate.  The  cases  of  sudden  and  rapid  death  caused  by  large  effusions 
have  not  all  been  published.  It  is  a  pity,  for  we  should  perhaps  be  less 
severe  on  thoracentesis,  and  should  see  its  indications  better. 

Trousseau  saw  sudden  death  in  the  course  of  pleurisy  on  three  occasions. 
One  of  his  patients  had  such  slight  distress  that  thoracentesis  was  post- 
poned, but  next  morning  the  patient  died.  Landouzy  has  reported  a  case 
in  which  dyspnoea  was  absent.  This  fact  did  not  prevent  sudden  death 
from  jjleural  effusion.  Dujardin-Beaumetz's  patient  had  neither  dyspnoea 
nor  cyanosis,  and  yet  his  death  was  sudden.  Oulmont  quotes  the  case 
of  a  man  who  was  talking  with  some  friends  in  his  garden.  He  went  to 
lie  down,  and  fell  dead  from  an  effusion  in  the  pleura. 

Two  patients  whose  hLstories  have  been  reported  by  Binet  and 
Lcgrand  had  no  dyspnoea.  One  suffered  so  little  that  he  refused  thora- 
centesis, and  asked  that  it  might  be  put  off.  Two  hours  later  the  effusion 
proved  fatal.  The  other  patient,  who  was  in  apparently  good  health,  also 
died  suddenly  from  the  same  cause. 

After  such  information,  is  dyspnoea  a  necessary  indication  for  the  urgency 
of  thoracentesis  ?  And  we  know  these  mishaps  are  not  the  only  ones  ;  the 
majority  are  never  published.  I  have  collected  forty  cases,  which  I  brought 
before  the  Academic.  How  many  would  there  be  if  we  could  make  a 
complete  list  ? 

These  cases  are,  for  the  most  part,  copies  of  one  another.  At  every  turn 
we  see  that  the  patient  who  dies  suddenly  has  been  suffering  from  an  effusion, 
causing  only  insignificant  dyspncca — so  insignificant,  in  fact,  that  in  many 
cases  thoracentesis  has  been  rejected,  or  imprudently  put  off  till  next  day. 

I  think  that  we  must  finally  dismiss  the  inexact  indications  upon  which 
the  question  of  urgency  in  thoracentesis  has  been  based.     The  duration  of 

17—2 


260  TEXT-BOOK  OF  MEDICINE 

the  pleurisy  matters  little.  It  is  not  a  matter  of  importance  whether  such 
troubles  as  fever  or  dyspnoea  be  present  or  absent.  The  amount  of  the 
effusion  is  the  key  of  the  situation. 

At  the  risk  of  repeating  myself  on  this  important  point,  I  say  that 
dyspnoea  is  a  false  sign  and  a  treacherous  guide  when  we  have  to  decide 
upon  the  urgency  of  thoracentesis.  To  wait  for  dyspnoea  and,  a  fortiori, 
to  wait  for  cyanosis  of  the  face  and  of  the  fingers,  is  gratuitously  to  antici- 
pate a  catastrophe.  If  we  search  in  the  hecatomb  of  patients  who  have 
died  suddenly  because  puncture  was  not  performed  in  time,  we  shall  find 
many  examples  which  show  clearly  that  a  large  effusion  may  prove  fatal, 
even  though  it  has  caused  but  slight  dyspnoea.  It  is  much  more  likely  to 
kill  if  dyspnoea  be  intense,  while  precious  time  is  lost  in  applying  blister 
after  blister. 

These  cases  of  sudden  or  rapid  death  may  result  from  various  causes. 
Sometimes  they  are  due  to  clots  (thrombosis  or  embolism)  which  arise  in 
the  heart,  the  large  vessels,  or  even  in  the  lung  itself.  If  the  clot  is  formed 
in  the  large  pulmonary  veins,  or  in  the  left  side  of  the  heart,  it  often  causes 
cerebral  embolism,  with  its  results — viz.,  apoplexy,  hemiplegia,  aphasia, 
etc.  If  the  clot  is  formed  in  the  right  heart  or  in  the  pulmonary  artery,  it 
may  produce  rapid  asphyxia  and  death,  as  in  cases  quoted  by  Paget,  Smith, 
and  Blachez.  The  patients  suffered  from  left  pleurisy,  and  died  suddenly 
from  syncope.  At  the  autopsy  the  clot  hat/  'originated  in  the  trunk  of  the 
pulmonary  artery,  and  reached  into  the  smaller  vessels. 

In  a  certain  number  of  cases  death  has  supervened  suddenly  from 
syncope,  the  effusion  being  situated  more  often  on  the  right  side  than  on 
the  left,  but  it  is  not  easy  to  explain  the  reason. 

Louis  was  therefore  wrong  in  stating  that  simple  pleurisy  is  not  a  cause 
of  immediate  death,  "  A  patient  may  die  suddenly  from  acute  pleuritic 
effusion  "  (Trousseau).  These  accidents  can  be  set  down  to  the  effusion, 
and  therefore,  I  repeat,  the  urgency  of  thoracentesis  must  be  based  solely 
upon  the  amount  of  the  effusion.  But,  it  will  be  asked,  at  what  moment 
does  urgency  arise  ?  Is  it  when  the  effusion  amounts  to  4  or  5  pints  ? 
And,  further,  how  can  the  quantity  be  estimated  ?  How  can  we  ascertain 
that  it  reaches  3  pints  or  more  ? 

My  analysis  in  cases  of  sudden  death  shows  that  death  has  never  been 
caused  by  an  effusion  of  less  than  4  pints.  Once  only  (Blachez)  the  pleura 
contained  3  pints  of  serous  fluid.  This  exceptional  case  ought  not  to  be 
included,  and  I  estimate  that,  in  a  well-made  adult,  when  the  effusion  reaches 
about  4  pints,  the  urgency  of  thoracentesis  is  clear. 

We  must  consider  the  estimation  of  the  amount  of  fluid.  Upon  what 
signs  and  symptoms  are  we  to  rely  ?  Careful  study  of  the  signs  of  pleurisy 
shows  that  m  small  effusions  tubular  breathmg  is  muffled  and  limited  to 


DISEASES  OF  THE  PLEURA  261 

expiration  ;  in  moderate  ones  (2  to  3  pints)  it  has  a  bronchial  tone,  and  is 
present  during  both  inspiration  and  expiration  ;  in  large  effusions  (4  pints 
or  more)  the  breathing  is  in  some  cases  cavernous,  but  in  others  it  is 
inaudible.  These  auscultation  data,  however,  are  not  absolute— that  is  to 
say,  thev  are  insufficient  for  the  estimation  of  the  amount  of  fluid  present. 
I  would  say  the  same  concerning  measurements  with  the  cyrtometer 
(Woillez).  This  method,  though  excellent  at  times,  is  often  faulty.  We 
must,  therefore,  associate  the  preceding  signs  with  the  more  exact  informa- 
tion furnished  by  the  extent  of  the  dullness  and  by  the  displacement  of 
organs. 

Let  us  take,  for  example,  a  left  pleurisy.  When  the  dullness  and  the 
absence  of  fremitus  reach  behind  as  high  as  the  spine  of  the  scapula,  the 
resonance  in  Traube's  space  has  disappeared,  and  a  dull  note  replaces  the 
skodaic  note  in  the  clavicular  region,  and  especially  when  the  heart  is  dis- 
placed, so  that  the  maximum  of  the  apex-beat  is  situated  at  the  right  edge 
of  the  sternum  or  between  the  sternimi  and  the  right  nipple,  although  at 
this  moment  the  pleural  cavity  may  not  be  filled  to  its  maximum,  such 
signs  in  an  adult  denote  that  the  effusion  is  about  4  pints.  Thoracentesis 
is  then  urgent.  Operation  is  imperative,  and  we  must  not  forget  that  pro- 
crastination is  an  unfortunate  formula  which  costs  patients  their  lives. 

When  the  effusion  is  situated  on  the  right  side,  the  problem  is  rather 
more  difficult,  because  there  is  no  displacement  of  the  heart.  Nevertheless, 
percussion  and  examination  of  the  vocal  fremitus  give  similar  information 
to  that  which  I  have  just  mentioned.  I  may  add  that  depression  of  the 
liver,  when  present,  is  a  sign  of  great  value.  The  liver  is  only  pushed 
down  by  large  effusions,  which  I  estimate  at  about  .3  pints.  The  estimation 
of  the  effusion  is  therefore  rather  more  difficult  on  the  right  side,  but  it 
is  quite  as  important,  for  the  statistics  given  above  show  that  sudden  death 
is  more  frequent  in  right  than  in  left  pleurisies. 

The  discussion  so  far  has  referred  only  to  simple  pleurisy.  Tiie  same 
principles  are  applicable  to  cases  with  complications.  The  direct  or 
indirect  compHcations  of  pleurisy,  such  as  pulmonary  congestion,  okl 
adhesions,  valvular  lesions  of  the  heart,  or  pericarditis— in  short,  all  the 
lesions  which  impair  the  pulmonary  circulation  or  narrow  the  field  of  lu-cma- 
tosis— are  not  a  contra-indication  to  thoracentesis.  On  the  contrary,  they 
demand  it  as  .soon  as  the  effusion  readies  large  proportions  ;  only  the 
evacuation  of  the  fluid  in  such  a  case  demands  precautions,  which  will  be 
indicated  later.  The  estimation  of  the  quantity  of  fluid  is  sometimes 
dillicult,  as  witness  the  very  numerous  cases  in  which  the  more  or  less  con- 
gested lung  makes  the  amount  of  fluid  appear  larger  than  it  really  is.  These 
facts  have  been  emphasized  by  Potain.  It  ls  really  only  by  the  moit 
delicate  differences  in  auscultation  and  percassion  that  we  can  clinically 


262  TEXT-BOOK  OF  MEDICINE 

distinguish  the  part  due  to  congestion  of  the  lung  from  that  due  to  efEusion. 
The  worst  that  could  happen  in  such  a  case  would  be  to  overestimate  the 
quantity  of  fluid.  But  where  would  be  the  harm  ?  Is  it  not  better  to 
withdraw  2  pints  of  fluid  when  the  urgency  is  not  absolute  than  to  expose 
the  patient  to  sudden  death  by  not  performing  thoracentesis  in  time  ? 

I  have  just  discussed  "  thoracentesis  of  urgency."  Apart  from  urgent 
thoracentesis,  in  which  the  surest  guide  is  the  quantity  of  fluid  effused,  the 
operation  is  disputable  in  all  other  cases.  Some  admit  it,  others  reject  it, 
and  certain  authorities,  indeed,  consider  it  harmful.  Let  us  discuss  these 
different  opinions. 

As  long  as  the  temperature  is  raised — that  is,  as  long  as  the  acute  stage 
of  pleurisy  exists — it  is  better  to  wait  for  defervescence  before  deciding. 
If  the  absorption  of  the  effusion  takes  place  naturally,  and  appears  to  be 
rapid,  it  is  useless  to  intervene.  If,  however,  the  effusion  remains  stationary, 
or  absorption  appears  slow  and  difficult,  the  fluid  must  be  drawn  off.  Fluid 
cannot  remain  long  in  the  pleura  with  impunity.  The  displaced  organs 
become  fixed  in  their  vicious  positions ;  the  flattened  and  adherent  lung 
acts  badly;  two  of  the  chief  functions  in  the  economy — i.e.,  hsematosis  and 
circulation — are  compromised,  without  counting  the  passage  of  the  inflam- 
mation into  a  chronic  state  and  the  liability  to  purulent  changes  (Trous- 
seau). Thoracentesis,  performed  at  the  right  moment,  may  shorten  the 
malady  by  some  weeks,  and  cause  the  fall  of  the  residual  fever  which  often 
accompanies  effusions  that  are  slow  to  absorb. 

Operation. — Up  to  1869  only  Trousseau's  method  was  in  use.  He 
punctured  in  the  sixth  or  seventh  intercostal  space,  and  2  inches  from  the 
outer  border  of  the  pectoralis  major — that  is,  in  the  axilla.  A  small 
incision  was  first  made  in  the  skin  in  order  to  prepare  the  way  for  the  pas- 
sage of  the  trocar,  which  was  at  once  thrust  into  the  chest.  The  tube  of 
the  trocar  was  armed  with  goldbeater's  skin,  which,  by  acting  as  a  valve, 
prevented  the  entrance  of  air  into  the  chest  during  inspiration.  The  fluid 
escaped  from  the  chest  first  in  jerks,  then  in  drips,  and  during  the  opera- 
tion the  patient  was  generally  seized  with  fits  of  coughing,  which  were  dis- 
tressing, and  sometimes  "  violent,  irrepressible,  and  very  sharp."  Trousseau 
considered  that  this  cough  favoured  the  outward  flow  of  the  fluid,  and  in 
some  persons  it  lasted  for  part  of  the  day.  Let  me  add  that  towards  the 
end  of  the  operation  the  fluid  was  commonly  coloured  red  by  admixture 
with  blood. 

Thoracentesis  thus  performed,  although  not  a  very  difficult  operation^ 
required  some  skill,  and  at  times  some  boldness,  on  the  part  of  the  surgeon,] 
and  some  resignation  on  that  of  the  patient.     It  was,  therefore,  reservec 
for  urgent  cases,  and  performed  by  a  restricted  number  of  physicians. 

When  I  invented  the  aspirator,  and  performed  aspiration   for  effusions 


DISEASES  OF  THE  PLEURA  263 

in  the  pleura,  the  old  technique  was  replaced  by  a  needle-prick  so  trifling  that 
hardly  any  mark  remained  on  the  skin  after  the  operation,  and  the  fluid, 
instead  of  being  forced  out  by  jerks,  with  distressing  attacks  of  coughing, 
passed  into  the  aspirator  from  the  thoracic  cavity  unknown  to  the  patient. 

Thoracentesis  was  thus  brought  within  reach  of  the  least  experienced 
physician.  It  became  the  most  easy  and  the  least  painful  of  all  operations, 
and  the  most  junior  student  has  to  perform  it  in  my  wards. 

My  method  is  as  follows  : 

The  patient  sits  up  in  bed,  with  his  arms  held  forward.  I  mark  the 
exact  spot  upon  the  skin,  which  has  previously  been  washed  with  a  solution 
of  sublimate,  and  insert  the  needle  behind  in  the  seventh  or  eighth  inter- 
costal space,  in  a  line  with  the  inferior  angle  of  the  scapula.  This  point  ls 
lower  and  more  posterior  than  in  the  old  procedure.  It  has  the  advantage 
of  attacking  the  fluid  in  a  more  dependent  position. 

Thoracentesis  should  be  performed  with  an  aseptic  No.  2  or  No.  3  needle, 
and  not  with  a  larger  instrument.  The  permeability  of  the  needle  is 
proved  by  means  of  a  silver  wire.  The  needle  is  connected  with  the  aspirator 
by  indiarubber  tubing  ;  a  vacuum  is  created  in  the  bottle,  and  the  puncture 
is  then  made.  For  this  purpose,  the  operator  with  his  left  index-finger 
finds  the  intercostal  space,  so  as  to  define  the  rib  above  with  the  dorsal 
surface  of  the  finger  and  the  rib  below  with  its  palmar  surface.  He  then 
uses  the  extremity  of  the  index-finger  as  a  guide,  and  holding  the  aspirating 
needle  in  the  right  hand,  penetrates  the  chest  wall  witli  a  sure  thrust. 
The  needle  is  pushed  in  about  1  inch,  the  tap  corresponding  with  the  aspirator 
is  opened,  and  the  fluid  flows  through  the  indicator  tube  into  the  bottle.  If 
the  fluid  does  not  appear,  the  needle  has  not  been  sufficiently  pushed  home. 
It  is  pushed  on  boldly,  the  previous  vacuum  indicating  the  exact  moment 
at  which  it  meets  the  fluid.  The  aspirator,  once  filled,  is  slowly  emptied, 
and  this  temporary  delay  is  beneficial  to  the  lung,  which  does  not  lend 
itself  to  too  rapid  expansion.  This  manoeuvre  is  repeated  several  times, 
according  to  the  capacity  of  the  aspirator,  and  the  flow  is  stopped  after 
2  pints  of  fluid  have  been  drawn  off.  The  needle  is  withdrawn,  and  the 
operation  only  takes  eight  or  ten  minutes.  Scarcely  any  trace  of  the  punc- 
ture is  to  be  found  on  the  skin,  and  no  dressing  is  needed. 

When  the  operation  is  properly  performed,  the  patient  should  suffer 
neitlier  fits  of  coughing  nor  pain.  If  pleurisy  is  associated  witli  other 
lesions,  and  the  field  of  haematosis  is  narrowed  by  cardiac  or  by  pulmonary 
lesions,  if  pleural  adhesions  are  thouglit  to  exist,  and  especially  if  during 
the  operation  the  patient  complains  of  a  feeling  of  tearing  or  pain  in  the 
interior  of  the  chest,  it  is  better  to  stop  the  flow,  and  repeat  the  opera- 
tion next  day.  These  precautions,  however,  which  are  rightly  very  neces- 
sary in  pleurisy  with  complications,  are  rarely  required  in  simple  |)leurisy. 


264  TEXT-BOOK  OF  MEDICINE 

What  must  be  our  line  of  action  as  regards  the  fluid  remaining  in  the 
chest  ?  If  the  effusion  is  very  large  and  exceeds  4  pints,  we  remove  2  pints 
next  day  or  the  day  after,  and  so  on  until  the  effusion  is  drained.  If,  how- 
ever, the  quantity  of  fluid  has  been  primarily  estimated  at  about  3  pints, 
and  2  pints  have  already  been  withdrawn,  is  it  then  necessary  to  repeat  the 
operation  ?  I  think  that  it  is  not  advisable.  In  effusions  estimated  at 
about  3  pints  I  have  often  removed  two-thirds  only,  and  have  found  that 
recovery  went  on  rapidly,  the  residue  being  more  quickly  absorbed  after 
part  of  the  fluid  had  been  withdrawn.  I  think  that  a  repetition  is  only 
indicated  when  the  fluid  remabiing  in  the  pleura  amounts  to  2  pints  or 
more. 

We  must  not  forget  that  in  some  cases  the  fluid,  after  evacuation, 
reforms  rapidly  and  obstinately.  We  must  then  perform  thoracentesis  as 
often  as  may  be  necessary,  carefully  examining  the  patient  for  some  days 
after  the  operation,  as  the  fluid  may  form  again  insidiously,  and  cause 
sudden  death.  If  thoracentesis  is  performed  in  time,  patients  should  not 
die  from  pleuritic  effusion. 

In  performing  thoracentesis,  the  choice  of  the  aspirator  is  indifferent. 
However,  the  rackwork  aspirator  appears  to  me  the  most  convenient.  The 
choice  of  the  needle  is  important,  and  I  recommend  exclusively  No.  2 
needle,  the  calibre  of  which  measures  only  r2  millimetres  in  diameter. 
Several  objections  have  been  made  to  this  needle — that  it  permits  but  a  slow 
flow  of  fluid,  that  it  is  easily  blocked,  and  that  its  sharp  point  may  injure 
the  lung.     What  foundation  is  there  for  these  objections  ? 

The  small  bore  of  the  needle  retards  the  flow  of  fluid,  but  this  is  bene- 
ficial to  the  patient,  for  the  slow  flow  allows  the  lung  to  expand  gradually, 
and  prevents  painful  fits  of  coughing. 

The  hypothesis  that  so  fine  a  needle  may  easily  be  blocked  is  hardly 
ever  realized,  and,  supposing  it  does  happen,  we  need  only  withdraw  the 
needle  and  make  a  fresh  puncture. 

Another  objection  to  the  needle  is  that  its  point  may  wound  the  lung. 
In  order  to  prevent  this  accident,  a  special  trocar  has  been  invented  (Castiaux). 

I  have  never  seen  the  lung  wounded  by  the  needle.  The  lung,  which  is 
compressed  and  pushed  back  by  the  fluid,  expands  slowly,  and  does  not 
meet  the  needle  quickly.  Further,  a  simple  manceuvre  prevents  every 
chance  of  this.  We  need  only  withdraw  the  needle  gradually  as  the  fluid 
flows  out,  and  to  make  it  turn,  so  as  to  bring  it  almost  parallel  with  the 
intercostal  wall. 

Consecutive  Accidents. — Congestion  and  oedema  of  the  lung,  albuminous 
expectoration,  slow  and  sudden  asphyxia,  syncope,  hemiplegia,  apoplexy, 
more  or  less  rapid  death,  and  purulent  changes  in  the  fluid,  have  been  seen 
after  thoracentesis. 


DISEASES  OF  THE  PLEURA  265 

Aspiration  has  more  than  once  been  accused  of  these  mishaps,  an  accusa- 
tion which  Reybard's  trocar  did  not  escape.  Let  me  at  once  say  that  these 
accusations  have  no  foundation. 

The  abuse  of  thoracentesis  has  arisen  from  aspiration.  I  know  this 
fact,  and  regret  it ;  but  as  regards  its  abuse,  there  is  at  times  a  question,  if 
not  of  inexperience,  at  least  of  imperfect  knowledge  of  the  technique.  It 
is  not  sufficient  to  have  in  hand  a  needle  and  an  aspirator  ;  it  is  also  necessary 
to  know  how  to  use  them. 

I  shall  analyze,  therefore,  the  accidents  imputed  to  aspiration,  seek 
their  cause,  and  discuss  their  worth,  hoping  to  prove  that,  with  precise 
indications  and  proper  technique,  thoracentesis  by  aspiration  is  the  most 
innocent  of  all  operations. 

1.  Albuminous  Expectoration — Asphyxia. — Dyspnoea  and  asphyxia, 
which  I  place  in  the  first  group,  arise  as  follows  :  Immediately  or  a  little 
while  after  thoracentesis,  the  patient,  who  is  seized  with  cough  and  distress, 
brings  up  frothy  and  blood-stained  albuminous  sputum,  and  the  fine  rales 
of  pulmonary  cedema  are  heard  on  auscultation.  In  mild  cases  the  symp- 
toms rapidly  improve,  but  in  other  cases  the  complication  is  very  formid- 
able. The  cough  is  paroxysmal,  the  dyspnoea  increases,  and  the  patient 
brings  up  as  much  as  3  or  4  pints  of  expectoration,  which  in  the  receiver  is 
divisible  into  several  layers,  the  upper  frothy  and  yellowish,  the  lower  more 
dense  and  albuminous.  The  intensity  of  the  dyspnoea,  the  duration  and 
the  quantity  of  the  expectoration,  are  variable,  and  the  patient  only  regains 
his  normal  condition  at  the  end  of  twelve  or  of  twenty-four  hours.  Lastly, 
in  some  exceptional  cases  (I  know  only  of  six)  the  results  have  been  fatal, 
and  asphyxia  has  come  on  so  rapidly  after  thoracentesis  that  patients  have 
died  in  a  few  minutes. 

Since  1853  these  cases  of  dyspnoea  have  been  studied  and  variously 
interpreted.  How  can  we  explain  the  albuminous  expectoration  and  the 
asphyxia  ?  No  wound  of  the  lung  has  been  found  post  mortem,  and  sup- 
posing that  puncture  of  tiiis  organ  may  have  allowed  the  fluid  to  pass  into 
the  bronchi,  it  would  also  have  allowed  air  to  pass  from  the  bronchi  into 
the  pleura,  causing  symptoms  of  hydro-pneumothorax.  Wounds  or  spon- 
taneous perforation  of  the  lung,  therefore,  cannot  be  blamed.  We  must 
look  to  acute  oedema  of  the  lung  as  the  cause  of  alltuminous  (^\i)('(i()ruti()ii, 
dyspmjea,  and  asj)hyxia  (llerard)  ;  but  the  cause  of  the  acute  oedema  still 
remains  to  be  explained. 

The  method  of  aspiration  has  been  blamed.  It  has  been  said  that 
asjdration  lowered  the  tension  in  the  pleura,  and  allowed  the  fluid  to  liow 
out  too  quickly.  How  little  foundation  exists  for  this  accusation  is  seen 
from  the  reports,  which  show  that  in  sixteen  cases  of  thoracentesis  followinl 
by  albuminous  expectoration   (Terillon's  thesis),   the  operation  had   been 


266  TEXT-BOOK  OF  MEDICINE 

performed  twelve  times  with  Reybard's  trocar,  and  only  four  times  by 
aspiration.  In  the  six  fatal  cases,  the  operation  was  performed  three  times 
with  the  trocar  and  three  times  with  aspiration.  Aspiration,  therefore,  is 
not  directly  responsible,  since  most  of  the  accidents  have  supervened  apart 
from  it. 

If  these  accidents  have  nothing  to  do  with  the  operative  procedure,  to 
what,  then,  are  they  due  ?  In  six  cases  in  which  operation  was  followed 
by  death,  five  were  cases  of  complicated  pleurisy.  In  the  first  (Gombault), 
the  opposite  lung  was  partly  fibrous  and  bound  down  by  old  pleuritic 
adhesions  ;  in  the  second  (G-irard),  the  patient  was  suiTering  from  acute 
rheumatism  with  double  pleurisy ;  in  the  third  (Behier),  tubercular 
broncho-pneumonia  was  also  present  on  the  right  side ;  in  the  fourth 
(Dumontpallier),  the  patient  had  bronchitis  and  adhesions  of  the  left  lung, 
in  addition  to  right  pleurisy ;  in  the  fifth  (Bouveret),  the  asphyxiated 
patient  had  old  tubercular  pleurisy,  with  adhesions  and  7  pints  of  fluid. 

Let  us  analyze  the  cases  in  which  thoracentesis  has  been  followed  by 
oedema  of  the  lung  (Terrillon's  thesis)  and  albuminous  expectoration.  Here 
also  complications  were  present  in  most  cases.  Thus,  in  Cases  13  and  17 
(Lasegue),  the  patients  had  aortic  and  mitral  lesions,  oedema  of  the 
lower  limbs,  etc.  ;  in  Case  3  (Bucquoy),  hypertrophy  of  the  heart,  with 
mitral  and  aortic  murmurs  ;  in  Case  15  (Lancereaux),  the  patient  was  four 
months  pregnant,  and  subject  to  chronic  bronchitis-,  with  night-sweats  ;  in 
Case  7  (Marotte),  the  patient  was  suffering  from  pleurisy  as  well  as  from 
pulmonary  tuberculosis. 

I  find  that  the  accidents  due  to  thoracentesis,  when  pleurisy  was  not 
associated  with  any  complication,  have  been  caused  by  withdrawing  rapidly 
and  at  one  sitting  too  large  a  quantity  of  fluid — 10  pints  in  Case  6  (Marotte), 
7  pints  (Worms),  5  pints  in  Case  18  (Faussillon),  and  4  pints  in  other  cases. 

The  benign,  grave,  or  fatal  cases  of  pulmonary  oedema  and  albuminous 
expectoration  have,  therefore,  always  been  associated  either  with  com- 
plications or  with  the  immediate  withdrawal  of  too  large  a  quantity  of 
fluid,  and  most  often  with  these  two  causes  combined.  These  accidents, 
then,  are  not  directly  referable  to  exaggerated  lowering  of  the  pleural 
tension  produced  by  aspiration,  since  the  same  accidents  supervene  with 
Reybard's  trocar  wlien  the  tension  is  the  same  inside  and  outside  the 
chest. 

When,  however,  aspiration  is  badly  performed,  trouble  follows ;  but  it 
is  not  a  question  of  the  quality  of  the  vacuum,  but  of  the  quantity.  Acci- 
dents do  not  occur  because  2  pints  of  liquid  have  been  withdrawn  with  a 
proper  vacuum,  but  because  4  or  5  pints  Lave  been  drawn  at  once  with 
an  incomplete  vacuum  or  with  none  at  all.  It  is  not  aspiration  which  is 
at  fault,  but  the  way  in  which  it  is  done.    A  patient  has  had  6  or  7  pints 


i 


DISEASES  OF  THE  PLEURA  267 

of  fluid  in  his  chest  for  five  or  six  weeks.  The  heart  and  the  pulmonary 
vessels  are  displaced,  the  lung  is  flattened,  the  circulation  is  hampered. 
These  organs  are  suddenly  deprived  of  6  pints  of  fluid  which  has  for  a  long 
time  impeded  their  functions,  and  the  blood  at  once  rushes  into  the  pul- 
monary vessels,  the  air  into  the  alveoli,  and  yet  we  are  astonished  that 
accidents  supervene.  What  astonishes  me  is  that  they  do  not  occur  more 
often.  It  is  not  aspiration,  nor  a  too  perfect  vacuum,  which  must  be  blamed 
for  these  accidents.  It  is  aspiration  prolonged  without  measure,  or  the 
emplojTnent  of  too  large  a  trocar.  It  is,  in  short,  the  ill-advised  method, 
which,  without  holding  to  principles  that  should  never  be  departed  from, 
allows  a  large  effusion  to  be  drawn  off  too  rapidly  at  one  sitting.  I  repeat 
again  that  the  secret  of  preventing  accidents  consists  in  using  a  No.  2 
needle  and  in  limiting  the  quantity  of  fluid  withdrawn  at  a  sitting  to  2  pints. 

I  have  always  carried  out  this  plan,  and  in  the  180  cases  which  served 
as  a  basis  for  my  discussion  at  the  Academic  de  Medecine,  we  find  that  the 
patients  suffered  no  mishap.  Pulmonary  congestion,  albuminous  expec- 
toration, and  threatening  asphyxia  were  never  seen. 

We  may,  then,  draw  the  general  conclusion  that  thoracentesis,  properly 
done,  never  causes  trouble  ;  while  thoracentesis,  if  imprudently  rejected  or 
postponed,  exposes  every  patient  suffering  from  a  large  effusion  to  the  risk 
of  sudden  death. 

2.  Early  or  Late  Syncope. — In  some  cases  patients  die  from  synco23e  one 
or  two  days  after  operation.  Analysis  of  these  cases  proves  that  the  acci- 
dents resulted  from  various  causes  which  were  in  every  case  independent 
of  thoracentesis,  and  included  clots  in  the  heart  or  the  pulmonary  vein, 
phlebitis,  and  thrombosis,  and  gangrene  of  the  pleura  (Besnier). 

3.  Purulent  Changes. — The  accusation  that  serous  fluid  may  become 
purulent  is  certainly  one  of  the  gravest  accusations  which  has  been  brought 
against  thoracentesis.  This  accusation  has  been  brought  up  durhig  the  last 
disciLssion  at  the  Academic,  but  it  has  no  foundation.  If  we  puncture  in 
the  early  stage  of  pleurisy,  and  do  not  examine  the  fluid  carefully,  we  may 
conclude  the  effusion  is  benign,  because  the  fluid  is  clear  and  citron-coloured  ; 
then,  if  a  fresh  puncture  is  made  later,  thoracentesis  is  ^vrongly  accused  of 
having  caused  infection,  because  we  forget  that  we  have  punctured  at  two 
different  stages  of  the  disease,  and  that  thoracentesis  has  nothing  to  do 
witii  this  change. 

A  similar  remark  holds  good  with  regard  to  the  pathogenic  agents  in 
the  fluid  of  sero-fibrinous  pleurisy.  Fluid  containing  the  pneumococcus 
or  the  staphylococcus  may,  on  the  first  ]nincture,  be  scro-fibrinous,  and  may 
become  purulent  from  the  nature  of  the  disease,  and  not  from  thoracen- 
tesis. 

The   question  of  this   purulent  change   in   pleuritic   effusion   htllowing 


2G8  TEXT-BOOK  OF  MEDICINE 

thoracentesis  appears  clear,  in  my  opinion.  Aseptic  thoracentesis  cannot 
cause  sero-fibrinous  fluid  to  become  purulent,  and  if  the  change  has  occurred, 
it  is  not  the  operation  which  should  be  blamed,  but  the  operator. 


II.  HOW  TO  TELL  IF  AN  ACUTE  SERO-FIBRINOUS  PLEURISY  IS 

OR  IS  NOT  TUBERCULAR— CYTO -DIAGNOSIS 

— SERO-DIAGNOSIS. 

Discussion. — As  we  have  studied  the  symptoms,  course,  and  treatment 
of  acute  pleurisy,  let  us  now  consider  the  tubercular  nature  of  these  cases. 
We  are  often  consulted  by  patients  who  have  been  attacked  while  in  good 
health  by  acute  sero-fibrinous  pleurisy.  The  case  appears  innocent,  and  it 
has  the  characters  of  primary  pleurisy.  The  conditions  under  which  it  has 
developed  appear  to  stamp  it  as  pleurisy  a  frigore,  and  yet,  learning  from 
experience,  we  doubt  the  benignity  of  the  disease,  and  ask  ourselves  whether 
the  condition  is  not  really  tubercular — a  fact  which  greatly  modifies  the 
prognosis. 

How  can  we  solve  this  problem,  which  sometimes  is  very  difficult  ?  Are 
we  in  a  position  to  say  that  the  case  is  tuberculous  or  not  ?  We  must  now 
discuss  this  question.* 

When  I  commenced  my  medical  studies,  acute  pleurisies  were  classed  as 
primary  and  secondary.  The  former  class  was  said  to  result  from  chill, 
whence  the  name  "  pleurisy  a  frigore."  It  was  called  idiopathic,  meaning  by 
this  that  it  was  not  secondary  to  any  other  pathological  process.  It  was 
also  called  "  frank  pleurisy,"  which  excluded  the  idea  of  any  original  taint. 
This  primary  form  served  as  the  general  descriptive  type  of  acute  pleurisy. 

In  opposition  to  this  primary  form,  writers  described  secondary  pleurisies 
which  supervened  in  the  course  of  some  other  disease,  such  as  pneumonia, 
rheumatism,  3right's  disease,  etc.,  or  were  consecutive  to  neighbouring 
lesions  of  the  thoracic  and  abdominal  organs.  In  this  incongruous  group 
pleurisy  due  to  tuberculosis  occupied  the  chief  place,  but  primary  pleuro- 
tuberculosis  was  not  yet  well  known,  and  tubercular  pleurisy  was  chiefly 
considered  as  a  complication  of  phthisis. 

The  question  of  tubercular  pleurisy  has  been  gradually  elucidated,  and 
it  is  evident  that  all  cases  do  not  resemble  one  another.  The  first  category 
includes  cases  supervening  in  phthisis  when  lesions  exist  in  the  lung  and 
bacilli  are  present  in  the  sputum.  Pleurisy  appearing  under  these  condi- 
tions is  almost  certainly  tuberculous ;  but  this  fact  is  of  minor  importance 
in  the  present  discussion,  since  we  know  in  advance  that  the  patient  is 
tubercular. 

*  Dieulafoy,  Clinique  Medicate  de  V Hotel- Dieu,  1905,  le9ons  1  et  2. 


DISEASES  OF  THE  PLEURA  269 

In  the  second  category  let  us  place  cases  supposed  to  be  tubercular. 
The  lung  appears  free,  it  is  true,  yet  the  patient  is  suspected  of  tubercu- 
losis. One  is  of  tubercular  stock ;  another  has  previously  had  obstinate 
bronchitis,  haemoptysis,  fistula  in  ano,  or  so-called  rheumatism,  which  is 
only  tubercular  pseudo-rheumatism  (Poncet).  Some  patients  in  their 
infancy  have  had  suppurating  glands  in  the  neck,  which  have  left  scars ; 
coxalgia,  which  has  left  slight  lameness  ;  or  adenoid  hypertrophy,  with  larval 
tuberculosis  of  the  tonsils.* 

In  short,  the  cases  belonging  to  this  category  have  been  preceded  at  a 
more  or  less  distant  date  by  previous  tubercular  lesions.  Sometimes  they 
follow  a  prodromal  phase  that  is  of  indefinite  duration,  and  is  characterized 
by  loss  of  strength  and  wasting.  Clinically,  I  repeat,  these  cases  are 
suspicious  of  tuberculosis. 

Quite  different  are  the  cases  of  tubercular  pleurisy  which  now  require 
notice.  We  find  no  trace  of  tuberculosis,  either  in  the  past  or  in  the  present. 
The  patient  has  been  attacked  with  pleurisy  while  in  good  health,  either 
without  appreciable  cause  or  following  a  chill,  just  as  a  patient  is  seized 
with  tonsillitis  or  with  coryza.  The  onset  and  course  of  the  disease,  the 
appearance  of  effusion,  the  results  of  thoracentesis  (if  it  has  been  per- 
formed), and  convalescence  itself,  recall  the  picture  of  so-called  pleurisy 
a  frigore.  Appearances,  however,  are  often  deceptive,  for  we  shall  find 
that  the  man  who  recovers  from  pleurisy  suffers  some  years  later  from  more 
or  less  advanced  pulmonary  tuberculosis.  The  pleurisy  from  which  he 
recovered  was  the  initial  manifestation  of  the  tubercular  infection  which 
has  developed  later.  Another  patient  who  has  been  completely  cured  of 
pleurisy  dies  six  months  or  a  year  later  from  tubercular  meningitis.  These 
cases,  moreover,  are  not  isolated.  On  the  contrary,  they  are  frequent,  and 
have  thrown  douljt  upon  the  existence  of  pleurisy  a  frigore. 

Landouzy  in  1884  deprived  pleurisy  a  frigore  of  its  ancient  privileges. 
"  Every  pleurisy,"  says  he,  "  which  does  not  stand  the  test  is  tubercular, 
although  the  patient  may  be  robust."  Kelsch  and  Vaillard  sustained  the 
accusation,  and  the  course  of  events  fitted  in  so  well  in  this  respect  that 
pleurisy  a  frigore  has  lost  part  of  its  importance. 

Landouzy's  opinion,  however,  aroused  sharp  protests,  and  facts  in 
opposition  to  his  opinion  were  sought  for.  Cases  of  acute  pleurisy  a  frigore 
were  published.  It  was  said  they  had  no  connection  with  tuberculosis, 
since  they  recovered  without  sequelae.  Partisans  arranged  themselves  into 
camps,  and  pleurisy  a  frigore  continued  to  be  admitted  by  many 
physicians. 

We  have  to  see  on  wliicli  side  the  truth  lies.     Lot  us  carefully  examine 

*  Diinilafov,  " 'i'lilxTCulosf!  Ijiirvrt!  dcs  Trois  Aniygflali-s  "  {Aradhnif  de  MCdecine, 
8('anco  du  'M  Avril,  18SJ5  ;  ut  "  Maiiuol  de  I'ttthologio  lutorao,"  t.  ii.,  p.  l'J7). 


270  TEXT-BOOK  OF  MEDICINE 

the  evidence,  for  it  is  important  in  prognosis  to  know  whether  pleurisy  is 
tubercular  or  not. 

Let  us  first  consider  the  cases  of  sudden  death  in  patients  suffering  from 
pleurisy  a  frigore,  and  see  whether  post-mortem  examination  discloses 
tubercular  lesions. 

The  following  case  (Landouzy)  might  be  quoted  as  a  type  of  pleurisy 

a  frigore. 

A  healthy  baker  went  out  while  in  a  profuse  sweat  to  buy  some  wine.  Whilst 
walking  he  felt  that  he  had.  caught  a  cold,  but  continued  his  work.  Pain  in  the  side, 
respiratory  distress,  and  fever  appeared.  The  j)leurisy  ran  its  course.  Some  months 
later  he  died  suddenly,  while  under  Landouzy's  care.  Post  mortem,  much  serous 
fluid  was  found  in  the  right  pleura,  and  the  right  lung  showed  small  foci  of  latent  tuber- 
culosis.    This  case,  although  apparently  one  of  pleurisy  a  frigore,  was  really  tubercular. 

Kelsch  and  Vaillard  have  published  the  following  cases : 

A  healthy  trooper  was  taken  ill  with  acute  pleurisy.  He  died  suddenly  while  talking 
Avith  his  comrades,  just  as  he  was  going  to  the  Val-de -Grace  Hospital.  At  the  autopsy 
a  large  effusion  was  found  in  the  right  pleura,  which  was  studded  with  tubercular 
granulations. 

Another  soldier,  who  was  suffermg  from  right  pleurisy,  was  reading  by  his  bed, 
when  he  suddenly  fainted  and  died.  A  large  right-sided  effusion  was  foimd  post 
mortem  ;  the  pleura  was  studded  with  tubercular  nodules.  These  cases  of  serous 
pleurisy,  say  Kelsch  and  Vaillard,  "  supervening  in  strong  men  without  any  tuber- 
cular taint  and  having  only  the  usual  signs  of  pleurisy,  would  certainly  have  been 
considered  as  inflammatory  if  sudden  death  had  not  revealed  their  true  nature." 

In  days  gone  by,  at  the  Saint-Antoine  Hospital,  I  saw  the  two  following 
cases,  which  have  been  published  by  Binet  and  Legrand  : 

A  man  in  good  health  was  taken  iU  with  right  pleurisy,  which  he  attributed  to  a 
chill.  For  several  days  we  followed  the  spread  of  the  effusion,  which  finaUy  reached 
about  4  pints.  Although  dyspncea  was  absent,  we  decided  on  thoracentesis  about 
11  a.m.  The  patient  protested,  and  the  operation  was  postponed  tiU  evening;  but 
an  hour  later  the  man  got  up,  and  died  from  sjTicope  before  help  could  reach  him.  At 
the  autopsy,  as  I  wished  to  know  the  exact  amount  of  the  effusion,  I  performed  thora- 
centesis on  the  corpse,  and  drew  off  4  pints  of  yeUowish  fluid.  Latent  tuberculosis  had 
been  present ;  at  the  apex  of  the  lung  we  foimd  a  cretaceous  tubercle. 

The  second  of  my  cases  refers  to  a  robust  man  who  had  no  tubercular  history.  His 
trade  exposed  him  to  sharp  changes  of  temperature,  and  especially  to  local  chiUs  :  he 
carried  blocks  of  ice  on  his  back.  The  pleura  and  the  lungs  were  therefore  much  exposed 
to  cold.  He  came  under  my  care  for  pleurisy.  At  the  right  side  we  found  an  effusion, 
estimated  at  about  6  jjints.  Two  pints  were  dra-mi  off  by  puncture  on  three  successive 
days.  He  felt  very  well,  but  the  hquid  continued  to  reform.  Some  days  later  he  got 
up,  but  had  gone  only  a  few  steps  when  he  fell  down,  his  face  cyanosed,  his  lips  blue, 
and  died  in  a  few  seconds.  At  the  post-mortem,  as  I  wished  to  know  exactly  the 
quantity  of  effusion  causing  his  sudden  death,  I  performed  thoracentesis  on  the  body, 
and  drew  off  71  ounces  of  fluid.  I  then  discovered  that  the  pleurisy,  which  appeared 
to  be  a  frigore  (contact  with  the  ice-basket),  was  really  tubercular;  I  found  tuberculosis 
of  the  pleura  and  a  tubercular  nodule  in  the  Ixmg. 

A  person  may  apparently  regain  his  health  after  acute  pleurisy,  but 
some  months  later  he  is  carried  off  by  acute  phthisis  or  by  menmgitis,  show- 


DISEASES  OF  THE  PLEURA  271 

ing  the  tubercular  nature  of  the  pleurisy.  In  1884  I  saw  the  following 
case  : 

A  mechanic,  aged  twenty-eight,  came  imder  my  care  for  pleurisy  a  frigoie  of  three 
weeks'  standing.  There  was  nothmg  to  make  me  think  of  tuberculosis  ;  it  was  a  typical 
case  of  pleurisy.     On  the  left  side  I  foimd  a  large  effusion,  which  I  estimated  at  4  pints. 

1  began  by  drawing  off  2  pints  of  sero -fibrinous  fluid.     A  few  days  later  I  drew  off 

2  pmts  more.  Everything  went  well — the  patient  regained  his  health  ;  bat  six  months 
afterwards  he  came  imder  my  care  with  signs  of  meningitis,  and  died  in  a  few  days. 
At  the  i)Ost-mortem  we  foimd  that  the  pleurisy  was  cured,  only  a  few  adhesions  remain- 
ing, but  tubercular  meningitis  and  some  tubercular  granulations  in  tho  lang  were 
present. 

In  his  anatomical  and  experimental  researches  on  tuberculosis  of  the 
pleura,  Peron  arrives  at  the  following  conclusions  :  "  Acute  pleurisy,  called 
'  frank,'  is  usually  tubercular  in  nature,  and  is  in  many  cases  due  to  dis- 
crete infection  of  the  pleura." 

Clinical  medicine  teaches  us  that  many  patients  who  are  a^jparently 
suffering  from  primary  pleurisy  are  really  affected  with  tuberculosis, 
because,  although  they  may  be  cured  of  pleurisy,  the  tubercular  infection 
invades  the  lung,  meninges,  peritoneum,  or  other  parts  of  the  body 
some  months  or  years  later.  Clinical  medicine,  however,  also  teaches  us 
that  there  are  other  patients  in  whoih  acute  pleurisy,  with  large  effusion, 
may  recover  without  leaving  any  tubercular  taint  ;  the  patient,  after 
having  recovered  his  health,  lives  for  ten  or  twenty  years,  but  yet  neither 
he  nor  his  descendants  show  any  signs  ol  tubercular  infection. 

Many  statistics  may  be  consulted  on  this  subject.  Fiedler,  in  Germany, 
reports  92  cases  of  sero-fibruious  pleurisy  which  he  punctured  :  of  this 
number,  17  died  in  hospital  from  tuberculosLs,  8  died  after  leaving,  66 
left  the  hospital  either  tubercular  or  suspected  of  tuberculosis,  and  21 
were  in  good  health  at  least  one  or  two  years  later.  The  statistics  of 
Barrs  and  Bowditch  in  England,  and  those  of  Mayor  and  Ricochon  in 
France,  give  results  which  are  not  in  agreement,  but  still  the  tubercular 
element  occupies  the  largest  part.  For  some  years  I  questioned  my 
colleagues  (Brouardel,  Grancher,  Vcrgely,  Lepiiie,  etc.),  in  order  to  learn 
their  opinion  and  the  result  of  their  observations.  Vergely  sent  me  four 
reports,  referring  to  patients  with  pleurisy  who  were  punctured  fifteen, 
twenty,  and  twenty-two  years  previously  ;  they  remained  in  good  health, 
as  did  their  children.  Lepine  has  furnished  me  with  six  cases,  seen  a  great 
number  of  years  ago,  and  never  followed  by  tubercular  miseliicf. 

Since  my  first  work  on  thoracentesis  by  aspiration,  which  dates  back 
more  than  thirty  years,  I  have  punctured  a  great  many  cases.  I  have  lost 
sight  of  nearly  all  the  hospital  patients,  but  have  been  able  to  follow  up 
many  of  those  treated  in  ])rivatc,  and  I  can  quote  cases  of  persons  who 
suffered  from  acute  pleurisy  and  recovered  without  any  signs  of  tuberculosis. 


272  TEXT-BOOK  OF  MEDICINE 

I  owe  the  following  notes  to  Dr.  Lamarre  (of  Saint-Grermain) : 

The  forage-store  at  Saint-Germain  was  formerly  situated  in  the  Rue  d' Alsace, 
nearly  a  mile  from  the  quarters.  The  square  of  the  Chateau  is  about  half-way  on  the 
road  from  the  forage-magazine  to  the  barracks.  When  Lamarre  was  appointed 
Assistant  Physician  to  the  Samt- Germain  Hospital,  the  outer  walls  of  the  trenches  of 
the  castle  had  just  been  raised  to  the  height  of  3  feet.  This  wall  became  a  natural 
lounge  for  the  soldiers  who  carried  forage  on  their  backs.  They  used  to  come  from  the 
store,  and,  while  in  a  sweat,  they  leant  their  backs  against  the  wall,  so  as  to  rest  their 
load  on  the  top.  Suddenly,  however,  an  epidemic  of  acute  pleurisy  a  frigore  broke 
out  in  the  regiment,  while  no  cases  were  seen  among  the  civil  population.  The  mischief 
always  affected  the  right  side.  The  men  made  good  recoveries,  with  or  without 
aspiration,  according  to  circumstances. 

They  were  clearly,  says  Lamarre,  cases  of  pleurisy  a  frigore.  The  angle  of  the 
Chateau  square  where  the  soldiers  rested  was  sheltered  except  from  the  cold  north- 
east wind,  which  lashed  the  right  side  of  their  chests.  At  the  request  of  Lamarre 
and  of  the  Surgeon-Major  of  the  regiment,  the  Colonel  forbade  the  men  to  stop  at  this 
dangerous  spot,  and  no  more  cases  of  pleurisy  occurred. 

The  regiments  on  guard  duty,  however,  change  every  six  months,  and  fresh  cases 
of  jjleurisy,  due  to  the  same  cause,  occurred  in  the  regiment  which  had  just  marched 
in.  It  was  again  necessary  to  prohibit  the  men  on  fatigue  duty  from  stopping  and 
resting  against  the  wall.  This  experiment  (for  this  fact  has  the  value  of  an  experi- 
ment) occurred  several  times,  ■with  the  same  regularity. 

By  confining  ourselves  to  clinical  facts  we  see,  then,  that  the  cure  of 
acute  pleurisy,  without  any  residue  of  tuberculosis,  is  not  so  rare.  These 
facts  furnish  an  argument  for  those  who  defend  acute  pleurisy  a  frigore  : 
"  You  see  clearly,"  they  say,  "  that  these  cases  of  pleurisy  are  not  tuber- 
cular." Moreover,  they  add  :  "  Since  pleurisy  a  frigore  exists  in  animals, 
why  should  it  not  exist  in  man  ?"  Trasbot,  in  an  interesting  paper,  has 
shown  that  pleurisy  a  frigore  is  common  in  horses,  dogs,  and  sheep,  and 
may  have  nothing  to  do  with  tuberculosis.  In  support  of  this  opinion,  the 
following  facts  have  been  quoted  :  In  1871  a  line  regiment  of  Cuirassiers 
who  had  just  been  supplied  with  clipped  horses  were  picketed  in  the  open, 
often  without  blankets,  and  in  a  few  weeks  thirty  cases  of  pleurisy,  nearly 
all  fatal,  occurred  among  the  animals.  This  fact  was  so  striking  that  the 
military  authorities  at  once  prohibited  the  purchase  of  all  clipped  horses. 

Duvieusart  saw  100  cases  of  pleurisy,  with  60  deaths,  in  a  flock  of 
400  sheep  which  had  just  been  shorn  during  a  very  cold  February.  These 
animals  were  not  tubercular,  and  the  pleuritic  fluid,  injected  mto  guinea- 
pigs,  never  caused  tuberculosis. 

Rousseau  saw  several  healthy  dogs  attacked  by  pleurisy,  after  havuig 
in  the  depth  of  winter  followed  a  stag  in  a  pond  for  almost  an  hour.  In 
all  these  cases,  adds  Trasbot,  there  was  no  question  of  tuberculosis. 

I  quote  Trasbot  word  for  word  :  "  The  three  domestic  species — horse, 
dog,  and  sheep — in  which  pleurisy  is  most  often  met  with  are  precisely 
those  in  which  tuberculosis  is  most  rare.  .  .  .  Thus,  the  facts  drawn 
from  extensive  clmical  observation  in  different  species  of  animals  are  in 


J 


DISEASES  OF  THE  PLEURA  273 

formal  contradiction  to  the  idea  that  pleurisy  may  in  these  species  be  a 
form  of  tuberculosis.  This  proposition,  which  is  derived  from  clinical  data, 
is  also  absolutely  confirmed  by  experiment.  The  injection  of  the  fluid 
from  sero-fibrinous  pleurisy  in  horses  or  in  dogs  has  never  caused  tuber- 
culosis in  guinea-pigs  or  rabbits." 

It  appears  undeniable,  then,  that  simple  pleurisy  a  frigore  is  frequent 
in  animals.  Veterinary  medicine  shows  the  power  of  chills  in  causing 
pleurisy  among  animals.  But  let  us  limit  our  study  to  human  medicine, 
and  state  the  question  afresh  :  Does  there  exist  in  man  true  pleurisy  a 
frigore  which  is  not  tubercular  ?  and  if  it  exists,  by  what  means  can  it  be 
distinguished  from  the  tubercular  form  ? 

Laboratory  Researches. — To  answer  this  question,  an  appeal  has  been 
made  to  the  multiple  resources  of  the  laboratory. 

Inoculations. — It  was  thought  that  the  introduction  of  pleuritic  fluid 
into  the  peritoneum  of  guinea-pigs  would  furnish  important  information, 
as  the  iiioculation  would  transmit  experimental  tuberculosis  to  the  animal 
if  the  fluid  were  tubercular.  The  method  of  inoculation  certainly  gives 
valuable  information,  but  in  a  fairly  large  number  of  cases  it  leaves  the 
tubercular  or  non-tubercular  nature  of  pleurisy  in  doubt ;  its  value  Is  abso- 
lute when  the  result  is  positive,  but  a  negative  result  does  not  prove  that 
pleurisy  may  not  be  tubercular.  AH  observers  are  agreed  that  tubercular 
pleurisy  may  give  negative  results  after  inoculation  of  pleural  fluid.  A 
negative  result  is  easily  understood,  because  the  fluid  may  have  very  little 
virulence,  and  the  bacilli  may  be  so  disseminated  that  the  few  organisms 
introduced  into  the  peritoneum  are  rapidly  destroyed. 

Injections  of  tuberculin  furnish  information  of  undeniable  value. 
According  to  the  official  figures  from  the  clinics  in  Prussia,  patients 
suffering  from  apparently  simple  but  really  tubercular  pleurisy  are  nearly 
as  sensitive  to  injections  of  tuberculin  as  frankly  tubercular  patients  are. 
Injection  with  tuberculin,  even  if  carried  out  according  to  Grasset's  rules, 
is  not  always  exempt  from  harm. 

Cultures. — The  application  of  culture  methods  to  the  search  for  the 
tubercle  bacillus  in  effusions  has  only  recently  been  successful.  If  we  are 
to  obtain  positive  results,  a  culture  medium  that  is  extremely  favourable 
to  Koch's  bacilli  should  be  employed.  Glycerinated  blood-agar,  as  used 
by  Bezan9on  and  Griffon,  is  the  best  medium. 

The  mixture  of  aseptic  rabbit's  blood  with  agar  furnishes  soil  on  which 
the  microbes  develop  in  abundance,  although  they  will  not  grow  on  the  usual 
media.  If  glycerine  is  previously  added  to  the  agar-agar,  glycerinated 
blood-agar  is  obtained,  on  the  surface  of  which  it  Is  only  necessary  to  place 
the  suspected  litpiid,  whether  it  be  pus,  cerebro-spinal  fluid,  removed  by 
puncture,  pleuritic  fluid,  etc. 

18 


274  TEXT-BOOK  OF  MEDICINE 

We  may  use,  in  place  of  ordinary  culture -tubes,  Erlenmeyer's  flasks, 
at  the  bottom  of  which  a  layer  of  the  mixture  of  the  blood  and  glycerine 
agar  is  allowed  to  settle. 

The  tube  is  carefully  sealed  and  placed  in  the  oven  at  37°  C.  After  three 
or  four  weeks,  colonies,  which  increase  in  number  and  have  the  following 
characters,  are  seen  to  appear.  At  first  the  colonies  are  smaller  than  a 
pm's  head,  but  they  soon  become  larger,  growing  in  prominent  mulberry- 
shaped  masses  of  a  chocolate  colour.  Under  the  microscope,  preparations 
show  bacilli,  isolated  or  in  clumps,  which  are  usually  of  a  twisted  form. 
The  number  visible  to  the  naked  eye  is  proportionate  to  the  amount  of 
fluid  sown,  and  especially  to  the  richness  of  this  fluid  in  bacilli. 

The  results  obtained  by  this  procedure  are  not  constant,  but  it  is  an 
excellent  control  measure,  often  used  in  our  clinic. 

Sero-Diagnosis. — What  may  we  expect  from  sero-diagnosis  ?  Let  me 
first  remind  the  reader  that  it  is  the  sero-diagnosis  of  tuberculosis.  Speaking 
generally,  sero-diagnosis  supposes  two  factors  ;  whether  the  case  be  one 
of  typhoid,  pneumonic,  or  tubercular  infection  we  need  :  on  the  one  hand, 
a  homogeneous  culture  in  a  fluid  medium,  in  which  the  microbes  are 
separated  one  from  another ;  and,  on  the  other  hand,  serum  from  the 
infected  patient,  which,  on  addition  to  the  culture,  produces  agglutina- 
tion of  the  microbes. 

In  1898  Arloing  tried  to  find  a  sero-diagnosis  for  tuberculosis,  comparable 
with  Widal's  method  in  typhoid  fever.  The  problem  was  solved  when  he 
obtained  homogeneous  cultures  of  Koch's  bacillus  in  a  fluid  medium.  In 
order  to  obtain  the  conditions  most  favourable  to  success,  we  must  employ 
a  culture  of  tubercle  bacilli  twelve  days  old.  A  small  quantity  of  the 
culture  is  placed  in  a  very  small  tube.  This  culture  is  mixed  with  blood- 
serum  from  the  finger  of  a  patient  who  is  thought  to  be  suffering  from 
some  tubercular  lesion.  The  mixture  is  so  made  that  it  represents  one 
part  of  serum  to  five  parts  of  culture,  or  one  part  of  serum  to  ten  parts  of 
culture,  etc.  The  tube  is  then  shaken,  to  favour  mixing,  and  the  effect 
is  watched.  If  the  result  is  positive,  agglutination  occurs  after  an  interval 
of  one  to  five  hours.  The  upper  layers  of  the  mixture  become  clear,  while 
flakes  accumulate  at  the  lower  part  of  the  tube  and  give  to  this  layer  a 
muddy  aspect,  contrasting  with  the  limpid  nature  of  the  upper  layers. 
Microscopic  examination  will  confirm  the  result  of  the  agglutination,  and 
the  Koch's  bacilli  appear  in  masses  instead  of  being  isolated. 

Sero-diagnosis  is  applicable  in  tubercular  pleurisy.  Courmont  found 
that  a  positive  reaction  may  be  obtained  by  mixing  cultures  of  Koch's 
bacilli  either  with  blood-serum  or  with  pleuritic  fluid  in  dilutions  of  1  to  20, 
1  to  10,  or  1  to  5. 

The  agglutinating  power  of  the  blood  is  not  always  equal  to  that  of  the 


I 


DISEASES  OF  THE  PLEURA  275 

serum ;  it  may  be  more  or  less  marked,  and  may  exist  while  that  of  the 
serum  is  absent,  or  vice  versa. 

Courmont  in  the  following  table  has  summarized  the  results  of  positive 
and  negative  reactions  with  pleuritic  fluid  and  with  blood-serum  ; 

-r.    .,.  ..         r>o  I  ^  case,  1  in  20 

/■Positive  reactions,  23  cases 


i\ 


In  31  cases  with  I      "^       (74nercent)  j  6  cases,  1  in  10 

pleui-itic  fluid    'I  ^      V  ■>  [16  cases,  1  in  5 

iNegative  reaction  8  cases,  1  in  5  (26  per  cent.). 

/Positive  reactions,  18  cases 


(3  cases,  1  in  20 
9  cases,  1  in  15,  1  in  10 
6  cases,  1  in  5 
INegative  reactions  4  cases  (19  per  cent.) 

The  results  obtained  at  the  Hotel-Dieu  confirm  the  value  of  sero- 
diagnosis  in  tubercular  pleurisy  ;  we  must,  nevertheless,  remember  that  the 
procedure  is  sometimes  at  fault. 

Cyto-Diagnosis. — Cyto-diagnosis  is  based  on  the  examination  of  the 
cellular  elements  found  in  the  fluid  of  pleurisy  and  of  serous  effusions  in 
general.  A  few  words  of  explanation  are  necessary.  Certain  cells  respond 
by  an  offensive  and  defensive  reaction  against  the  attack  of  the  patho- 
genic agents,  but  the  same  cells  do  not  always  react  to  different  provoking 
agents.  The  polynuclear  neutrophUes,  or  microphages  (Metchnikoff), 
engulf  the  streptococcus  or  the  pneumococcus.  The  large  mononuclear 
cells,  or  macrophages,  have  a  more  powerful  action ;  they  absorb,  and 
sometimes  succeed  in  destro3dng,  the  tubercle  bacillus ;  they  readily  digest 
large  cells,  such  as  red  corpuscles  and  polynuclears.  It  was  therefore 
natural  to  suppose  that  the  presence  of  a  particular  cell  in  the  fluid  would 
indicate  the  nature  of  the  pathogenic  agent.  From  this  idea  cyto-diagnosis 
has  arisen. 

In  1900,  under  the  name  of  "  Cyto-diagnosis,"  Widal  and  Ravaut  first 
published  their  valuable  work,  of  which  the  chief  features  are  as  follows  : 

In  a  case  of  pleurisy  we  desire  to  know  the  cellular  elements  in  the 
fluid.  For  this  purpose  we  draw  off,  with  a  sterile  syringe,  some  pleuritic 
fluid,  and  centrifugalize  it,  A  sediment  forms  at  the  bottom  of  the  tube  ; 
we  pour  off  the  fluid,  so  as  to  leave  in  the  tube  only  a  little  liquid,  which 
forms  a  cloudy  emulsion  with  the  cellular  debris.  A  drop  of  this  emulsion 
is  placed  on  a  slide  and  stained  with  thiouin,  eosin  -  ]ia)inatin,  or  with 
Erlich's  tri-acid  mixture. 

On  microsco])ical  examination,  we  see  cells  of  various  kinds — red  cor- 
puscles, polynuclear  leucocytes,  large  mononuclear  cells,  lymphocytes, 
isolated  endothelial  cells,  and  endothelial  plaques.  These  elements,  how- 
ever, do  not  exist  indifferently  in  all  cases.  A  slide  does  not  at  the  same 
time  show  numbers  of  polynuclears,  lymphocytes,  and  endothelial  cells. 

18-2 


276  TEXT-BOOK  OF  MEDICINE 

Except  for  the  red  corpuscles,  which  exist  in  most  pleuritic  fluids,  one  speci- 
men will  contain  chiefly  lymphocytes,  while  the  polynuclear  and  the 
endothelial  cells  are  absent,  or  in  very  small  numbers.  Another  specimen  of 
fluid  contains  almost  nothing  but  polynuclear  cells,  while  the  lymphocytes 
and  endothelial  cells  are  absent,  or  very  few  in  number.  Lastly,  a  third 
specimen  contains  chiefly  endothelial  cells  and  plaques — the  lymphocytes 
and  polynuclear  cells  are  absent,  or  few  in  number. 

The  preponderance  of  one  or  other  variety  of  cell  in  the  pleuritic  fluid 
constitutes  the  cellular  formula  for  this  fluid,  and  leads  to  the  cjrto-diag- 
nosis.  From  this  point  of  view,  Widal  and  Ravaut  have  described  three 
kinds  of  pleurisy,  each  with  its  own  cyto- diagnosis. 

The  first  variety  comprises  effusions  in  cardiac  disease,  Bright's  disease, 
and  cancer,  as  well  as  those  due  to  irritation  or  to  compression  by  neigh- 
bouring organs.  No  infective  agents  are  present,  and  consequently  we 
find  no  phagocytosis,  but  only  the  processes  of  transudation  and  desquama- 
tion ;  the  condition  is  a  kind  of  congestive  oedema.  To  use  an  old  expression, 
it  is  here  less  a  case  of  exudate  than  of  transudate ;  it  is  by  transudation 
that  the  liquid  carries  away  the  endothelial  cells  from  the  serosa  into  the 
fluid.  Accordingly,  these  so-called  mechanical  effusions  have  a  special 
formula  ;  the  fluid,  as  a  rule,  contains  neither  lymphocytes  nor  polynuclear 
cells  (at  any  rate,  in  the  first  stage).  Endothelial  cells  from  the  serosa 
are  almost  exclusively  met  with. 

These  cells  are  very  large  in  comparison  with  the  size  of  the  red  cor- 
puscles and  the  leucocytes.  They  may  be  isolated  or  agglomerated,  bilobed, 
trilobed,  or  fused  in  large  endothehal  plaques  with  polycyclical  edges. 
After  staining  with  eosin-ha^matin,  the  nucleus  is  seen  to  be  much  darker 
than  the  protoplasm.  The  outline  of  the  cells  is  almost  circular ;  in  the 
endothelial  plaques,  however,  the  outline  of  the  cells  disappears  at  the 
points  where  the  protoplasm  is  fused.  These  plaques,  which  vary  in  size 
and  in  number,  are  characteristic  of  mechanical  effusions.  Widal  and 
Ravaut  met  with  them  in  twelve  cases.  The  post-mortem  examination  of 
three  patients  with  this  variety  of  pleurisy,  and  the  negative  results  of 
the  intraperitoneal  inoculations  in  guinea-pigs  with  pleuritic  fluid  from 
seven  similar  cases  prove  that  tuberculosis  is  not  in  evidence.  These 
endothelial  masses  are  not  only  characteristic  of  mechanical  pleurisy,  but 
their  presence  in  the  fluid  excludes  the  hypothesis  of  tuberculosis.  They 
are  not  found  in  the  fluid  in  recent  cases  of  tubercular  pleurisy,  no  doubt, 
"  because  the  tubercular  neomembrane  prevents  the  patchy  desquamation 
of  the  endothelium."  Similar  observations  have  been  made  in  my  wards  : 
the  fluid  in  every  case  of  tubercular  pleurisy,  though  very  rich  in  lympho- 
cytes, did  not  contain  endothelial  plaques.  A  similar  assertion  may  be 
made,  especially  with  regard  to  the  first  stages  of  mechanical  effusions, 


I 


DISEASES  OF  THE  PLEUEA  277 

but  later  the  lymphocytes  may  abound.  The  presence  of  the  plaques 
suffices,  nevertheless,  to  specify  the  diagnosis. 

In  the  second  variety  of  pleurisy  the  fluid  has  quite  a  different  cellular 
formula.  This  variety  includes  acute  infective  pleurisies.  The  patho- 
genic agents,  which .  include  the  streptococcus,  the  pneumococcus,  the 
Bacillus  typhosus,  etc.,  after  causing  cellular  reactions  of  attack  and  defence, 
may  no  longer  be  present,  but  the  phagocytes  or  polynuclear  leucocytes 
exist  in  abundance.  We  also  meet  with  large  mononuclear  cells,  which 
may  be  large  leucocytes,  or  may  be  derived  from  the  serous  membrane  ; 
while  we  may  also  recognize  the  presence  of  endothelial  cells,  which  are 
isolated  or  have  remained  absolutely  normal. 

With  regard  to  these  cases,  Widal  and  Ravaut  give  the  following 
information  :  In  three  out  of  seven  cases  of  pleurisy  in  typhoid  fever, 
the  relative  abundance  of  large  polynuclear  leucocytes  characterized  the 
formula  of  the  effusion.  In  a  case  of  sero-fibrinous  streptococcal  pleurisy, 
there  were  only  neutrophile  polynuclears,  with  deformed  nuclei.  In  sero- 
fibrinous pneumococcal  pleurisy,  the  formula  gives  rather  the  impression 
of  attack  and  defence.  This  formula  is  characterized  by  the  presence  of 
red  corpuscles  and  of  a  few  lymphocytes,  but  especially  by  the  abundance 
of  the  polynuclears  and  by  the  presence  of  a  greater  or  less  number  of 
large  mononuclear  cells,  some  of  which  are  really  macrophages  and  engulf 
the  polynuclears.  It  is  quite  exceptional  to  meet  with  two  or  three  endo- 
thelial cells  fused  together. 

Some  odourless  fluid  was  withdrawn  by  exploratory  puncture  from  one 
of  my  patients  who  had  pleurisy  on  the  right  side.  The  fluid  was  examined 
by  Apert,  and  contained  only  polynuclears  ;  neither  lymphocytes  nor  endo- 
thelial plaques  were  met  with.  The  absence  of  lymphocytes  excluded  acute 
tubercular  pleurisy ;  the  absence  of  endothelial  plaques  put  mechanical 
pleurisy  out  of  court.  A  few  days  later  turbid  foul-smelling  liquid,  like 
dirty  water,  was  withdrawn.  The  fluid,  which  was  rich  in  polynuclears  at 
the  first  puncture,  now  contained  only  a  few  cells  in  the  shape  of  granular 
masses,  which  did  not  stain  well ;  they  were  dead  leucocytes  in  process  of 
granulo-fatty  degeneration.  Aerobic  and  anaerobic  cultures  of  the  liquid 
revealed  a  varied  microbic  flora.  In  aerobic  cultures  the  Staphylococais 
(dbus  appeared.  In  anaerobic  cultures,  colonies  in  the  form  of  whitish 
points,  composed  of  a  small  micrococcus  en  masse,  appeared.  The  leuco- 
cytic  formula  of  this  foetid  pleurisy  was  the  same  as  in  other  infectious 
varieties.  In  short,  polynuclear  and  mononuclear  elements  characterize 
acute  infective  pleurisies  ;  lymphocytes,  when  met  with,  are  less  numerous, 
and  it  is  exceptional  to  find  endothcilial  masses,  with  two  or  three  nuclei, 
l^^ig.  14  represents  the  cellular  formula.  We  see  several  polynuclear 
leucocytes  and  one  large  uninuclear  cell. 


278  TEXT-BOOK  OF  MEDICINE 

We  now  come  to  the  third  variety,  which  is  the  most  important 
of  all,  and  corresponds  best  to  acute  pleurisy  a  frigore.  On  micro- 
scopic examination  of  the  pleuritic  fluid,  we  see  that  the  cellular 
formula  is  characterized  "by  the  almost  exclusive  presence  of  lympho- 
cytes, which  are  confluent  and  mixed  with  a  relatively  large  number 
of  red  corpuscles.  At  times  we  perceive  here  and  there  mononuclear  cells, 
as  well  as  lymphocytes,  which  at  first  sight  seem  to  be  the  only  leucocytes 
in  the  specimen."  The  polynuclears,  when  met  with,  are  not  numerous ; 
they  are  perhaps  the  result  of  secondary  infection.  The  endothelial  cells 
must  be  very  rare,  because  in  seventeen  cases  Widal  and  Ravaut  never  met 
with  them. 

I  have  examined  the  cellular  formula  of  these  cases,  employing  prepara- 
tions made  with  fluid  from  seven  patients  in  the  Saint-Christophe  and 


^ 


?$u 


Fig.  14. — PoLYNtr clear  LEtrcocyTEs, 

Sainte-Jeanne  wards.  Numerous  lymphocytes  and  some  red  corpuscles 
are  met  with ;  neither  polynuclears  nor  endothelial  plaques  are  seen. 
This  description  corresponds  to  that  given  by  Widal  and  Ravaut. 

This  cellular  formula,  or  pleural  lymphocytosis  with  red  corpuscles, 
indicates  that  the  case  is  tubercular.  Histological  examination  of  the  pleura 
and  inoculation  of  the  peritoneum  in  guinea-pigs  with  the  pleuritic  fluid 
confirm  their  tubercular  nature.  'The  following  case  was  related  to  me 
by  Widal,  and  is  a  strikmg  example  : 

A  youth  was  taken  ill  with  the  symptoms  of  pleurisy  a  frigore — i.e.,  repeated  rigors, 
stitch  in  the  right  side,  and  cough,  but  no  expectoration.  On  the  ninth  day  he  was 
admitted  under  Widal,  with  the  signs  of  abundant  effusion  on  the  right  side.  Thora- 
centesis was  performed,  and  4  pints  of  yellow  liquid  were  withdrawn.  The  liquid 
showed  a  typical  lymphocytic  formula,  indicating  pleuro -tuberculosis.  On  the  follow- 
ing day  the  temperature  varied  between  102°  and  104°  F.  Four  days  after  the  puncture 
the  patient  suddenly  sat  up,  choked,  and  died  in  a  few  seconds. 

Post  mortem  :  The  left  lung  looked  like  an  infarct  engorged  with  blood ;  this  conj 
dition  seemed  to  depend  upon  an  extensive  pulmonary  embolism.     Tubercles  were  nol 


DISEASES  OF  THE  PLEURA  279 

present  in  either  lung.  The  pleural  cavity  contained  3  pints  of  sero-fibrinous  fluid. 
The  pleura  was  much  thickened.  No  tubercles  were  visible  to  the  naked  eye,  but 
histological  sections  showed  everywhere  tubercular  tissue.  Many  giant  cells  were  seen 
in  the  fibroas  tissue  of  the  inflamed  serous  membrane.  Fig.  15  represents  these 
lesions.  In  this  section  of  the  thickened  pleura  tissue  is  infiltrated  with  numerous 
cells.  We  see  a  giant  cell,  containing  numerous  nuclei,  arranged  like  a  crown  at 
the  periphery  of  the  cell. 

The  entire  pleura  was  really  a  tubercular  membrane  studded  with  giant  cells,  but 
the  lung  was  unaffected.  The  condition  was  primary  tuberculosis  of  the  pleura.  The 
fluid  produced  tuberculosis  in  guinea-pigs. 

This  case  sums  up  the  whole  question  ;  it  would  formerly  have  been  con- 
sidered as  a  case  of  simple  pleurisy  a  frigore,  when  it  was  really  tubercular. 
The  cytoscopic  examination  of  the  fluid  was  undertaken,  but  lymphocytes 
alone  were  found ;  the  diagnosis  of  tubercular  pleurisy  was  verified  by  the 


Fio.  15, — Section  of  Pleura. 

histological  examination  of  the  pleura  and  by  the  results  of  inoculation  of 
guinea-pigs  with  the  pleuritic  fluid. 

We  have,  therefore,  several  methods  of  ascertaining  the  tubercular  nature 
of  acute  pleurisy,  but  I  much  prefer  cyto-diagnosis,  because  it  is  simple  and 
expeditious. 

In  acute  pleurisy  (the  patient  being  in  good  health)  abundance  of  lympho- 
cytes and  absence  of  endothelial  plaques  from  the  fluid  point  to  tubercular 
mischief.  Cytoscopic  examination  of  the  fluid  is  as  necessary  as  bacterio- 
logical analysis  of  the  sputum  in  a  doubtful  case  of  pulmonary  tuberculosis. 
In  every  case  of  pleurisy  cyto-diagnosis  is  necessary.  Every  report  in 
which  cyto-diagnosis  is  wanting  is  incomplete.  In  my  wards  this  fact  is 
never  neglected. 

We  must  not  be  satisfied  even  though  the  diagnosis  is  clinically  evident, 
because   surprises   may   happen.     Pleurisy,    considered    to    be   tubercular 


280  TEXT-BOOK  OF  MEDICINE 

because  it  has  supervened  in  the  course  of  phthisis,  may  not  be  tubercular  ; 
pleurisy,  considered  influenzal  because  it  has  occurred  in  the  course  of 
influenza,  may  be  tubercular  ;  the  influenzal  infection  has  here  favoured  the 
development  of  pleurisy.  Cases  of  traumatic  pleurisy,  which  might  have 
been  referred  to  the  trauma  alone,  are  really  tubercular,  the  injury  having 
awakened  the  latent  germs.  I  have  so  far  considered  tubercular  pleurisy, 
which  is  acute  or  of  recent  date.  The  leucocytic  formula  of  the  fluid  may  be 
quite  different  in  a  case  of  tubercular  hydropneumothorax,  which  results 
from  gross  tubercular  lesions  in  the  lung.  Under  such  conditions  the  lympho- 
cytosis is  not  the  chief  point :  "  old  deformed  polynuclears  with  much  divided 
nuclei  are  seen,  as  well  as  cells  with  vesicles  in  their  protoplasm,  and  some- 
times also  amorphous  masses,  which  appear  to  be  derived  from  the  endo- 
thelium." The  diagnosis  in  this  variety  depends  chiefly  on  clinical  research. 
Nattan-Larrier  has  devised  an  ingenious  method,  which  consists  in  the 
injection  of  |  c.c.  of  pleuritic  fluid  into  the  mamma  of  a  female  guinea-pig 
which  is  suckling.  The  mamma  acts  as  a  living  culture  medium.  The 
bacilli  begin  to  appear  in  the  milk  after  five  to  ten  days.  When  we  wish  to 
examine  the  milk,  the  animal  is  put  on  its  back,  and  the  mammary  gland  is 
squeezed  with  the  fingers  of  the  left  hand  ;  a  drop  of  milk  exudes  from  the 
nipple.  The  drop  is  spread  out  over  a  slide  in  a  thin  layer.  The  films  are 
fixed  with  alcohol,  stained  with  Ziehl's  fuchsin,  and  decolourized  with 
30  per  cent,  nitric  acid  ;  the  ground  substance  is  stained  with  Kiihn's  blue. 
We  see  even  as  early  as  the  fifth  day  that  some  bacilli  are  engulfed  by  the 
macrophages,  or  are  isolated  between  the  leucocytes.  A  few  days  later  the 
bacilli  are  more  numerous,  and  their  recognition  is  more  easy.  This  method 
has  been  extended  to  other  fluids  (peritoneal  effusion,  cerebro-spinal  fluid, 
etc.).  It  has  been  used  in  my  wards  at  the  Hotel-Dieu,  and  I  have  proved 
the  correctness  of  the  results.  By  this  method  the  daily  search  for  bacilli 
allows  us  to  follow  the  course  of  the  inoculation,  and  reveals  tuberculosis  as 
soon  as  it  begins  to  develop  in  the  gland.  We  also  see  that  the  glands  become 
larger  in  a  few  days  and  that  the  inguinal  glands  swell ;  the  mamma  is  there- 
fore the  starting-point  of  widespread  lesions. 

Let  us  return  to  the  origin  of  our  discussion.  The  original  question  was  : 
Are  we  in  a  position  to  know  whether  acute  sero -fibrinous  pleurisy  is  or  is  not 
tubercular  ?     The  answer  is  an  affirmative  one. 

Henceforth  it  will  be  possible  for  us  to  estimate  correctly  the  so-called 
"  essential "  pleurisy.  We  shall  see  from  the  first  that  most  cases  which 
answer  to  the  description  of  so-called  frank  pleurisy  a  frigore  are  really  tuber- 
cular ;  cyto-diagnosis  stamps  them,  and  lymphocytosis  unmasks  their  origin. 
We  shall  see,  further,  that  there  are  infectious  agents  capable  of  causing 
acute  pleurisies  which  have  nothing  to  do  with  tuberculosis.  An  individual 
suffers  from  sero-fibrinous  pleurisy  with  effusion,  as  he  might  from  pneu- 


I 


DISEASES  OF  THE  PLEURA  281 

monia  ;  the  pneumococcus  is  the  provoking  agent.  Another  person  has 
acute  pleurisy  with  effusion  ;  here  the  streptococcus  is  the  pathogenic  agent. 
In  a  third  person,  who  also  has  acute  pleurisy  with  effusion,  we  find  fcetid 
or  non-foetid  infection  of  the  pleura  by  aerobic,  or  by  anaerobic,  germs,  etc. 
This  group  of  acute  pleurisies,  which  I  might  further  enlarge,  has  nothing 
to  do  with  tuberculosis.  Bacteriology  has  classed  them  according  to  their 
pathogenic  agents ;  cyto-diagnosis  includes  them  in  the  same  cellular  formula; 
they  are  cases  of  pleurisy  with  polynuclear  and  mononuclear  cells. 

The  pathogenic  diagnosis  of  pleurisies  which  were  formerly  indefinite  is 
now  so  clearly  elucidated  that  we  may  ask  what  place  can  be  assigned  in 
medicine  to  "  essential  "  pleurisy,  in  which  cold  was  considered  the  only 
cause.  Ought  this  variety  of  pleurisy  to  surrender  its  place  in  our  nosology 
for  ever,  after  having  occupied  the  chief  place  ?  Should  it  be  definitely  cut 
out,  or  should  a  place  still  be  reserved  for  it  ?     The  future  will  tell  us. 

Curability  of  Tubercular  Pleurisy. — Let  us  now  approach  another  side 
of  the  question.  How  can  we  explain  the  fact  that  acute  pleurisy,  called 
a  frigore,  but  recognized  as  tubercular,  may  recover  without  leaving  any 
traces  ?  This  very  curability  was  the  chief  argument  against  tuberculosis. 
Our  reply  is  that  if  these  cases  recover  it  does  not  say  that  they  may  not  be 
tubercular.  The  disease  is  sometimes  limited  to  the  pleura  (primary  pleuro- 
tuberculosis),  the  lung  is  free,  and  the  rest  of  the  organism  is  healthy  ;  as  the 
serosa  is  well  armed  for  defence  and  the  virulence  is  feeble,  it  is  not  surprising 
that  pleurisy  may  recover  without  the  infection  of  other  parts. 

Further,  recovery  is  not  special  to  tuberculosis  of  the  pleura  ;  other  sero- 
membranes  have  the  same  privilege.  Tuberculosis  of  synovial  membranes, 
from  simple  arthritis  to  tubercular  pseudo-rheumatism,  is  cured  fairly  often. 
Tuberculosis  of  the  pericardium  (Rendu)  belongs  to  the  same  category. 

Cases  of  recovery  from  tubercular  peritonitis  with  ascites  are  no  longer 
reckoned.  Cases  of  ascites,  formerly  catalogued  under  the  terms  "essential," 
or  "  a  frigore,"  are  certainly  cases  of  tubercular  peritonitis,  which  are 
attenuated  and  readily  curable.  Some  recover  under  medical  treatment 
without  the  help  of  surgical  intervention,  some  after  puncture,  with  or 
without  consecutive  injections,  while  others  are  cured  by  laparotomy.  The 
cure  of  one  of  these  cases  formerly  caused  much  stir.  On  March  20,  1840, 
at  a  time  when  no  one  dared  to  touch  the  peritoneum,  my  uncle,  Paul 
Dieulafoy,  of  Toulouse,  was  bold  enough  to  inject  tincture  of  iodine  into  the 
peritoneal  cavity  after  removal  of  the  fluid.  This  operation  was  successful, 
and  since  then  other  cases  have  been  reported. 

I  have  often  recognized  this  curability  in  simultaneous  tuberculosis  of 
the  pleura  and  the  peritoneum. 

Tubercular  pleurisy  is  therefore  perfectly  curable  ;  indeed,  it  may  be  said 
that  it  is  sometimes  quite  benign  in  nature.     Peron,  who  studied  this  question 


282  TEXT-BOOK  OF  MEDICINE 

from  the  anatomical  and  experimental  point  of  view,  comes  to  the  same 
conclusion :  '*  In  tubercular  sero-fibrinous  pleurisy,  which  assumes  the 
clinical  bearing  of  acute  tuberculosis,  the  infection  is  at  its  minimum  ;  the 
reaction  of  the  organism  is  considerable." 

Griffon,  in  collaboration  with  Bezan9on,  has  just  verified  this  idea 
experimentally  by  measuring  the  degree  of  virulence  of  the  pleuritic  fluid  in 
several  patients  under  my  care.  Their  researches  show  that  the  effusion  in 
frank  pleurisy  which  tuberculizes  the  guinea-pig,  a  most  sensitive  animal, 
is  generally  benign  in  a  more  resisting  animal,  such  as  the  rabbit.  Only  one 
of  my  patients  had  pleuritic  fluid  of  sufiicient  virulence  to  cause  experi- 
mental tuberculosis  in  an  inoculated  rabbit.  The  affection  was  of  long  dura- 
tion, with  high  fever,  and  this  patient  has  come  back  to  my  wards  suffering 
from  pulmonary  tuberculosis,  which  is  secondary  to  the  pleurisy. 

The  curability  of  tubercular  pleurisy  suggests  some  reflections.  When 
we  speak  of  cure  in  tubercular  pleurisy,  are  not  our  thoughts  limited  to  the 
pleura  ?  What  will  happen  later  to  the  lungs  after  the  pleurisy  is  cured  ? 
Is  the  patient  destined  to  become  tubercular  ?  This  is  the  whole  point  of 
the  question.  The  answer  is  somewhat  difficult.  It  is  said,  with  good  reason, 
that  definite  cure  without  sequelae  results  when  the  disease  is  limited  to  the 
pleura  and  the  lung  is  free.  This  statement  is  true,  but  how  can  we  say  that 
the  lung  is  absolutely  free  in  an  individual  who  is,  suffering  from  primary 
pleuro-tuberculosis  ?  Do  we  not  know,  as  Potain  has  taught,  that  acute 
pleurisy  is  often  accompanied  by  an  inflammatory  condition  of  the  lung  ? 
What  is  the  nature  of  the  pleuro-congestion  ?  A  small  focus  of  tuberculosis 
may  exist  in  the  lung  without  showing  any  symptom,  and  yet  this  latent  focus 
may  become  the  origin  of  tuberculosis.  Rapidly  fatal  miliary  tuberculosis  of 
the  lung  may  appear  to  be  primary,  though  it  is  really  consecutive  (the  autopsy 
shows  this)  to  a  small  tubercular  focus  that  was  insidious  in  its  growth. 

The  same  arguments  apply  to  tubercular  pleurisy.  An  individual  while 
in  good  health  is  taken  ill  with  acute  pleurisy.  Cyto-diagnosis  shows  that  the 
disease  is  tubercular,  and  everything  points  to  primary  pleuro-tuberculosis  ; 
the  most  minute  examination,  according  to  Grancher's  scheme,  reveals  no 
lesions  in  the  lung,  and  yet  the  apparently  primary  mischief  in  the  pleura 
may  well  be  consecutive  to  a  small  focus  in  the  lung  which  has  infected  the 
pleura.     We  have  the  proof  of  this  in  the  case  quoted  above. 

Landouzy's  patient  while  in  good  health  was  seized  with  apparently 
primary  tubercular  pleurisy  ;  he  died  suddenly,  and  the  autopsy  revealed  a 
small  focus  in  the  lung.  My  two  patients  who  died  suddenly  had  both  been  ] 
taken  ill  with  apparently  primary  pleurisy.  At  the  autopsy  we  found  aj 
small  focus  in  the  lung,  which  had  given  rise  to  infection  of  the  pleura. 

These  cases  prove  that  true  primary  pleuro-tuberculosis,  associated  with  j 
no  pre-existing  lesions  in  the  lung,  and  secondary  pleuro-tuberculosis,  setup 


DISEASES  OF  THE  PLEUEA  283 

by  a  small  latent  focus  in  the  lung,  may  both  assume  the  symptoms  of  so- 
called  frank  pleurisy.  In  many  cases  it  is  not  possible  to  distinguish 
them  ;  clinically,  they  may  show  no  differences,  and  cyto-diagnosis  includes 
them  in  the  same  cellular  formula. 

These  two  varieties  of  tubercular  pleurisy,  however,  are  not  comparable 
as  regards  prognosis ;  one  is  less  grave  than  the  other.  In  the  primary  form 
the  lesion  in  the  pleura  may  recover  without  producing  general  infection  of 
the  lung,  or  of  the  other  organs.  If  the  lung  is  already  affected,  although  the 
lesion  is  small,  the  prognosis  is  not  so  good,  for  we  have  to  cure  tuberculosis, 
both  of  the  pleura  and  of  the  lung.  The  prognosis  in  acute  cases  of  long 
duration  is  evidently  uncertain. 

Treatment. — I  would  refer  the  reader  to  the  preceding  section ;  I  have, 
however,  some  remarks  to  add.  Acute  pleuro -tuberculosis  is  generally 
accompanied  by  much  effusion.  Perhaps  this  effusion  is  a  mode  of  defence  ; 
perhaps  the  lung  which  is  compressed  by  the  fluid  has  less  tendency  to  be 
infected  from  the  pleura.  If  this  hypothesis  be  true,  it  would  be  better  not 
to  perform  thoracentesis  too  hastily ;  but  yet,  on  the  other  hand,  we  know 
how  dangerous  it  is  to  allow  too  much  fluid  to  accumulate  in  the  pleura  : 
sudden  death  may  be  the  consequence,  whatever  be  the  theory  employed  to 
explain  it.     It  is  therefore  necessary  to  perform  thoracentesis  in  good  time. 

There  is  another  question  which  is  also  of  importance.  In  the  case  of 
acute  tubercular  pleurisy  the  fluid  may  reform  rapidly,  even  when  it  appears 
to  have  been  drained  away  by  thoracentesis.  I  have  found  that  this  rapid 
and  obstinate  reproduction  of  fluid  is  much  less  marked  in  acute  infective 
pleurisies  that  are  not  tubercular.  I  have  often  in  tubercular  cases  had 
occasion  to  draw  off  4  or  5  pints  of  sero-fibrinous  fluid  by  two  or  three 
successive  punctures.  The  effusion  seemed  to  cease  for  the  moment,  and  the 
patient  was  considered  cured ;  but  yet  the  fluid  reformed  without  fever, 
dyspnoea,  or  pain,  and  in  a  few  days  amounted  to  3  pints  or  more.  The 
patient  must  be  kept  under  observation,  even  if  the  acute  phase  appear  to  be 
ended  ;  and  we  must  not  forget  that  fluid  may  reform  rapidly  after  puncture, 
and  cause  sudden  death,  if  we  be  not  forewarned. 

I  have  just  given  my  recommendations  in  the  acute  phase  of  pleurisy, 
but  treatment  does  not  stop  there.  The  patient  is  convalescent,  but  the 
tubercular  lesion  lies  hidden,  though  health  is  apparently  regained.  What 
will  happen  in  this  case  ?  Will  it  be  cured  without  leaving  any  scquolno,  or 
may  it  not  rather  be  the  first  stage  of  tubercular  infection,  which  will  later 
attack  the  lung  or  the  other  organs  ?  We  know  nothing  of  this,  but  we  do 
know  that  the  patient  has  tuberculosis,  and  we  should  place  him  under  the 
best  therapeutic  and  hygienic  conditions. 

An  individual  who  is  convalescent  from  acute  pleurisy  should  for  a  long 
while  take  care  of  himself,  even  though  he  be  considered  as  cured  of  active 


284  TEXT-BOOK  OF  MEDICINE 

disease.  Tubercular  infection  lies  in  wait  for  him.  Years  must  pass  before 
he  can  be  considered  free  from  all  risk  of  tuberculosis. 

Special  attention  must  be  paid  to  hygiene.  The  patient  should  avoid 
all  causes  of  over-fatigue.  Nourishment  should  be  substantial  and  varied ; 
food  and  diink  which  excite  the  appetite  should  be  chosen.  As  regards 
residence,  preference  should  be  given  to  high  altitudes,  and  life  should  be 
passed  in  the  open  air.  All  kinds  of  exercise  are  permissible,  provided  they 
are  never  carried  to  excess. 

As  regards  tonic  and  constitutional  remedies,  cod-liver  oil  should  be  given 
in  increasing  doses — e.g.,  2  to  4  ounces  daily — if  it  is  well  tolerated  ;  many 
patients  will  swallow  a  tumblerful  of  cod-liver  oil  before  meals.  In  order  to 
render  it  less  disagreeable,  it  may  be  cooled  by  placing  the  glass  in  ice. 

In  patients  who  do  not  take  cod-liver  oil  well  we  should  recommend  fatty 
foods,  such  as  cream  or  bread  and  butter.  Oysters,  caviare,  sardines  in  oil, 
tunny  fish,  smoked  fish,  and  meat  should  form  part  of  the  diet.  Raw  meat 
and  meat-juice  are  of  benefit  in  cases  of  tuberculosis  (Richet  and  Hericourt, 
Josias  and  Roux).     Injections  of  cacodylate  of  soda  should  also  be  given. 

III.  HEMORRHAGIC  PLEURISY. 

General  Considerations. — For  many  years  while  I  was  occupied  with  the 
histological  examination  of  fluid  from  acute  pleurisies,  I  had  seen  that  my 
specimens  contained  some  thousands  of  red  corpuscles  per  cubic  millimetre. 

With  1,500,  2,000,  and  3,000  red  corpuscles  per  cubic  millimetre  the 
colour  of  the  fluid  was  not  sensibly  altered ;  the  colour  only  becomes  rosy 
when  the  fluid  contains  5,000  to  6,000  red  corpuscles  per  cubic  millimetre. 
I  have  called  these  pleurisies  histologically  hsemorrhagie,  in  order  to 
differentiate  them  from  true  hsemorrhagic  pleurisies,  which  are  quite  distinct. 
Fluid  which  is  very  rich  in  red  cells  may  remain  histologically  hsemorrhagic 
without  becoming  hsemorrhagic  in  the  true  sense  of  the  word. 

In  this  section  I  shall  leave  out  hsemorrhage  into  the  pleura  from  injury, 
and  shall  only  take  count  of  hsemorrhagic  pleurisy  from  the  medical  aspect. 

It  is  customary  to  include  various  morbid  conditions  under  the  term 
"  hsemorrhagic  pleurisy."  Hsemorrhagic  effusions  into  the  pleura  which 
are  consecutive  to  tubercular  or  to  cancerous  lesions  are  the  most  frequent. 
These  effusions  are  sometimes  only  symptomatic,  and  develop  as  a  complica- 
tion in  the  course  of  cancer,  or  of  pleuro-pulmonary  tuberculosis  ;  at  other 
times  they  attract  attention  from  the  first,  and  appear  as  the  prodromata 
of  hidden  tubercular  or  cancerous  lesions.  In  some  cases  hsemorrhagic 
effusions  into  the  pleura  appear  independent  of  tuberculosis  or  cancer  ;  they 
seem  to  be  simple  hsematomata  of  the  pleura.  This  simple  hsematoma, 
however,  must  be  extremely  rare,  and  the  more  I  study  the  question  the  more 


DISEASES  OF  THE  PLEURA  285 

I  believe  that  the  hsematoma  is  only  a  benign  or  curable  haemorrhagic 
tubercular  pleurisy. 

We  do  not  see  therefore  one,  but  several  kinds  of  haemorrhagic  pleurisy. 
The  fluid  is  reddish  or  blackish,  and  contains  fibrin,  haematin,  red  cor- 
puscles, and  dissolved  elements  ;  the  composition  depends  upon  the  nature 
of  the  pleurisy  and  on  the  abundance  and  the  age  of  the  fluid. 

I  may  say  in  advance  that  the  haemorrhagic  nature  of  the  pleural  fluid 
usually  comes  as  a  surprise  ;  thoracentesis  is  performed,  and  the  fluid  is 
found  to  be  haemorrhagic.  It  is  practically  impossible  to  afflrm  before 
thoracentesis  that  pleurisy  is  haemorrhagic.  What  are  the  signs  and 
symptoms  which  would  lead  to  such  a  diagnosis  ?  In  the  great  majority  of 
cases  haemorrhagic  pleurisy  is  just  like  the  sero-fibrinous  form  ;  I  see  no  dis- 
tinctive signs  between  them  :  the  course  may  in  both  cases  be  acute,  sub- 
acute, or  latent.  On  palpation  the  same  modifications  of  the  vocal  fremitus  ; 
on  percussion,  the  same  character  of  the  dullness  ;  on  auscultation,  the  same 
tubular  breathing  and  aegophony,  as  well  as  aphonic  pectoriloquy  which  has 
been  given  as  a  distinctive  sign  between  sero-fibrinous  and  purulent  or 
haemorrhagic  effusions.  I  have  found  aphonic  pectoriloquy  in  most  of 
my  cases,  and  it  was  very  clearly  marked  in  a  case  of  haemorrhagic  pleurisy 
described  by  Jaccoud,  and  hence  I  repeat  the  haemorrhagic  nature  of  the 
fluid  is  a  surprise.  We  perform  thoracentesis,  thinking  to  draw  off  sero- 
fibrinous fluid  from  the  pleura,  and  we  are  often  astonished  to  find  it 
haemorrhagic. 

Under  some  conditions  haemorrhagic  pleurisy  may  simulate  empyema  ; 
the  general  symptoms  which  lead  to  this  error  in  diagnosis  are  due  to  the 
tubercular  or  to  the  cancerous  lesions  which  have  set  up  pleurisy.  The 
patient  is  feeble,  has  an  earthy  colour,  and  shows  oedema  of  the  lower  limbs 
and  of  the  chest-wall ;  thoracentesis  is,  performed  with  the  idea  that  pus  will 
result,  but  here  again  we  are  much  astonished  to  withdraw  blood-stained 
fluid.  We  make  this  mistake  because  we  are  too  accustomed  to  consider 
ffidema  of  the  che.st-wall  as  a  sign  of  suppuration ;  it  is,  indeed,  a  valuable 
sign,  but  it  is  not  limited  to  purulent  effusions.  It  is  also  met  with  in 
haemorrhagic  and  even  in  some  sero-fibrinous  effusions. 

Htemorrhagic  pleurisy  may  at  times  be  suspected  beforehand — e.g.,  when 
the  trouble  develops  in  a  cancerous  patient.  Whether  the  cancer  be 
primary  or  secondary,  we  may  prophesy  in  such  a  case  that  the  effusion  k 
perhaps  haemorrhagic.  I  say  perhaps,  for  effusion  of  cancerous  origin  is 
sero-fibrinous  in  at  least  one-third  of  the  cases. 

In  short,  the  diagnosis  of  the  haemorrhagic  nature  of  the  fluid  rests  upon 
no  certain  sign  ;  its  existence  may  be  suspected  and  reservations  made  as  to 
the  qualities  of  an  effusion  which  shows  unusual  characters,  but  it  is  impossible 
to  affirm  the  haemorrhagic  nature.     After  these  few  remarks  it  will  be 


286  TEXT-BOOK  OF  MEDICINE 

evident  that  the  study  of  haemorrhagic  pleurisies  is  surrounded  by  difficulties  ; 
therefore,  in  order  to  facilitate  the  description,  I  shall  divide  them  into  four 
groups : 

First  Group. — These  cases  supervene  in  the  course  of  hepatic  cirrhosis 
and  of  Bright's  disease,  or  appear  as  a  pleural  haemorrhage  in  the  course 
of  scurvy  and  the  eruptive  fevers.  In  this  group  I  shall  also  place  haemor- 
rhage from  the  opening  of  an  aortic  aneurysm,  or  from  the  rupture  of  an 
atheromatous  aorta.  This  group,  then,  contains  the  most  dissimilar 
varieties. 

Second  Group. — This  group  comprises  the  tubercular  pleurisies.  Three 
varieties  must  be  distinguished.  In  the  first  variety  the  condition  forms 
part  of  an  acute  tuberculosis  ;  in  the  second  variety  pleurisy  supervenes 
in  the  course  of  ordinary  chronic  tuberculosis  ;  in  the  third  variety 
haemorrhagic  pleurisy  appears  as  the  first  symptom  of  tuberculosis  :  it  is  the 
result  of  local  or  primary  tuberculosis  of  the  pleura. 

Third  Group. — To  this  category  belong  cancerous  pleurisies,  whether 
the  cancer  be  j)rimary  or  secondary. 

Fourth  Group. — Simple  haematoma  of  the  pleura  forms  the  fourth  group. 

First  Group. 

Description. — The  most  dissimilar  effusions  are  found  in  this  group. 
Does  cirrhosis  of  the  liver  deserve  the  place  assigned  to  it  in  the  pathogenesis 
of  haemorrhagic  pleurisy  ?  I  think  not.  In  Moutard-Martin's  remark- 
able work  two  cases  of  haemorrhagic  pleurisy  are,  in  my  opinion,  wrongly  con- 
sidered as  dependent  on  cirrhosis  of  the  liver.  One  of  them  is  taken  from 
Laennec's  famous  memoir,  in  which  the  lesions  of  atrophic  cirrhosis  were 
first  described.  A  patient  with  atrophic  cirrhosis  had  also  haemorrhagic 
pleurisy  on  the  left  side.  Laennec,  however,  did  not  say  that  the  pleurisy 
resulted  from  the  cirrhosis ;  I  am  more  inclined  to  believe  that  the  pleurisy 
was  tubercular  in  nature,  for  at  the  autopsy  "  the  deep  layer  of  the  pleura 
contained  innumerable  greyish  tubercles."  The  other  case  which  has  also 
been  considered  as  dependent  on  cirrhosis  of  the  liver  may,  I  think,  have 
been  due  to  independent  lesions  of  the  pleura  ;  for  if  we  look  up  the  details  of 
the  autopsy  we  shall  agree  that  it  is  difficult  to  admit  atrophic  cirrhosis  in  a 
liver  of  "  normal  size,  which  showed  remarkable  friability,  and  broke  up  on 
pressure  with  the  finger  into  a  pulp." 

I  do  not  deny,  of  course,  the  haemorrhagic  form  of  pleurisy  in  the  course 
of  hepatic  cirrhosis,  for  I  have  seen  several  cases ;  but  I  think  that  it  is  rare  as 
opposed  to  the  sero-fibrinous  form,  which  is  fairly  common. 

I  also  regard  haemorrhagic  pleurisy  associated  with  Bright's  disease  as 
exceptional,  though  Bright's  disease  predisposes  on  the  one  hand  to  effusion, 
and  on  the  other  to  haemorrhage. 


DISEASES  OF  THE  PLEURA  287 

In  pleuro-pulmonary  inflammations  of  infectious  origin  (influenzal 
pleuro-pneumonia,  typhoid  fever),  the  fluid  is  sometimes  hsemorrhagic. 

In  the  hsemorrhagic  forms  of  the  eruptive  fevers  haemorrhagic  effusion  is 
sometimes  met  with,  but  it  is  here  a  case  of  haemorrhage  into  the  pleura 
rather  than  that  of  an  inflammatory  condition,  properly  speaking. 

Haemorrhagic  effusion  may  also  result  from  opening  of  an  aortic 
aneurysm,  or  from  the  rupture  of  an  atheromatous  aorta.  Several  cases 
have  been  published  ;  the  following  case  is  given  by  Ribail : 

A  man,  thirty-five  years  of  age,  suffering  from  palpitation,  breathlessness,  and 
angina  pectoris,  came  into  the  Beaujon  Hospital,  under  Gombault.  The  diagnosis  of 
aortic  aneurysm,  with  aortic  insufficiency,  was  made.  A  month  later  the  patient  felt  a 
sharp  pain  on  the  left  side.  Pleural  effusion  was  recognized,  and  punctures  gave 
issue  to  12  ounces  of  bloody  fluid  on  the  first,  16  ounces  on  the  second  and  third  occa- 
sions. The  patient  died  suddenly  from  angina  pectoris.  Post  mortem,  the  left  pleura 
was  found  covered  by  a  clot,  which  was  continuous  with  the  clot  in  an  aortic  aneurysm. 

Second  Group. 

Description. — This  group  includes  haemorrhagic  pleurisies  of  tuber- 
cular nature.  I  shall  divide  them  into  three  varieties.  The  first  variety 
is  associated  with  acute  granular  tuberculosis,  or  with  acute  tubercular 
broncho-pneumonia.  The  lesions  in  the  pleura  and  in  the  lung  appear 
together  ;  the  general  symptoms  are  usually  very  marked  :  fever  is  acute, 
temperature  is  very  high,  dyspnoea  is  severe  and  continuous,  or  sometimes 
paroxysmal.  The  estimation  of  the  quantity  of  fluid  is  very  difficult,  because 
the  signs  of  pleurisy  are  distorted  by  the  subjacent  lesions  in  the  lung. 

The  dyspnoea  is  sometimes  so  violent  and  the  quantity  of  fluid  appears 
so  large  that  thoracentesis  is  performed  ;  1  or  2  pints  of  haemorrhagic  fluid 
are  withdrawn,  but  practically  no  relief  follows,  because  the  dyspnoea,  like 
all  the  other  symptoms,  is  due  rather  to  the  lung  trouble  than  to  the  effusion. 

The  effusion,  however,  either  from  its  early  appearance  or  its  abundance, 
sometimes  appears  to  be  the  chief  lesion.  The  patient  experiences  some  relief 
after  the  evacuation  of  the  fluid,  and  may  even  ask  for  a  second  or  a  third 
operation;  but  the  severity  of  the  general  symptoms,  the  elevation  of 
the  temperature,  the  persistent  or  rapid  reappearance  of  dyspnoea  after 
evacuation  of  the  fluid,  the  wasting  and  the  signs  found  on  auscultation, 
prove  that  the  effusion  is  associated  with  acute  tuberculosis  of  the  lung  and 
pleura.  The  sputum  must  be  examined  for  bacilli.  The  prognosis  is  nearly 
always  fatal  in  these  forms. 

In  the  second  variety  haemorrhagic  pleurisy  is  associated  with  tlio 
ordinary  chronic  forms  of  plitliisis,  and  I  am  surprised  tliat  Moutard-Martin 
has  stated  that  it  never  coexists  with  chronic  tuberculosis.  I  have  collected 
several  cases  which,  on  the  contrary,  prove  that  the  chronic  as  well  as  the 
acute  forms  of  tuberculosis  may  cause  haemorrhagic  pleurisy. 


288  TEXT-BOOK  OF  MEDICINE 

The  pathogenic  diagnosis  is  very  simple.  The  patient  presents  both  the 
symptoms  of  pulmonary  tuberculosis  and  of  pleurisy.  Fever,  pain,  and 
dyspncBa  may  be  absent ;  the  mischief  may  end  after  one  or  more  punctures, 
because  it  has  been  only  an  incident  in  the  course  of  the  tuberculosis,  just  as 
sero-fibrmous  pleurisy  may  be. 

In  the  third  variety — and  I  draw  special  attention  to  this  point — pleurisy 
appears  as  the  initial  symptom  of  tuberculosis.  It  is  the  result  of  primary 
tuberculosis  of  the  pleura.  Tuberculosis  may  commence  in  the  pleura,  just 
as  it  may  in  the  synovial  membrane,  testis,  prostate,  eye,  skin,  pericardium, 
etc.  ;  remain  localized  for  a  lengthy  period,  and  recover  without  becoming 
general. 

As  we  have  seen  in  the  section  on  sero-fibrinous  pleurisy,  it  often 
happens  that  pleurisy  is  met  with  m  an  individual  who  recovers,  but  shows 
signs  of  pulmonary  tuberculosis  some  months  or  years  later.  In  this  case 
pleurisy,  though  simple  in  appearance,  was  only  the  result  of  tuberculosis, 
which  showed  itself  by  effusion,  and  then  became  generalized  throughout  the 
Imig. 

Hsemorrhagic  pleurisy,  therefore,  may  result  from  local  or  from  initial 
tuberculosis  of  the  pleura ;  and  just  as  persons  have  haemoptysis  long 
before  other  signs  of  tuberculosis,  so  others  have  hsemorrhagic  pleurisy  as 
the  first  symptom,  and,  if  I  may  use  the  expression,  these  people  "  reject 
their  hsemoptysis  into  their  pleura."  These  cases  may  present  all  the  signs 
of  sero-fibrinous  pleurisy,  and  the  haemorrhagic  nature  of  the  fluid  is  only 
recognized  on  puncture  ;  thoracentesis  is  performed  once,  twice,  three,  or 
four  times,  the  fluid  is  drawn  off,  the  pleurisy  cured,  and  the  case  thought 
to  be  one  of  simple  hsematoma  of  the  pleura  ;  but  yet  signs  of  pulmonary 
tuberculosis  appear  a  few  months  later,  and  show  the  error  in  diagnosis. 

These  considerations  show  that  the  pathogenic  diagnosis  of  this  variety 
may  be  fairly  easy  or  very  difficult.  It  is  easy  if  the  patient  has  signs  of 
acute  or  of  chronic  pulmonary  tuberculosis  ;  if  the  pleurisy  arises  during 
apparently  good  health,  the  diagnosis  cannot  be  settled  either  by  the  quality 
or  by  the  quantity  of  the  fluid,  or  by  the  course  of  the  pleurisy,  which  may 
be  acute,  subacute,  or  latent.  In  such  a  case  the  various  methods  of  labora- 
tory research  given  above  must  be  employed. 

In  a  patient  under  my  care  for  diabetes  and  haemorrhagic  pleurisy,  the 
lymphocytosis  demonstrated  the  tubercular  nature  of  the  pleurisy. 

This  form  of  pleurisy,  when  accompanied  by  fever,  becomes  much  more 
serious,  and  the  gravity  arises  from  the  lesions  in  the  lung.  Nevertheless, 
the  condition  may  recover  perfectly  after  one  or  several  punctures.  Ii 
have  pubhshed  cases,  and  Lereboullet  has  quoted  others.  The  patient  is] 
sometimes  definitely  cured,  in  which  case  it  is  probable  that  the  haemorrhagicj 
pleurisy  was  the  result  of  local  tuberculosis  of  the  pleura  ;  at  other  times 


DISEASES  OF  THE  PLEURA  289 

the  patient,  after  recovering  from  pleurisy,  subsequently  develops  tuber- 
culosis in  the  lung. 

Pathological  Anatomy. — The  lesions  show  some  peculiarities.  Some- 
times the  lesion  is  found  at  the  same  time  in  the  lung,  in  the  pleura,  beneath 
the  pleura,  or  in  the  false  membranes  ;  at  other  times  it  is  limited  to  the 
pleura  or  the  false  membranes.  The  walls  of  the  vessels  show  coagulation 
necrosis,  and  Kelsch  thinks  that  the  haemorrhage  is  due  to  this  change. 
Numerous  vessels  are  obstructed  by  hyaline  thrombi ;  the  vessel  walls  are 
no  longer  distinct,  and  are  surrounded  by  fibroid  networks. 

The  newly-formed  membranes  are  generally  stratified  and  rich  in  vessels, 
friable  if  yomig,  thick  and  firm  if  old.  These  membranes  are  composed  of 
granulation  tissue,  and  of  deeper  layers  that  are  made  up  of  lymphatic  cells, 
connective  bundles,  and  fibrous  tissue  (Malassez). 

Third  Group. 

Description. — Pleurisy  in  the  course  of  pleuro-pulmonary  cancer  is 
not  always  hsemorrhagic  ;  the  fluid  is  sero-fibrinous  in  at  least  one-tliird  of 
the  cases,  and  this  fact  must  carefully  be  borne  in  mind,  for  it  would  be 
wrong  to  reject  the  hypothesis  of  cancer  because  the  effusion  was  sero- 
fibrinous. The  haemorrhagic  form  alone,  however,  must  now  occupy  our 
attention.  Haemorrhagic  pleurisy  in  cancer  may  arise  quite  suddenly,  like 
acute  pleurisy,  or  have  an  insidious  onset,  so  that  the  patient  finds  some 
difficulty  in  fixing  the  date.  These  different  varieties  are  found,  moreover, 
in  sero-fibrinous,  haemorrhagic,  purulent,  tubercular,  or  cancerous  pleurisy. 

From  the  clinical  point  of  view  I  shall  divide  haemorrhagic  pleurisy  in 
cancer  into  two  varieties. 

In  the  first  variety,  pleurisy  appears  in  an  individual  who  has  obvious 
cancer.  We  find  in  one  patient  cancer  of  the  stomach,  oesophagus,  intes- 
tines, rectum,  omentum,  liver,  kidney,  bladder,  prostate,  testis,  eye,  skin, 
or  of  one  of  the  vertebrae  ;  in  another  patient  we  see  cancer  of  the  uterus  or 
of  the  breast.  Cough,  thoracic  pain,  continuous  or  paroxysmal  dyspnoea 
and  currant- jelly  expectoration,  appear  during  the  course  of  these  cancers. 
Pleural  effusion  is  then  discovered,  and  thoracentesis  gives  vent  to  haemor- 
rhagic fluid.  In  such  a  case  the  pathogenic  diagnosis  is  clear — viz.,  secondary 
cancer  of  the  lung  and  of  the  pleura  ;  and  it  may  be  stated  that  the  hajmor- 
rliagic  pleurisy  is  of  cancerous  origin. 

In  some  cases  we  do  not  witness  the  evolution  of  tlie  cancerous  lesions, 
but  the  patient  shows  traces  of  a  more  or  less  recent  scar,  resulting  from  an 
operation  for  epithelioma  of  the  nose  or  of  tlie  lip,  for  cancer  of  the  breast 
or  of  the  testis,  or  for  osteo-sarcoma.  Pleurisy  then  aj)pears  and  thora- 
centesis yields  haemorrhagic  fluid.  The  lung  and  the  pleura  have  evidently 
been  attacked  by  secondary  cancer. 

19 


290  TEXT-BOOK  OF  MEDICINE    . 

The  pathogenic  diagnosis,  however,  is  not  always  so  simple.  In  the 
cases  wliich  constitute  the  second  variety,  hsemorrhagic  pleurisy  is  not 
preceded  by  otherwise  appreciable  cancerous  lesions.  Primary  cancer  may 
afEect  the  pleura  and  only  give  rise  to  symptoms  of  pleurisy,  which  may  be 
acute  or  insidious  in  its  onset.     The  pathogenic  diagnosis  is  sometimes 

difficult. 

If  hemorrhagic  pleurisy,  consecutive  to  mediastino-pulmonary  cancer, 
were  always  accompanied  by  special  symptoms,  such  as  dysphagia,  aphonia, 
oedema  of  the  arm  or  of  the  face,  and  well-marked  collateral  circulation,  which 
are  so  common  in  tumours  of  the  mediastinum,  and  if  the  patient  suffering 
from  pleurisy  showed  supraclavicular  glands,  currant- jelly  expectoration,  and 
violent  attacks  of  dyspnoea,  which  are  seen  in  cancer  of  the  lung,  the  patho- 
genic diagnosis  of  the  pleurisy  would  be  signally  simphfied ;  there  are 
cases  in  which  nothing  leads  us  to  suppose  the  existence  of  cancer  of  the 
mediastinum  or  of  the  lung.  There  are  also  cases  in  which  cancer  of  the 
pleura  is  primary,  or  associated  with  early  cancer  of  the  lung,  which  may 
pass  unnoticed  ;  the  pleural  effusion  is  then  the  chief  feature,  and  we  find 
hsemorrhagic  pleurisy  which  presents  much  difficulty  as  to  its  origin. 

The  following  signs  and  symptoms  helped  me  to  make  a  diagnosis  in  a 
case  of  hemorrhagic  pleurisy,  consecutive  to  primary  cancer  of  the  lung,  in 
a  man  twenty-two  years  old  : 

Pain  constitutes  an  important  symptom;  it  is  frequent,  sometimes 
sharp,  persistent,  unhke  the  "  stitch  in  the  side  "  of  common  pleurisy.  It 
may  be  worse  at  the  base  of  the  thorax,  and  radiate  to  the  shoulder,  the 
arms,  and  the  wrists,  so  that  patients  beheve  themselves  to  be  suffering 
from  rheumatism.  Acuteness  and  radiation  of  the  pain  are  fairly  frequent 
symptoms  in  pleuro-pulmonary  cancer.  Neuralgia  of  the  brachial  plexus 
was  the  cliief  symptom  in  one  of  Behier's  cases.  One  of  Lancereaux's 
patients  complained  of  "  a  sharp  pain  in  the  left  side  of  the  neck,  and  in  the 
shoulder  on  the  same  side,"  and  later  swelhng  of  the  joints  of  the  left  arm 
supervened.  In  several  of  my  cases  I  have  noted  pains  in  the  joints,  so 
that  I  have  asked  myself  whether  pseudo-rheumatism  may  not  be  one  of 
the  manifestations  of  cancer.  These  pains  are  not  found  in  hemorrhagic 
tubercular  pleurisy. 

Dyspnoea  is  one  of  the  usual  symptoms  of  cancerous  pleurisy.  It  may 
be  continual  or  paroxysmal,  and  is  relieved  by  thoracentesis,  but  the  relief 
is  only  of  short  duration.  This  dyspnoea  is  found  in  most  of  the  cases  of 
cancerous  pleurisy,  and  I  have  seen  it  cause  terrible  agony  on  three  occa- 
sions ;  it  depends  chiefly  upon  the  cancerous  lesions  in  the  mediastinum 
and  the  lung.  Similar  dyspnoea  is  not  found  in  chronic  tubercular  hsemorj 
rhagic  pleurisy.  Some  cases  of  hemorrhagic  pleurisy,  associated  witr 
acute  tuberculosis  of  the  lung  and  of  the  pleura,  may  be  accompanied  bj 


DISEASES  OF  THE  PLEURA  291 

acute  dyspnoea ;  in  these  cases,  however,  the  fever  is  liigh ;  this  does  not 
happen  in  cancerous  pleurisy. 

Permanent  displacement  of  the  heart  is  seen  in  left  cancerous  pleurisy, 
at  first  on  account  of  the  fluid,  and  later  because  the  growth  in  the  pleura 
and  the  lung  may  help  to  cause  deviation.  Further,  the  heart  sounds  are 
heard  all  over  the  chest,  as  though  they  were  transmitted  to  the  ear  by 
soUd  lung,  which  is  a  good  conductor  of  sound. 

Acceleration  of  the  pulse  has  often  been  observed,  and  the  pulse-rate 
may  be  100  or  120,  although  fever  is  absent.  It  may  be  asked  whether 
this  acceleration  is  not  due  to  the  pressure  of  the  growth  on  the  pnsumo- 
gastnc  nerve.  In  one  of  my  patients  who  had  continuous  tachycardia  I 
found  a  cancerous  nodule  of  the  size  of  a  hemp-seed  in  the  interventricular 
septum  of  the  heart. 

The  nature  of  the  fluid  drawn  off  by  thoracentesis  may  furnish  evidence 
in  favour  of  cancer.  The  fluid  is  often  brownish  or  blackish,  blood  forming 
a  tenth  or  a  twelfth  part.  The  fluid  contains  very  httle  fibrin,  in  contra- 
distinction to  the  effusion  in  tubercular  pleurisy,  which  usually  contains  a 
large  amount.  In  some  cases  (Fraenkel,  Quincke)  agglomerated  or  isolated 
polymorphous  epithehal  cells,  with  a  large  nucleus  and  vacuoles,  have  been 
found  in  the  fluid. 

Nattan-Larrier  has  studied  the  cases  of  cancerous  pleurisy  in  my  wards, 
and  has  worked  out  their  cytological  formula.  In  addition  to  red  corpuscles, 
two  different  types  of  cells  may  be  met  with  :  (1)  Masses  of  cells  which  are 
large,  thick,  and  have  polycyclical  outHnes ;  masses  of  cells,  disposed  in 
layers,  of  variable  size  and  indefinite  outlines,  protoplasm  refracting  and 
vacuolated ;  irregular  nuclei,  which  stain  unequally.  (2)  Isolated  cancer 
cells,  which  are  easily  recognized  by  their  inequality  in  size,  by  the  fact  that 
they  are  larger  than  the  leucocytes  or  the  endothehal  cells,  by  their  ovoid 
or  irregular  shape,  by  their  clear  outUne,  by  their  refracting  protoplasm, 
which  is  studded  with  basophile  granules  and  clear  vacuoles,  and  by  their 
multiple  nuclei,  which  are  irregularly  placed  and  stain  imequally.  I  have 
noticed  the  existence  of  polynuclear  cells  in  cancerous  pleurisy  with  much 
effusion.  Eosinophile  polynuclear  cells  are  never  met  with  in  the  fluid  from 
these  cases  of  hsemorrhagic  pleurisy. 

Bard  has  laid  stress  on  the  characters  of  the  serum  after  centrifugaliza- 
tion.  The  serum  is  said  to  remain  coloured  with  hajmoglobin  in  cancerous 
pleurisy,  while  it  is  colourless  in  other  hajmorrhagic  affusions.  This  hajmo- 
lytic  action,  which  is  easily  recognized  with  the  naked  eye,  is  made  certain 
by  the  addition  of  tincture  of  guaiacum  and  turpentine  (blue  coloration 
of  the  laky  serum  by  this  reaction).  These  findings  have  been  confirmed 
by  all  authorities. 

In  some  cases  the  pleuritic  fluid  is  composed  of  nearly   pure   bloud. 

"  19-2 


292  TEXT-BOOK  OF  MEDICINE 

Thoracentesis  is  performed,  and  fluid  which  has  the  aspect  of  arterial  or 
of  venous  blood  is  drawn  off.  In  one  of  my  patients  puncture  gave  exit  to 
a  fluid  having  the  appearance  of  arterial  blood,  and  caused  me  at  first  sight 
to  think  that  it  might  be  a  case  of  intrapleural  hgematoma,  due  to  rupture 
of  an  atheromatous  or  a  dilated  aorta.  Lymphosarcoma,  colloid  cancer, 
epithelioma,  and  endothelial  carcinoma,  may  cause  such  intrapleural 
haemorrhages.     The  blood  does  not  clot,  but  remains  fluid. 

The  rapid  and  persistent  reproduction  of  haemorrhagic  fluid  after 
thoracentesis  is  common  to  tuberculosis  and  to  cancer  ;  it  is,  however,  much 
more  marked  in  the  case  of  cancer.  Thus,  in  one  of  my  cases  thoracentesis 
was  performed  thirty-three  times  in  five  months,  and  44  pints  of  haemor- 
rhagic fluid  withdrawn.  In  one  of  Desnos'  cases  thoracentesis  was  per- 
formed thirty  times  in  six  months,  in  a  woman  with  cancer  of  the  pleura, 
and  80  pints  of  haemorrhagic  fluid  were  withdrawn.  I  have,  however,  seen 
cases  in  which  the  fluid  of  pleuro-pulmonary  cancer  may  dry  up  after  a  few 
punctures  ;  and,  on  the  other  hand,  I  have  seen  cases  of  tubercular  haemor- 
rhagic pleurisy  in  which  the  fluid  formed  with  such  obstinacy  that  six,  ten, 
and  fifteen  punctures  were  necessary.  It  would,  therefore,  be  wrong  to 
base  an  absolute  opinion  upon  the  drying  up,  or  upon  the  obstinacy  of  the 
haemorrhagic  fluid,  in  order  to  banish  the  idea  of  cancer. 

The  youth  of  the  patient  is  no  argument  agaujst  the  hypothesis  of  can- 
cerous pleurisy,  for  this  lesion  has  been  found  in  patients  who  were  only 
eighteen  years,  twenty-four  years,  twenty-three  years,  twenty-two  years, 
and  ten  years  of  age  respectively.  One  of  my  patients  was  only  twenty- two 
years  of  age. 

Fourth  Group. 

Description.— Under  the  term  "  pleural  haematoma  "  we  must  include 
cases  of  haemorrhagic  pleurisy,  which  are  not  due  to  tuberculosis  or  to 
cancer.  The  anatomical  process  is  in  some  points  comparable  to  chronic 
hydrocele  and  to  pachymeningitis  ;  the  condition  is  a  haemorrhagic  pachy- 
pleuritis. 

In  some  cases  the  haematoma,  according  to  Wintrich,  is  said  to  be  genuine 
pleurisy,  in  which  the  intensity  of  the  initial  inflammation  determines 
haemorrhage  into  the  pleura.  A  typical  case  of  simple  haematoma  may 
be  thus  described  :  A  patient  has  haemorrhagic  pleurisy.  The  symptoms 
sometimes  resemble  those  of  simple  pleurisy,  but  at  other  times  the  appear- 
ance of  the  patient  and  the  general  symptoms  may  lead  us  to  fear  tuber- 
culosis or  cancer  of  the  jjleura.  Thoracentesis  is  performed,  and  haemorrhagic 
fluid  drawn  off.  In  simple  haematoma  the  liquid  is  fibrinous,  and  the  ten 
dency  to  reaccumulation  is  shght.  The  condition  sometimes  yields  to  a  single 
puncture,  and  we  are  rarely  obUged  to  aspirate  more  than  two  or  three 


DISEASES  OF  THE  PLEURA  293 

times.  The  relief  is  notable,  and  the  general  condition  shows  progressive 
improvement. 

The  diagnosis  of  simple  haematoma  must  not  be  hastily  made,  even  though 
the  conditions  have  yielded  to  thoracentesis.  In  some  cases,  as  I  have 
already  said,  hsemorrhagic  pleurisy  is  the  only  indication  of  local  or  primary 
tuberculosis  of  the  pleura.  Hsemorrhagic  pleurisy  may  recover  after 
thoracentesis,  when  a  favourable  prognosis  holds  good ;  on  the  other  hand, 
a  pleural  hematoma  is  thought  to  have  been  cured,  and  the  error  is 
recognized  some  months  later,  when  undoubted  signs  of  tuberculosis  appear. 

The  more  I  see,  the  more  I  believe  in  the  rarity  of  pleural  haematoma  ; 
the  condition  is  nearly  always  tubercular.  In  my  wards  at  the  Necker 
Hospital  I  had  a  patient  with  every  sign  of  pleural  hsematoma.  The  fluid, 
which  dried  up  after  a  single  puncture,  did  not  cause  inoculation  tuber- 
culosis in  guinea-pigs.  The  patient,  who  had  never  had  any  sign  of 
pulmonary  tuberculosis,  left  the  hospital  in  good  health.  If  I  had  lost  sight 
of  him,  I  should  have  thought  that  it  was  a  case  of  simple  haematoma,  but 
he  came  back  to  me  a  year  later  with  pulmonary  tuberculosis.  The  ao-called 
pleural  haematoma  was  therefore  haemorrhagic  tul^ercular  pleurisy. 

Treatment  of  Haemorrhagic  Pleurisies. 

The  treatment  is  very  simple.  Revulsives,  bhsters,  and  other  medical 
means,  such  as  diuretics  and  purgatives,  etc.,  give  here  no  more  benefit 
than  they  do  in  sero-fibrinous  pleurisy. 

What  line  of  treatment  must  be  adopted  in  a  case  of  haemorrhagic 
pleurisy  ?  One  treatment  alone  is  rational — viz.,  aspiration  of  the  fluid. 
Pleurotomy,  customary  in  empyema,  should  not  be  employed  in  these 
cases. 

The  rules  for  aspiration  laid  down  under  simple  pleurisy  are  in  every 
way  applicable  to  haemorrhagic  effusions.  The  pleura  is  punctured  with  a 
No.  2  or  No.  3  needle,  care  being  taken  never  to  withdraw  more  than  2  pints 
of  fluid  at  one  sitting.  In  this  way  we  can  avoid  fits  of  coughing,  attacks 
of  dyspnoea,  intrathoracic  pain,  and  other  much  more  serious  troubles  which 
sf)metinies  ac(;ompa?iy  thoracentesis  when  too  large  a  quantity  of  fluid  has 
wrongly  been  withdrawn  at  one  sitting.  As  I  have  discussed  the  important 
question  of  thoracentesis  fully,  further  notice  is  needless.  The  evacuation 
of  2  pints  of  fluid  at  a  sitting,  which  represents  the  maximum  amount  in 
simple  pleurisy,  is  usually  too  high  in  the  haoniorrhagic  variety.  After 
evacuation  of  20  to  30  ounces,  the  patient  often  experiences  dragging  pains, 
and  I  have  been  several  times  obliged  to  stop  the  flow  after  10  or  15  ounces. 

The  patient  rarely  experiences  the  marked  relief  which  follows  the 
evacuation  of  the  fluid  in  simple  pleurisy.  This  fact  depends  much  on  the 
condition  of  the  pleura  and  of  the  lung,  as  well  as  of  their  respective  lesions. 


294  TEXT-BOOK  OF  MEDICINE 

I  have  always  seen  that  the  relief  is  more  marked  in  cases  of  tuberculosis 
than  of  cancer. 

When  the  fluid  reaccumulates  rapidly,  we  are  obliged  to  perform  thora- 
centesis repeatedly,  and  the  patient  finally  clamours  for  it,  because  the 
operation  gives  momentary  relief  to  his  distress. 

I  recently  treated  a  lady  who  had  been  sent  to  me  from  Lisbon.  She 
begged  me  to  perform  thoracentesis  every  four  or  five  days.  I  succeeded 
in  lessening  her  terrible  dyspnoea  by  means  of  repeated  punctures  and 
injections  of  morphia.  Thoracentesis  is  only  to  be  performed  when  there 
is  necessity,  and  only  the  surplus  in  the  pleura  should  be  drawn  off.  As 
the  fluid  is  sometimes  very  rich  in  blood  cells,  thoracentesis  is  a  form  of 
bleeding,  and  repeated  punctures  cause  weakness. 

In  certain  cases  of  hsemorrhagic  pleurisy  the  fluid  yields  after  one,  two, 
or  three  punctures  ;  this  happens  in  simple  haematoma  of  the  pleura,  and  in 
some  cases  of  tubercular  pleurisy.  In  cancerous  pleurisy  the  fluid  is  repro- 
duced with  more  obstinacy.  In  some  malignant  cases,  however,  we  succeed 
in  drying  up  the  fluid.  All  hsemorrhagic  pleurisies  may,  then,  be  curable. 
The  tuberculosis  is  but  little  curable,  the  cancer  is  incurable.  Under 
some  circumstances  the  fluid  which  contained  much  blood  at  the  first 
puncture  contains  less  in  the  following  ones ;  it  loses  its  tint  and  becomes 
serous.  These  changes  are  seen  both  in  tuberculosis  and  in  cancer,  as  I 
have  reported.  These  very  important  facts  show  us  that  it  would  be  wrong 
to  take  the  drying  up  or  the  decoloration  of  a  hsemorrhagic  fluid  as  the 
basis  of  a  favourable  or  of  an  unfavourable  prognosis  as  to  the  cause  of  the 
haemorrhage.  The  evolution  of  hsemorrhagic  fluids  in  the  pleura  gives  us 
imperfect  information  as  to  the  cause  and  the  nature  of  the  lesion  which 
produces  the  haemorrhage. 

Hsemorrhagic  pleurisies  only  become  purulent  (a  change  which  is  very 
rare)  if  organisms  of  suppuration  produce  secondary  infection.  In  the 
contrary  case,  whatever  be  the  number  of  the  punctures,  the  fluid  does  not 
become  purulent,  either  in  simple  hsematoma  or  in  tubercular  and  cancerous 
pleurisy. 

I  have  performed  more  than  thirty  punctures  on  the  same  patient,  but 
the  hsemorrhagic  fluid  did  not  become  purulent. 

Thoracentesis  is  the  only  means  available  in  cancerous  pleurisy.  The 
dyspnoea  is  commonly  so  acute  that  we  are  obUged  to  give  several  injections 
of  morphia  daily. 

The  commonplace  treatment  by  tonics  and  constitutional  remedies,  such 
as  arsenic,  lecithin,  and  preparations  of  coca  and  kola  remains. 


DISEASES  OF  THE  PLEURA  295 


IV.  TRAUMATIC  HiEMOTHORAX. 

Traumatic  haemothorax  demands  the  physician's  attention,  and  therefore 
deserves  notice  in  a  text-book  of  medicine.* 

Resume  of  a  Case. — On  September  24,  1906,  man,  aged  twenty-two,  admitted  to 
the  Hotel -Dieu,  under  De  Deuke,  for  a  stab  in  the  back.  Pain  in  chest  and  dyspnoea 
were  severe  two  days  later  ;  he  was  therefore  transferred  to  my  care.  The  woimd, 
which  had  healed  over,  was  in  the  fifth  left  intercostal  space,  about  an  inch  from  the 
spine.  Inspection  showed  slight  bulging,  ynth  absence  of  vibrations,  and  dullness  at 
the  left  base.     Traube's  space  was  resonant. 

Soft  tubular  breathing  on  expiration,  aegophony,  and  pectoriloquy  pointed  to 
pleural  effusion.  No  signs  of  pneumothorax.  Heart  not  displaced  ;  cough  frequent ; 
dyspnoea  somewhat  marked  ;  temperature  103°  F.  (this  fact  attracted  my  notice).  No 
haemoptysis  ;  no  blood-stained  sputum.     Diagnosis  :  traumatic  hasmothorax. 

Exploration  in  order  to  examine  the  fluid,  and  also  to  see  if  the  pleura  were  infected  . 
20  c.c.  of  fluid,  almost  as  red  as  pure  blood,  withdra^Ti. 

During  the  first  week  in  October  the  only  change  was  an  increase  in  the  amount  of 
effusion,  and  during  the  next  week  it  was  clearly  abundant.  The  dullness  now  extended 
higher,  vocal  fremitus  was  absent  over  the  lower  two-thirds  of  the  chest,  and  the  heart 
was  displaced  to  the  right.  The  increase  in  the  effusion  was  not  due  to  blood,  but 
resulted  from  serofibrinous  pleurisy,  as  proved  by  punctures.  On  October  18  the 
fluid  had  lost  its  former  red  tint.  Friction  sounds  above  the  effusion  proved  pleurisy 
following  hfemothorax. 

On  November  1  the  fluid  had  partially  absorbed  ;  friction  sounds  wore  present  in 
the  axillary  region.  The  fluid,  on  puncture,  was  pale  yellow  and  fibrinous.  Patient's 
appetite  was  good,  his  general  condition  excellent,  and  he  left  for  Vinconnes  on 
November  11. 

He  came  back  a  week  later  for  slight  dyspnoea.  There  was  a  good  deal  of  fluid, 
and  on  puncture  200  c.c.  of  sero-fibrinous  liquid  were  drawn  off.  A  fortnight  later  he 
went  out  well. 

The  nature  of  the  fluid  withdrawn  at  the  different  punctures  was  determined  in  my 
laboratory.  As  aerobic  and  anaerobic  cultures  on  solid  and  fluid  media  showed  tho 
absolute  sterility  of  the  Hquid,  the  fever  clearly  did  not  depend  on  infection  of  the  pleura. 
At  the  first  puncture  (September  27)  the  fluid,  which  was  almost  blood-red,  contained 
2,100,000  red  and  4,000  white  corpuscles.  The  fluid  was  put  in  a  tube ;  twenty-four 
hours  later  we  found  a  red  sediment,  containing  blood  cells,  and  amounting  to  a  fifth 
of  the  contents  of  the  tube.  The  supernatant  fluid  was  not  laky,  but  pale  yellow  ;  it 
was  not  fibrinous,  and  showed  no  trace  of  coagulation.  No  clot  had  formed  in  this 
tube  on  December  10.  We  were  surprised  that  tho  sediment  formed  one-fifth  and  tho 
serum  four-fifths.  Did  this  excess  of  serum  come  from  clots  in  the  pleura  ?  If  this 
were  so,  some  of  the  blood  effused  must  have  clotttid. 

Puncture,  October  18  :  the  fluid  was  quite  different.  It  was  no  longer  red,  and  its 
rosy  tint  showed  how  quickly  the  red  cells  had  been  absorbed.  The  proportion  of 
red  to  white  cells  was  only  35,000  to  0,200. 


Eosinophiles 

Lymphocytes 

Macrophages 

Colls  from  tho  pleura 

Nucleated  red  corpuscles  :  1  or  2< 


Per  Cout. 
.      35 
.     35 
,     20 
,      10 


*  TiiewMoy,  Clinique  Medicale  de  V Hotel-Dieu,  llUKi.  I  !">«  et  12"'"  l<'(M)n. 


296  TEXT-BOOK  OF  MEDICINE 

The  deposit,  on  standing,  was  not  red,  but  of  a  rose  colour,  and  its  amount  about 
one-thirtieth  of  the  total  contents.     Flakes  of  fibrin  were  floating  in  the  yellow  fluid. 

On  November  11  the  fluid  resembled  that  of  an  ordinary  pleurisy,  and  contained 
13,000  red  to  8,500  white  corpuscles.  It  was  practically  a  "  histologically  hsemor- 
rhagic  "  pleurisy.  No  deposit  appeared  on  standing  ;  a  thin  layer  of  sediment,  with  a 
rosy  tint,  appeared  only  after  centrifugalization.-  The  fluid  was  sero -fibrinous,  and 
clotted  in  the  tube. 

Blood-counts  showed  : 

Red  Corpuscles.  White  Corpuscles. 

November  1      ..  ..     3,200,000  ..  5,000 

November  11     ..  ..     3,840,000  ..  4,400 

November  22     ..  ..     4,200,000  ..  6,000 

The  eosinophiles  amounted  to  10  per  cent. 

Pathological  Physiology. — Does  the  blood  effused  in  hsemothorax 
remain  fluid,  or  does  it  form  clots  ?  Trousseau  and  Leblanc,  from  experi- 
ments on  the  horse,  have  shown  that  clotting  occurs  if  blood  be  allowed  to 
flow  into  the  pleura  after  section  of  an  intercostal  artery.  Trousseau  hence 
concluded  that  similar  coagulation  might  take  place  in  haemothorax  in  man. 

This  view  has  recently  been  opposed  by  Tuffier  and  MiUan,  who  state 
"  the  bloody  effusion  in  the  pleura  does  not  clot  in  cases  of  traumatic 
hsemothorax."  We  can  decide  the  point  by  consulting  the  pubUshed  cases 
of  traumatic  haemothorax  (C.  de  Gery). 

Case  1. — Very  severe  haemothorax  on  the  left  side.  -  Six  pints  of  bright  blood 
drawn  off.  Later,  4  pints  of  blood,  "  mixed  with  clots,  which  at  times  stopped  the 
flow,"  drawn  off  by  thoracentesis. 

Case  2. — Young  woman  wounded  by  a  revolver  bullet.  Hsemothorax  formed 
quickly  ;  repeated  haemoptysis  occurred  ;  weakness  was  extreme,  and  syncope  im- 
minent. Two  inches  of  the  eleventh  rib  resected.  Blood  gushed  out,  and  blackish 
clots,  as  large  as  oranges,  were  expelled  on  expiration. 

Cases  3  and  4. — Haemothorax,    Resection  of  ribs  ;  fluid  blood  and  clots  removed. 

These  quotations  prove  that  Trousseau  was  right.  The  blood  may  clot  in 
the  pleura,  just  as  it  does  in  the  peritoneum,  the  pericardium,  the  meninges, 
and  the  joints.  This  fact  has  an  important  practical  apphcation  ;  the  clot 
may  plug  the  wound  in  the  lung.  The  results  of  Trousseau's  experiments 
may  be  stated  as  follows  : 

Haemothorax  was  produced  by  making  a  penetrating  wound  of  the  lung 
in  a  horse.  The  animal  was  killed,  and  the  wound  in  the  lung  examined. 
"  A  clot  of  fibrin  filled  up  the  wound  in  the  lung  like  a  sword  in  its  scabbard." 
This  protecting  clot  sometimes  formed  half  an  hour  after  the  injury,  and  on 
attempting  to  draw  the  clot  out  it  was  necessary  to  break  it,  because  it  was 
embedded  in  the  interlobular  cellular  tissue  by  numberless  fibrinous  radicles^ 
which  broke  on  traction. 

If  the  post-mortem  was  not  performed  till  forty-eight  or  seventy- 
two  hours  after  the  injury,  the  wound  was  closed  by  a  remarkable 
process. 


DISEASES  OF  THE  PLEURA  297 

The  woimd  in  the  hmg  was  inflamed,  and  the  pleura  itself  was  also 
affected  to  a  variable  extent.  A  plastic  exudate  was  adherent  to  the  serous 
membrane,  and  blended  with  the  fibrinous  nucleus  of  the  wound,  intimately- 
adhering  to  it.  The  whole  track  of  the  injury  was  thus  obhterated  by 
fibrinous  clot,  and  the  edges  were  covered  by  a  fibrinous  disc,  adherent  to 
the  pleura,  to  the  lips  of  the  wound,  and  to  the  plug  of  clot. 

The  effusion  of  blood,  therefore,  in  traumatic  hgemothorax  may  form  clots 
in  the  pleural  cavity ;  yet,  strange  to  say,  the  same  blood,  when  drawn  of? 
and  placed  in  a  test-glass,  does  not  clot,  or  at  least  coagulation  is  imperfect 
or  delayed.     The  study  of  cases  clears  up  this  point. 

In  my  own  case,  the  bloody  fluid  did  not  coagulate  in  the  tube,  which  was  kept 
in  the  laboratory  for  two  months. 

In  Sacquepee's  case  the  fluid  from  the  pleura  was  set  aside,  and  behaved  like  de- 
fibrinated  blood  ;  it  did  not  clot,  although  it  was  kept  for  two  months. 

Patel  and  Leriche  ptmctured  the  pleura  four  days  after  a  wound,  and  drew  off 
7  ounces  of  blood.     The  fluid  had  not  clotted  by  night. 

In  a  case  published  by  Gaultier  and  Fran^ais  puncture  was  performed  on  the  tw(mty- 
first  day.  Three  pints  of  bloody  fluid  were  drawn  off.  The  fluid  did  not  begin  to  clot 
till  six  hours  later,  and  the  clot  did  not  retract  till  twelve  hours  later,  while  fresh  blood 
from  the  patient's  finger  clotted  normally  at  the  end  of  half  an  hour. 

Milian  quotes  a  case  in  which  the  fluid  was  drawn  off  sixteen  days  after  the  injury. 
It  clotted  at  the  end  of  an  hour,  and  the  retraction  of  the  clot  expressed  yellowish 
senjm. 

These  examples  prove  that  we  have  not  yet  exact  knowledge  as  to  the 
properties  of  the  fluid  in  heemothorax.  As  a  rule,  the  fluid  does  not  clot, 
though  it  may  do  so,  and  in  the  latter  event  coagulation  is  delayed. 

The  blood  in  haemothorax  remains  aUve,  haematolysis  does  not  occur,  and 
the  serum  does  not  become  laky,  but  remains  of  a  straw  colour.  All  authori- 
ties agree  upon  this  point,  as  the  following  examples  prove  : 

In  my  case,  hsematolysis  was  quite  absent,  the  red  corpuscles  were  intact,  and  the 
exuded  serum  kept  its  yellow  tint  for  six  weeks.  In  Tufiier  and  Milian's  case  "  it  was 
not  possible  to  find  blood  cells  in  process  of  mortification.  The  red  corpuscles  and  the 
leucocytes  preserved  their  normal  shape  and  their  usual  reactions  ;  they  took  stains 
perfectly,  and,  in  fact,  remained  alive.  The  serum  exuded  in  vitro  after  retraction  of 
tlie  clot  was  yellowish,  and  did  not  show  the  least  tinge  of  red.  This  fact  shows  that 
hiematolysis  did  not  occur  in  the  effusion,  and  that  the  intact  red  corpuscles  wore 
d<^stin(;d  to  be  absorlx^d."  In  Sacquepee's  case  "  the  serous  fluid  above  the  red  sedi- 
ment had  a  vfiry  marked  ycillow  colour  ;  it  showed  no  colouring  due  to  hyemoglobin,  and 
Wius  not  laky  ;  \\w  same  characters  obtained  in  all  the  samph^s  taken." 

The,  ])()int  is  therefore  decided,  and  we  may  state  that  hcematolysis  does 
not  occur  in  traumatic  haemothorax. 

C'ytological  oxamiiKiiioii  of  tlu^  blood  gives  intor(^stiii<^'  information. 
When  I  gav(^  the  cellular  forimila  in  my  case,  I  mentioned  that  llie  cftsino- 
philes  were  as  high  as  35  per  cent.  The  eosinophiles  in  the  hlood  weri^  10  per 
eont.,  while  normal  blood  only  shows  2  to  4  per  cent. 


298  TEXT-BOOK  OF  MEDICINE 

Other  cases  show  this  enormous  predominance  of  the  eosinophiles.  In 
Sacquepee's  counts  they  amounted  to  33  per  cent. 

I  do  not  wish  here  to  discuss  eosinophilia  in  hsemorrhagic  pleurisies, 
and  in  traumatic  hsemothorax.  Burnet  thus  writes  on  pleural 
eosinopliilia  : 

"  The  affinities  for  stains  between  the  eosinophiles  and  the  red  blood- 
corpuscles  would  lead  us  to  suppose  that  the  eosinophile  is  a  polynuclear  cell 
charged  with  red  corpuscles.  Klein  describes  a  case  of  hsemorrhagic  pleurisy, 
with  marked  eosinophiha  in  the  exudate  and  in  the  blood.  He  holds  that  the 
eosinopliiles  are  not  leucocytes  normally  charged  with  haemoglobin,  but 
phagocytes  which  have  ingested  degenerated  red  corpuscles." 

Widal  and  Faure-BeauUeu  arrive  at  the  following  conclusions  upon 
pleural  eosinophilia  :  "  Our  cytological  findings  lend  support  to  Dominici's 
idea  that  the  eosinophiles  may  be  of  lymphatic  origin.  We  conclude  from 
our  researches  that  the  pleural  eosinophilia  takes  place  in  situ,  and  that  the 
blood  eosinopliilia  results  from  the  migration  of  cells  which  have  their  origin 
in  the  morbid  focus." 

However  this  may  be,  it  is  certain  that  my  patient  had  35  per  cent,  of 
eosinopliiles  in  the  effusion,  and  10  per  cent,  in  his  blood. 

The  absorption  of  the  red  corpuscles  may  be  very  rapid  in  hsemothorax. 
The  colour  may  change  from  red  to  rose  in  a  week  or  a  fortnight.  The 
number  in  my  patient  fell  from  2,100,000  to  35,000  in  three  weeks.  In 
Tuffier  and  Milian's  case  the  red  corpuscles  fell  from  390,000  to  22,500  in 
sixteen  days.  "  As  we  know  by  blood-counts  that  the  number  of  corpuscles 
diminishes  daily  in  the  effusion,  and  as,  on  the  other  hand,  we  know  that 
these  red  corpuscles  are  not  destroyed,  they  can  only  be  absorbed."  The 
method  of  this  rapid  absorption  of  the  red  corpuscles  in  hsemothorax  has 
been  repeatedly  discussed.  We  can  eHminate  hsematolysis  because  the  red 
corpuscles  remain  intact,  and  do  not  lose  their  haemoglobin,  as  the  yellow 
tint  of  the  serum  proves.  How,  then,  do  they  disappear  ?  Do  the  eosino- 
philes absorb  the  red  corpuscles  ?  "  It  is  probable  that  the  polynuclear  and 
mononuclear  cells  destroy  the  red  corpuscles,  and  carry  away  the  debris.  On 
the  other  hand,  the  endothehal  cells  do  not  remain  inactive  ;  we  often  find 
perfectly  intact  corpuscles  in  their  protoplasm,  while  others  are  swollen,  pale, 
and  surrounded  by  a  vacuole.  A  certain  number  disappear,  therefore,  by 
intracellular  digestion.  These  two  modes,  however,  do  not  appear  sufficient 
to  produce  such  a  rapid  effect.  Other  unknown  causes  doubtless  play  some 
part "  (Sacquepee). 

It  is  strange  that  the  number  of  white  cells  increases,  while  the  number  of 
red  corpuscles  rapidly  diminishes.  In  my  patient  the  white  cells  rose  from 
4,000  to  8,500.  The  polynuclears  first  disappear  ;  the  lymphocytes  are  found 
in  the  fluid  for  a  Ions  while. 


I 


DISEASES  OF  THE  PLEURA  299 

Symptoms. — We  may  now  commence  our  clinical  study  of  traumatic 
hsemothorax.  Gross  injuries  of  the  chest,  the  heart,  and  the  great  vessels 
demand  surgical  treatment,  and  are  therefore  foreign  to  our  subject,  which 
embraces  only  those  forms  of  haemothorax  that  are  amenable  to  medical 
science. 

We  shall  here  consider  the  course  of  haemothorax  apart  from  complica- 
tions, wliich  will  be  dealt  with  later. 

A  patient  has  been  wounded  in  the  chest.  The  injury  may  involve  all  the 
layers  of  the  chest-wall,  or  may  not  be  visible  externally  (fracture  of  ribs) ; 
the  bleeding  may  come  from  some  vessel  in  the  wall  or  from  a  wound  of  the 
lung,  but  yet  in  each  case  the  blood  very  readily  finds  its  way  into  the  pleura, 
and  forms  a  haemothorax. 

The  initial  symptoms  vary  somewhat  with  the  nature  of  the  wound  and 
with  the  amount  of  bleeding.  The  injured  man  may  become  pale,  complain 
of  pain  and  distress,  and  lose  consciousness.  The  injury,  however,  may  be 
almost  unnoticed,  and  the  only  sign  may  at  first  sight  be  the  external 
bleeding. 

The  wound  of  the  lung  may  show  itself  by  early  haemoptysis.  In  some 
instances  the  patient  brings  up  blood-stained  sputum,  but  in  others  we  find 
frothy  bright  red  blood,  which  is  coughed  up  at  intervals.  One  of  my 
patients,  with  a  bullet  wound,  had  a  severe  attack  of  haemoptysis,  which  was 
followed  by  slighter  attacks.  In  Sacquepee's  case  the  haemoptysis  lasted  for 
several  days.  The  case  reported  by  Connelsville  is  exceptional :  the  patient 
died  from  haemoptysis  in  a  few  minutes,  and  it  was  found  post  mortem  that 
a  fragment  of  rib  had  pierced  the  lung. 

It  would  be  reasonable  to  suppose  that  a  wound  of  the  lung  would  always 
be  followed,  if  not  by  abundant  haemoptysis,  at  least  by  blood-stained 
sputum.  Our  supposition  does  not  hold  good  ;  slight  or  profuse  haemoptysis 
is  far  from  being  frequent.  My  patient  who  was  stabbed  in  the  chest  did  not 
bring  up  any  blood.  Haemoptysis  was  noted  only  eight  or  ten  times  in  forty- 
four  cases  of  traumatic  haemothorax  collected  by  de  Gery.  It  is  true  that 
haemothorax  is  not  always  associated  with  a  wound  of  the  lung  ;  the  blood  in 
the  pleura  may  come  solely  from  the  chest- wall,  in  which  case  the  absence  of 
haemoptysis  is  readily  explained. 

When  blood  invades  the  pleural  cavity,  dullness,  absence  of  vocal  fremitus^ 
tubular  breathing,  and  perhaps  aegophony  enable  us  to  determine  the 
presence  and  tlie  amount  of  tlie  effusion.  Cough,  dyspnoea,  weakness,  and 
Itallor  vary  with  the  severity  of  the  case. 

Haemothorax  may  not  be  accompanied  by  fever,  but  in  some  rases,  from 
the  third  to  the  fifteenth  day,  the  temperature  rises  to  10.3°  or  101°  F.,  and 
remains  high  for  some  time.  We  may  then  ask  whether  the  pleura  has  not 
been  infected  by  the  foreign  body.     The  fever  leads  us  to  fear  pneumonia  or 


300  TEXT-BOOK  OF  MEDICINE 

empyema,  and  we  are  the  more  anxious  in  that  the  injured  man  has  more 
pain  and  more  distress  while  the  fluid  in  the  pleura  increases. 

Such  an  attack  naturally  awakens  our  attention,  but  fortunately  it  does 
not,  as  a  rule,  indicate  any  serious  complication.  When  my  patient  had  a 
temperature  of  103°  F.  four  days  after  the  injury,  we  were  not  greatly  sur- 
prised ;  cultures  of  the  fluid  remained  quite  sterile,  and  we  therefore  con- 
cluded that  the  attack  of  fever  indicated  absorption  of  the  blood  and  the 
onset  of  secondary  pleurisy. 

We  know  that  fever  may  last  some  time  in  cases  of  hsemothorax,  quite 
apart  from  infection,  and  we  now  admit  that  absorption  of  the  red  corpuscles 
gives  rise  to  fever,  and  to  effusion  of  serous  fluid  in  the  pleura. 

The  same  condition  obtains  in  subarachnoid  haemorrhage,  when  blood 
passes  into  the  ventricles  of  the  brain  and  into  the  subarachnoid  space  of  the 
spinal  cord.  The  blood,  as  Prus  says,  may  have  a  very  irritant  action  upon 
the  parts  with  which  it  comes  in  contact.  "  The  recognition  of  Kernig's 
sign  and  the  haematolytic  reactions  in  subarachnoid  haemorrhage  show  that 
the  extravasated  red  corpuscles  undoubtedly  cause  inflammatory  changes." 

Further,  whatever  truth  there  may  be  in  these  hypotheses,  it  is  certain 
that  fever  in  haemothorax  may  coincide  with  absorption  of  the  red  corpuscles, 
with  the  gradual  decoloration  of  the  haemorrhagic  effusion,  with  the  appear- 
ance of  serous  fluid,  and  with  the  subsequent  discavery  of  pleural  friction 
sounds.     The  following  cases  prove  this  point : 

In  my  patient  the  temperature  was  105°  F.  on  admission,  and  the  attack 
was  of  short  duration.  We  found  soon  after  an  increase  in  the  pleural  fluid, 
which  coincided  with  the  rapid  decoloration  of  the  original  effusion,  the 
fibrinous  condition  of  the  newly-formed  fluid,  the  marked  diminution  in  the 
number  of  red  corpuscles,  and  the  appearance  of  friction  sounds.  In 
Sacquepee's  case  the  fluid  is  said  to  have  remained  stationary  for  some 
time,  although  the  number  of  red  corpuscles  diminished. 

"  We  must  conclude  that  a  large  amount  of  serous  fluid  passed  into  the 
pleura,  and  thus  compensated  for  the  absorption  of  the  solid  part."  In 
Tuffier  and  Mihan's  case  the  patient  had  fever,  the  serous  effusion  increased 
in  amount,  and  the  specimens  showed  progressive  diminution  in  the  red 
corpuscles.     Friction  sounds  were  heard  later  in  the  axilla. 

Secondary  pleurisy  may  appear  early  or  late,  but  it  is  impossible  to  fix 
the  exact  moment  of  its  onset,  for  the  same  signs  (dullness,  absence  of 
fremitus,  tubular  breathing,  aegophony)  are  common  both  to  serous  effusion 
and  to  haemothorax. 

Unless  we  are  on  our  guard,  we  may  wrongly  suppose  that  more  blood  is 
being  poured  out  into  the  pleura,  when  a  serous  effusion  is  really  being 
formed.  In  order  to  gain  information  as  to  the  relative  importance  of  the 
bloody  and  of  the  serous  effusion,  we  may  take  samples  of  the  fluid,  which 


DISEASES  OF  THE  PLEURA  301 

are  placed  in  small  tubes.  On  comparison  of  the  samples,  the  presence  of 
pleurisy  is  shown  by  the  rapid  attenuation  of  the  red  tint  of  the  lowest 
layer,  which  coincides  with  the  diminution  in  the  number  of  red  corpuscles, 
and  by  the  appearance  of  fibrin  in  the  serous  layer.  Friction  sounds  later 
make  the  diagnosis  certain. 

We  may  fear  that  the  fever  is  due  to  infection  of  the  lung,  or  to  com- 
mencing empyema  ;  we  have,  however,  a  simple  means  of  deciding  this 
point :  "  Make  cultures  of  the  fluid.  If  you  find  them  sterile,  you  can 
eUminate  any  idea  of  infection." 

Complications. — I  have  first  sketched  the  course  of  an  uncomplicated 
case  of  traumatic  hsemothorax.  The  prognosis  is  nearly  always  good,  and 
recovery  results  in  a  few  weeks,  without  the  need  for  surgical  intervention. 
Let  us  now  pass  on  to  the  complications  of  haemothorax,  and  first  consider 
the  condition  known  as  "  hsemopneumothorax."  Air  may  enter  the  pleural 
cavity  either  through  a  woimd  of  the  chest- wall  or  of  the  lung.  This  double 
channel  of  entrance  might  lead  us  to  suppose  that  pneumothorax  would  be 
a  frequent  comphcation  of  chest  wounds.  I  am  of  opinion,  however,  that 
tliis  complication  is  somewhat  rare.  It  was  not  seen  in  the  cases  quoted 
above,  and  was  found  in  only  twelve  out  of  forty-four  cases  collected  by 
De  Gery.  It  may  perchance  pass  unnoticed,  because  we  can  only  make 
a  summary  examination  in  a  patient  who  is  fainting  from  loss  of  blood. 

The  presence  of  pneumothorax  makes  the  situation  worse  :  distress, 
suffocation,  weakness  of  the  pulse,  and  lipothymia  are  more  marked  when 
this  complication  is  present.  Consideration  for  the  patient  does  not  always 
allow  us  to  make  a  complete  examination,  and  we  cannot  try  for  a  succussion 
splash  ;  yet  the  tympanitic  note  on  Ught  percussion  over  the  upper  part  of 
the  chest  is  usually  sufficient,  especially  if  amphoric  breathing  is  also 
present. 

In  some  cases  we  may  hear  the  air  entering  and  leaving  the  chest  at  each 
respiration. 

Let  us  now  consider  suppurating  haemothorax.  In  some  patients  the 
pleura  is  infected,  and  the  fluid  becomes  purulent,  as  in  the  following 
examples  : 

Haemothorax  occurred  on  the  right  side  from  a  bullet-wound  (Grecnleaf).  A 
little  blood  wa.s  drawn  oflf  by  thoracentesis.  Empyema  supervened ;  P^stlander's  opera- 
tion was  performed,  and  the  patient  linally  recovered. 

Case.  rejHjrtcd  by  dhrisUnitch. — A  boy  was  shot  at  close  range  with  a  revolver.  He 
wius  kept  quiet  for  three,  days.  On  the  fourth  day  effusion,  fever,  and  dyspnoea.  On 
the  sixth  day  ho  nearly  died  from  suffocation.  Foul-smelling  bloody  Huid  was  with- 
drawn on  jjuncture  in  the  seventh  space.  Resection  of  the  fifth  and  sixth  ribs.  On 
incision  of  the  pleura  and  the  lung  much  pus  and  blood  came  out,  th<!  bullet  and  three 
bits  (if  gangrenous  lung  being  removed.     Perfect  recovery  in  two  months. 

l']limoff  has  pub!ish(;d  the  following  case  :  A  man  was  wounded  in  the  axilla  with  a 
shot-gun.     Signs  of  hiemopncumothorax.     Operation  postponed,  as  patient  was  weak. 


302  TEXT-BOOK  OF  MEDICINE 

Some  days  later  foul-smelling  bloody  fluid  escaped  from  the  wound  at  each  fit  of  cough- 
ing ;  the  wad  of  the  charge  soon  came  away  in  the  secretion.  Twelve  days  after  the 
accident  much  pus  escaped  from  the  wound.  Thoracotomy  was  proposed,  but  patient 
refused.     Rapid  improvement  took  place,  and  cure  was  complete  in  six  weeks. 

Peyrot  says  :  A  boy  was  shot  in  the  •second  intercostal  space.  Hsemo thorax 
resulted.  Symptoms  of  infection  appeared  twelve  days  later  :  temperature,  103°  F.  ; 
pulse-rate,  112  ;  rapid  breathing  ;  and  great  collapse.  As  these  symptoms  became 
worse,  the  ribs  were  resected,  but  he  died  on  the  table.  Almost  6  pints  of  reddish  fluid, 
with  foul-smelling  gas,  were  let  out  by  the  incision.  Examination  of  the  fluid  showed 
streptococci  and  anaerobic  microbes. 

Loeper  related  the  following  case  to  me  :  A  boy  had  been  stabbed  in  the  third 
left  space  a  week  before.  He  had  some  distress,  and  complained  of  acute  pains  in  the 
chest  on  the  left  side.  Vocal  fremitus  was  abolished  on  that  side  up  to  the  subclavicular 
region.  Dullness  was  absolute  over  the  same  area.  That  night  the  temperature  rose 
to  103-5°  F.,  and  next  night  to  104°  F.  ;  it  then  varied  between  100°  and  104°  F. 

Normal  blood  was  taken  from  the  finger  ;  clotting  was  rapid,  and  the  clot  retracted 
well.  The  serum,  rather  dark  in  colour,  contauied  urobilin,  and  a  normal  amoimt  of 
chlorides.  Freezing-point  was  0-57°  and  0-60°.  The  red  corpuscles  were  much  reduced 
in  number  ;  the  count  showed  2,650,000,  with  a  fair  number  of  poikilocytes.  The 
white  corpuscles  were  much  increased  in  number  ;  the  count  showed  17,500,  84  per  cent, 
being  polynuclears  and  16  per  cent,  mononuclears.  The  patient  had  signs  of  a  left 
effusion,  but  the  high  temperature,  the  severe  general  symptoms,  and  the  existence  of 
marked  leucocytosis  were  against  simple  heemothorax  or  sero -fibrinous  effusion. 

The  fourth  space  was  punctured,  and  fluid  of  a  chocolate  tint  was  drawn  off.  The 
fluid  was  odourless,  and  froze  at  0-47°.  The  microscope  showed  normal  red  corpuscles 
and  nimierous  polynuclear  cells,  of  which  some  were  normal  and  others  were  in  process 
of  disintegration,  indicating  suppuration  in  the  fluid.  The  fluid  was  sown  on  agar  and 
on  broth.  The  latter  culture  at  the  end  of  twenty-four  hours  showed  a  thin  bacillus, 
which  was  mobiis  and  present  in  a  pure  state  ;  it  appeared  to  be  the  coli  bacillus.  Forty- 
eight  hours  later  the  culture  became  green,  as  though  the  pyocyaneus  were  present. 
The  green  tint  later  changed  to  a  blackish-brown  colour.  The  colonies  on  agar  showed 
similar  colour  changes.  The  patient's  serum  agglutinated  the  baciUi  in  the  fluid.  The 
case  was  one  of  suppurating  hsemothorax.  Thoracotomy  gave  exit  to  brownish  fluid, 
containing  many  clots.  No  gas.  The  fever  at  once  fell,  and  recovery  was  complete 
in  six  ^\eek3. 

Infection  of  the  pleura  is  therefore  fairly  common  in  traumatic  hsemo- 
thorax.  When  fever  appears  in  a  case  of  hsemothorax,  we  must  at  once 
look  for  the  cause.  The  condition  may  simply  coincide  with  absorption 
of  blood  and  with  the  onset  of  pleurisy  ;  but  it  may  also  be  due  to  infection 
of  the  pleura,  which  requires  early  operation.  The  diagnosis  must  be  made 
promptly.  Leucocytosis  is  in  favour  of  pus,  but  cultures  furnish  the  more 
rehable  information. 

Both  in  my  case  and  in  that  of  Sacquepee  the  cultures  were  sterile, 
and  it  was  therefore  clear  that  the  pleura  was  not  infected,  in  spite  of  the 
fever  present.  The  same  result  obtained  in  the  case  reported  by  Tuffier 
and  Mihan.  Inoculation  on  broth,  on  agar,  and  on  agar  with  sugar  (tubes 
of  Liborius  and  Veillon)  showed  absolute  sterility,  although  the  patient 
had  fever.  In  the  cases  of  Peyrot  and  of  Loeper,  on  the  contrary,  the 
hsemothorax  was  infected,  and  cultures  showed  the  nature  of  the  organisms. 


DISEASES  OF  THE  PLEURA  303 

Infection  of  the  pleura  is  to  be  feared  both  in  haemothorax  and  in  hsemo- 
pneumothorax.  Every  infected  case  should  undergo  operation.  If  the 
patient  dies  in  spite  of  operation,  he  does  so  because  the  operation  has  been 
performed  too  late. 

I  have  spoken  of  the  acute  forms,  but  infected  haemothorax  may 
show  another  variety.  The  initial  symptoms  at  times  subside,  and  the 
patient  appears  on  the  road  to  recovery,  but  yet  the  infection  persists  in  a 
chronic  form.  Peyrot  tells  how  a  patient  was  about  to  be  discharged 
after  the  apparent  cure  of  a  wound  in  the  right  axilla.  He  had  no  fever, 
and  would  have  been  looked  upon  as  well  if  he  had  not  shown  signs  of  a  large 
effusion.  Puncture  in  the  eighth  space  showed  the  existence  of  granular 
pus,  which  was  not  homogeneous  and  had  a  slight  colour. 

In  two  cases  reported  by  Ch.  Nelaton  the  collections  of  pus  were  emptied 
through  the  bronchi  long  after  the  wound  of  the  chest.  Peyrot' s  second 
case  was  as  follows  : 

A  woman  had  been  stabbed  in  the  cliest.  The  signs  of  an  effusion  of  blood  into  the 
pleura  were  present.  She  made  good  progress,  but  several  weeks  later  she  suddenly 
coughed  up  a  quantity  of  very  foul-smelling  blood.  The  condition  again  became 
normal.  She  thought  that  she  was  cured,. and  her  health  appeared  excellent,  when  the 
same  thing  occurred  some  weeks  later.  Several  recurrences  took  place  during  the  next 
year. 

Traumatic  haemothorax  is  often  accompanied  by  subcutaneous  emphy- 
sema, which  gives  the  well-known  feeUng  of  downy  crepitation.  It  com- 
mences around  the  wound,  especially  if  the  latter  is  narrow  and  anfractuous. 
It  usually  remains  limited,  and  rarely  extends  to  a  distance. 

Traumatic  pneumonia  is  chiefly  seen  in  the  case  of  fractured  ribs.  It  is 
somewhat  difficult  to  diagnose,  because  the  crepitant  rales,  the  tubular 
breathing,  and  the  rusty  sputum  are  obscured  by  the  signs  of  haemothorax 
or  of  haemopneumothorax.  Pneumonia  is  a  serious  complication  per  se, 
and,  further,  it  may  give  rise  to  infection  of  the  pleura. 

Treatment. — We  may  first  consider  cases  that  recover  without  surgical 
treatment.     Two  of  our  patients  belong  to  this  category. 

A  person  has  just  received  a  penetrating  wound  of  the  chest.  You  are 
called  to  see  him.  The  wound  is  bleeding.  The  patient,  who  is  pale  and 
distressed,  is  breathing  badly  and  is  coughing  up  blood,  showing  that  the 
lung  is  injured.  There  is  no  fever.  The  pulse  is  quick,  but  is  of  fair  strength, 
so  that  you  may  suppose  the  intrapleural  bleeding  to  be  moderate. 

Do  not  tire  the  patient  by  useless  manipulation  ;  do  not  probe  the 
wound,  but  be  content  to  disinfect  it,  and  to  apply  an  occlusion  dressing. 
Absolute  rest  in  bed  must  be  ordered.  Be  very  careful  to  auscultate  and 
to  percuss  the  chest.  If  you  do  not  find  either  tympanitic  resonance 
or  amphoric   breathing,  pneumothorax  is   absent.      The  dullness  in  the 


304  TEXT-BOOK  OF  MEDICINE 

dependent  partswill  indicate  the  amount  of  blood  effused.  If  the  patient 
has  much  pain  in  the  chest,  give  an  injection  of  morphia,  which  is  repeated 
if  need  be.  If  the  heart  is  weak,  use  injections  of  caffeine  ;  and  if  the  weak- 
ness increases,  give  injections  of  serum  every  three  hours,  and  stimulants. 
A  mixture  of  Rabel  water  and  syrup  of  rhatany  may  be  given  for  haemop- 
tysis. The  diet  should  consist  of  milk,  eggs,  and  broth.  In  order  to 
ascertain  whether  the  blood  continues  to  flow  into  the  pleura,  be  careful 
at  your  first  visit  to  take  some  blood  from  the  finger,  and  to  count  the  red 
corpuscles.  Repeat  this  examination  every  two  or  three  hours,  if  the  con- 
dition becomes  worse.  If  you  find,  after  two  or  three  examinations,  that 
the  number  falls  rapidly,  you  may  reasonably  hold  that  the  intrapleural 
haemorrhage  is  still  going  on. 

Let  us  suppose  that  the  patient  is  not  growing  worse.  A  day  passes, 
and  the  general  condition  is  better.  More  exact  examination  shows  an 
effusion,  which  may  amount  to  about  a  pint.  The  situation  remains 
practically  unchanged  during  the  next  few  days.  It  is  then  unnecessary  to 
evacuate  the  fluid,  because  absorption  of  the  effusion  is  sometimes  very 
rapid  ;  you  need  only  await  events.  Recovery  in  traumatic  haemothorax 
is  very  frequent,  even  though  the  fluid  has  not  been  evacuated.  The  cases 
reported  by  Millard,  Sacquepee,  Tuffier,  De  Gery  and  Bergeaud  are  of  this 
nature. 

Events,  however,  do  not  always  follow  tliis  course,  and  you  will  see 
patients  whose  condition  some  hours  after  the  injury  causes  anxiety,  because 
the  intrapleural  bleeding  continues. 

Haemoptysis  and  pneumothorax  may  or  may  not  be  present,  but  yet 
the  condition  grows  worse.  The  breathing  is  not  so  easy,  dyspnoea  follows 
the  least  movement,  the  pulse  becomes  quick,  the  strength  fails,  syncope 
threatens,  and  the  effusion  may  amount  to  3  or  4  pints. 

What  fine  of  treatment  is  to  be  adopted  ?  If  it  were  simply  a  question 
of  an  eflusion,  which  by  its  large  amount  threatened  hfe,  the  problem 
would  be  quickly  solved  by  performing  thoracentesis.  The  matter,  how- 
ever, is  not  always  so  simple.  The  source  of  the  bleeding  may  not  be 
exhausted ;  the  blood  from  the  lung  or  from  the  chest- wall  may  be  still 
flowing  into  the  pleura,  and  the  situation  is  most  serious.  The  surgeon  must 
now  take  up  the  tale,  and  decide  the  question  of  resecting  the  ribs  in  order 
to  make  a  complete  exploration  of  the  thoracic  cavity  and  to  arrest  all 
bleeding. 

I  have  described  two  extreme  cases  :  on  the  one  hand,  haemothorax  of 
moderate  severity ;  on  the  other,  grave  haemorrhage,  in  wliich  operation  is 
imperative.  We  see,  however,  intermediate  forms  in  which  puncture  may 
replace  thoracotomy.  Thoracentesis  has  been  performed  with  success  on 
the  third,  fourth,  sixth,  eleventh,  and  twenty-first  days  respectively. 


I 


DISEASES  OF  THE  PLEURA  305 

What  are  the  indications  for  puncture  ?  Are  we  to  do  it  early  or  late  ? 
Are  we  to  be  content  with  drawing  off  part  of  the  fluid,  or  must  we  evacuate 
a  large  quantity  at  one  sitting  ? 

I  would  first  state  that  the  expediency  of  thoracentesis  should  depend 
solely  upon  the  condition  of  the  patient.  If  aggravation  of  the  symptoms 
coincides  with  signs  indicating  abundant  effusion,  and  if  immediate  surgical 
intervention  is  not  justifiable,  thoracentesis  is  indicated,  in  my  opinion. 

As  regards  the  quantity  of  fluid  that  should  be  drawn  off,  some  authors 
say  that  we  must  only  draw  off  a  small  amount,  while  others  give  the  opposite 
advice.     To  quote  examples  : 

A  case  of  traumatic  haemothorax  was  admitk^d  under  Jaboulay.  As  the  symptoms 
were  alarming,  he  performed  thoracentesis  on  the  fourth  day,  and  drew  off  only  8  ounces. 
The  result  was  excellent,  and  he  insists  on  the  benefit  of  thoracentesis  in  such  a  case. 

A  man  had  hsemopneumothorax.  Dyspnoea  became  very  acute  some  days  later. 
Examination  of  the  chest  revealed  a  large  effusion.  Souligoux  performed  thoracentesis, 
but  only  drew  off  8  ounces  of  bloody  fluid.     The  patient  recovered. 

Lejars  quotes  a  case  of  traumatic  ha-mothorax  in  which  3  pints  of  blood-stained 
fluid  were  draA\Ti  off  ten  days  after  the  injury.     Recovery  was  uninterrupted. 

In  a  case  in  which  the  fluid  was  slow  to  absorb,  Gaultier  and  Fian^ais  performed 
thoracentesis  three  weeks  after  the  injury.  Three  pints  of  bloody  fluid  were  drawn  off. 
The  patient  recovered. 

A  man  fell  on  the  shaft  of  a  waggon,  and  his  chest  was  squeezed  by  the  wheel.  No 
fracture  was  found,  and  the  surgeon  gave  a  good  prognosis.  Dr.  Jagot  was  called  to 
him  at  9  p.m.  The  patient  was  pale  and  breathless  ;  the  left  side  of  the  chest  was 
dull,  and  the  heart  was  pushed  over  to  the  right.  Jagot  diagnosed  traumatic  hemo- 
thorax, and  drew  off  6  pints  of  bright  blood  by  thoracentesis.  Relief  followed,  but 
the  fluid  reformed,  and  4  pints  of  chocolate  fluid,  mixed  with  clots,  were  drawn  off. 
Recovery  now  followed. 

These  examples  prove  that  recovery  followed  whether  much  or  little 
fluid  was  drawn  off.  For  ray  part,  I  do  not  see  the  necessity  for  drawing 
off  at  one  sitting  several  pints  of  fluid  ;  I  should  be  afraid  of  starting  fresh 
hemorrhage,  or  of  causing  a  fresh  pneumothorax.  I  would  rather  with- 
draw a  pint  of  fluid,  and  then  repeat  the  procedure,  according  to  the  result 
obtained.  We  must  not  lose  sight  of  the  cases  in  which  surgical  intervention 
is  imperative  ;  delay  or  indecision  may  cost  the  patient  his  life. 


V.  PURULENT  PLEURISIES  OF  THE  GENERAL  PLEURAL 

CAVITY. 

Discussion. — Writers  formerly  spoke  of  "  purulent  pleurisy,"  but  we 
should  really  speak  of  "  purulent  pleurisies."  Bacteriology  has  completely 
modified  certain  questions  in  medicine,  and  purulent  pleuri-sy  is  among  the 
number.  I  shall  now  describe  purulent  pleurisies  of  the  general  pleural 
cavity,  and  later  discuss  the  interlobar,  mediastinal,  and  diaphragmatic 
varieties. 

20 


306  TEXT-BOOK  OF  MEDICINE 

It  is  not  possible  to  write  a  set  chapter  on  purulent  pleurisies,  because 
each  variety  necessitates  a  special  description,  according  as  it  is  due  to  the 
pneumococcus,  to  the  streptococcus,  to  tuberculosis,  to  appendicitis,  etc. 
Each  of  these  types  will  be  described  in  turn,  and  we  shall  see  how  they  differ 
from  one  another  ;  each  type  owes  its  special  characters  and  its  degree  of 
gravity  to  a  special  pathogenic  agent,  and  this  new  view  of  the  question  is  of 
much  interest.  Nevertheless,  there  are  some  general  considerations  which 
may  find  their  place  here. 

Pathological  Anatomy. — The  older  the  mischief,  the  more  are  the  lesions 
marked.  At  the  onset  the  fluid  is  turbid  and  sero-purulent,  or  sometimes 
purulent ;  the  false  membranes  are  not  thick.  Later,  however,  the  lesions 
are  well  marked,  false  membranes  spread  over  both  layers  of  the  pleura,  and 
may  be  ^  inch  thick,  especially  on  the  parietal  pleura.  The  adhesions 
between  the  two  layers  of  the  serosa  divide  up  the  cavity,  and  form  pockets 
of  pus  ;  they  extend  their  harmful  action  still  farther,  fix  the  ribs  by  restrain- 
ing their  action,  and  contribute  to  deformity  of  the  chest-wall,  which  becomes 
flattened  and  retracted  in  the  lateral  and  posterior  region. 

The  fluid  may  amount  to  4,  6  or  8  pints.  The  lung,  though  pushed  back 
and  flattened,  is  but  httle  changed  if  the  pleurisy  is  recent ;  in  old-standing 
cases,  the  lung  is  reduced  to  a  kind  of  stump  of  the  size  of  the  fist,  and  is 
indurated,  fibrous  (Brouardel),  compressed  against  the  costo-vertebral 
groove,  surrounded  by  false  membranes,  and  consequently  reduced  to  a 
condition  that  renders  it  incapable  of  regaining  its  normal  size  and  func- 
tions. The  skeleton  of  the  thorax  is  affected ;  the  periosteum  is  adherent 
to  the  pleural  membranes,  and  the  ribs  are  the  seat  of  osteitis.  The  pus 
may  make  its  exit  by  various  channels,  by  the  bronchi  (vomica),  or  by  r.n 
intercostal  space  (this  is  most  frequent  in  the  fifth  space).  The  rela-*-ive 
frequency  of  these  perforations  is  thus  given  by  Flammarion  : 

Pleuro-cutaneous  fistulge  . .  . .  . .  . .  10 

Pleuro-broncho-cutaneous  fistulas  . .  . .  . .  5 

Pleuro-bronchial  fistulse  . .  . .  . .  . .  3 

Pleuro-abdominal  fistulse  . .  . .  . .  . .  1 

These  statistics  prove  that  empyemata  empty  themselves  more  often  by 
an  intercostal  space  than  by  the  bronchi,  and  the  remarkable  fact  is  that  the 
perforation  does  not  occur  behind  at  the  most  dependent  part,  but  in  front, 
at  the  middle  of  the  intercostal  space,  in  the  proportion  of  eleven  to  three. 
Let  me  hasten  to  add  that  these  terminations,  which  were  fairly  frequent  at 
a  time  which  I  have  called  the  prehistoric  period  of  pleurisy,  have  become 
almost  unknown  since  early  operations  for  empyema  have  been  performed. 

The  presence  of  air  in  the  pleural  cavity  (pneumothorax  by  perforation), 
or  the  formation  of  gas  (pneumothorax  by  putrefaction)  in  the  case  of 
putrid  pleurisies,  constitutes  pyopneumothorax.     The  kidney,   the  liver, 


DISEASES  OF  THE  PLEURA  307 

and  the  spleen,  are  sometimes  affected  by  amyloid  degeneration  in  chronic 
cases  of  empyema. 

Common  Signs. — Some  signs  may  be  common  to  the  various  forms  of 
empyema. 

Dullness  is  absolute  over  the  whole  extent  of  the  effusion,  or  alternates 
with  resonant  zones  if  the  pleurisy  is  partial  or  encysted.  Sometimes,  by 
reason  of  adhesions,  the  pus  accumulates  at  the  base  of  the  thorax,  depresses 
the  diaphragm  at  the  expense  of  the  abdominal  organs,  which  are  pushed 
down,  and  the  encysted  pleurisy  at  the  base  then  simulates  a  tumour  of 
the  Uver,  the  spleen,  or  the  kidney. 

The  vocal  fremitus  is  abohshed  or  diminished  over  the  effusion,  but 
often  persists  at  the  site  of  the  adhesions.  The  thorax  on  the  affected  side 
undergoes  a  transient  bulging,  which  is  followed  by  retraction  and  flattening 
of  the  lower  intercostal  spaces ;  this  flattening  is  seen  in  spite  of  the  presence 
of  the  fluid,  unless  it  be  very  abundant.  In  the  latter  case  the  spaces  are 
dilated,  and  the  thorax  forms  a  large  curve.  The  deformity  in  time  becomes 
very  marked,  especially  after  tlie  natural  or  the  artificial  evacuation  of  the 
effusion.  The  shoulder  is  depressed,  the  chest  is  flattened,  the  muscles  are 
atrophied,  and  the  vertebral  column  becomes  concave  towards  the  affected 
side.  This  deformity,  which  may  persist  indefinitely,  is  a  natural  and  neces- 
sary device,  destined  to  fill  up  the  void  caused  by  the  partial  atrophy  of  the 
lung. 

(Edema  of  the  chest- wall  is  often  seen  on  the  diseased  side  ;  it  may  occur 
early  in  the  disease,  and  may  be  limited  to  the  posterior  border  of  the  axilla, 
or  may  extend  to  the  arm  and  hand.  In  long-standing  cases  the  fine  arboriza- 
tions of  a  complementary  circulation  may  be  seen  on  the  skin  of  the  thorax. 

The  neighbouring  organs  are  pushed  back  by  the  effusion,  the  heart  is 
displaced,  and  the  liver  is  pushed  down  according  as  the  pus  is  on  the  left 
or  tlie  right  side,  and  these  vicious  positions  are  the  more  durable  in  that 
they  are  maintained  by  the  false  membranes. 

The  signs  on  auscultation  are  variable,  especially  when  the  disease  has 
las^ited  some  time  ;  in  some  cases  they  are  negative.  We  may  examine  and 
find  a  total  absence  of  normal  and  abnormal  sounds  ;  at  other  times  we  may 
hear  bronchial,  cavernous,  or  amphoric  breathing  (Landouzy). 

^gophony,  which  may  exist  when  the  onset  is  acute  and  the  liquid  is  sero- 
purulent,  is  wanting  in  other  cases,  and  aphonic  pcctorilo(iuy,  which  is  so 
clear  in  sero-fibrinous  effusions,  may  lose  its  characters  (Bacelli).  At  points 
where  the  false  membranes  exist  alone,  without  adhesions  and  fluid,  a  harsh 
and  sawing  friction  sound  may  be  heard. 

In  some  cases  on  the  left  side  wc  find  in  the  region  of  the  effusion  a 
pulsating  tumour,  or  expansile  movements,  like  those  of  an  aneurysm. 
Pulsating  empyema  is  the  term  applied  to  this  form. 

20-2 


308  TEXT-BOOK  OF  MEDICINE 

The  fever  has  no  definite  character  ;  it  is  more  or  less  acute  and  inter- 
mittent ;  it  may  be  absent,  or  may  in  time  take  a  hectic  course,  with  evening 
rise  and  abundant  sweats.  The  dyspnoea  varies  with  the  amount  of  the 
fluid,  the  extent  of  the  adhesions,  and  the  condition  of  the  neighbouring 
organs  (pulmonary  tuberculosis,  pericarditis,  and  broncho-pneumonia). 

When  pus  is  left  to  make  its  way  through  an  intercostal  space,  the  patient 
feels  pain  at  a  point  which  soon  becomes  more  prominent  than  the  neighbour- 
ing parts.  The  tumour  takes  several  days  or  weeks  to  form ;  it  becomes 
fluctuating,  invades  one  or  two  intercostal  spaces,  has  an  elongated  form,  and 
is  reducible.  The  skin  becomes  thin,  red,  and  perforated,  and  a  fistula  forms, 
through  which  the  pus  flows  out.  According  to  the  nature  of  the  fistulous 
tract,  the  external  air  may  or  may  not  enter  the  pleura,  and  in  the  former 
case  symptoms  of  pneumothorax  arise.  The  pus  sometimes  has  a  foetid 
odour,  and  after  a  transient  improvement,  which  coincides  with  the  first 
evacuation  of  the  pus,  symptoms  of  septic  absorption  and  hectic  fever  may 
occur  if  appropriate  treatment  be  not  at  once  employed. 

The  pus  may  traverse  the  tissues  like  a  congestion  abscess,  and  point  in 
the  lumbar  region,  most  often  on  the  left  side.  In  order  to  reach  this  spot 
it  may  follow  various  routes.  Sometimes  it  takes  quite  a  superficial  route 
across  the  posterior  part  of  the  lower  intercostal  spaces  beneath  the  latissimus 
dorsi,  and  in  this  case  the  progressive  raising  of  the  integument  indicates  the 
course  of  the  collection.  Sometimes  it  chooses  a  deeper  route,  passes  through 
the  diaphragm  near  the  vertebral  column,  follows  the  anterior  surface  of  the 
psoas  magnus,  or  the  outer  border  of  the  quadratus  lumborum,  and  appears 
in  the  lumbar  region.  The  lumbar  tumour  may  eventually  reach  a  large 
size  ;  it  is  oblong,  fluctuating,  painless,  partly  reducible,  and  sometimes  shows 
expansile  pulsations  {vide  section  on  Pulsating  Empyema)  ;  it  may  become 
ulcerated  when  evacuation  of  the  empyema  follows  pleurisy.  When  the 
pus  passes  into  the  bronchi  (pleuro-bronehial  fistula),  there  is  a  vomica 
(see  Section  XV.). 

The  change  from  sero-fibrinous  or  hsemorrhagic  fluid  to  pus,  after  thora- 
centesis, is  now  denied  no  longer.  I  may  say  that  this  change  cannot  occur 
provided  the  operator  takes  proper  care.  I  have  discussed  tliis  question  in 
detail  under  thoracentesis. 

Micro-organisms  must  be  regarded  as  the  final  cause  of  empyema.  After 
these  general  remarks  we  may  consider  the  chief  varieties  of  empyema, 
which  owe  their  special  characters  to  their  pathogenic  agents.  This  side  of 
the  question  has  been  examined  with  the  greatest  care  by  Netter. 


I 


DISEASES  OF  THE  PLEUKA  309 

Purulent  Pleurisy  due  to  Streptococci. 

Description. — The  streptococcus,  which  often  causes  suppuration  in  the 
serous  membranes,  is  perhaps  the  most  usual  microbe  when  the  disease  occurs 
in  adults.  I  say  in  adults,  because  in  children  the  most  usual  microbe 
appears  to  be  the  pneumococcus. 

The  presence  of  the  streptococcus  in  the  pleural  fluid  does  not  always 
determine  piLS  ;  some  cases  are  sero-fibrinous.  Pus  is  seen  especially  when 
the  plem'a  is  in  contact  with  a  focus  rich  in  streptococci  (focus  of  influenzal 
broncho-pneumonia,  broncliial  dilatation,  tuberculosis,  pulmonary  gan- 
grene), yet  the  focus  may  be  so  small  that  it  would  pass  unseen  post  mortem 
without  a  minute  examination.  In  other  cases  the  focus  is  remote  (lesions 
of  the  mediastinum,  breast,  puerperal  infection,  etc.).  Sometimes  purulent 
streptococcal  pleurisy  arises  in  the  course  of  an  infectious  disease  (scarlatina, 
typhoid  fever,  erysipelas,  diphtheria,  etc.)  ;  it  may  also  occur  as  a  primary 
infection,  the  point  of  entrance  of  the  organism  being  unknown.  The  fluid 
in  streptococcal  pleuiisy  is  rarely  purulent  from  the  start ;  it  is  usually  first 
turbid,  then  sero-purulent,  and  finally  purulent  fluid.  The  turbid  appearance 
may  be  so  slight  that  a  sample  on  superficial  examination  will  be  taken  for 
sero-fibrinous  fluid,  but  microscopic  examination  usually  reveals  red  cor- 
puscles and  polynuclear  cells.  Bacteriological  examination,  including  cul- 
tures, reveals  micrococci  in  little  chains. 

When  the  liquid  becomes  purulent,  the  pus  is  not  homogeneous  and 
laudable,  like  that  due  to  the  pneumococcus  ;  it  separates  into  two  layers  in 
the  glass,  the  upper  being  serous,  the  lower  dense,  with  a  sediment  which 
falls  to  the  bottom.  The  false  membranes  which  cover  the  pleura  are  not  so 
tliick  and  firm  in  streptococcal  as  in  pneumococcal  pleurisy. 

Endocarditis,  pericarditis,  meningitis,  otitis,  etc.,  are  much  rarer  in  this 
variety  than  in  pneumococcal  pleurisy,  but  suppurative  meningitis  is  fairly 
common. 

The  symptoms  and  course  show  nothing  special.  Sometimes,  however, 
the  fever  and  the  temperature  undergo  great  variations,  while  oedema  of  the 
chest-wall  is  more  frecjuent  than  in  pneumococcal  pleurisy  ;  in  some  cases, 
too,  the  disease  takes  a  rapid  typhoid  course,  which  answers  to  the  descrip- 
tion of  septic  pleurisies  ;  often,  too,  the  course  of  the  disease  is  slow,  the 
symptonLs  are  moderate,  the  fever  is  not  high,  and  tlu;  disease  is  ahnost  latent. 
It  is  therefore  (;lear  that  the  disease  may,  clinically  speaking,  assume  all 
forms.  Vomica  is  more  rare  in  streptococcal  than  in  pneumococcal  pleurisy. 
In  puer[)eral  cases  the  disease  may  have  a  rapid  course,  an  excessive  viru- 
lence, and  a  most  grave  prognosis  ;  it  used  to  appear  in  epidemic  form  when 
epidemics  of  puerperal  fever  were  seen.  These  epidemics  are  no  longer  seen, 
or,  at  least,  they  ought  not  to  be  seen. 


310  TEXT-BOOK  OF  MEDICINE 

The  diagnosis  can  only  be  made  by  bacteriological  examination  of  the 
pus.  The  sample  fluid,  as  I  have  already  said,  may  be  turbid,  sero-purulent, 
or  purulent.  Bacteriological  examination  and  cultures  will  indicate  the 
micro-organism.  "  The  appearance  of  chains,  after  staining  with  gentian 
violet,  proves  the  streptococcus ;  only  if  the  chains  be  long,  bent,  and  have 
very  round  granules,  we  must  not  forget  that  the  pneumococci  in  serous 
membranes  are  often  disposed  in  little  chains,  though  they  are  straighter  and 
less  bent  than  those  of  streptococci,  and  are  composed  of  more  elongated  and 
less  numerous  elements  "  (Netter).  We  may  add  that  the  pneumococcus  is 
encapsuled. 

The  treatment  consists  in  thoracotomy.  The  operation  for  empyema, 
with  or  without  resection  of  ribs,  is  the  rational  treatment  for  these  cases. 
It  is  extremely  rare  indeed  for  the  streptococcal  form  to  recover,  Uke  pneumo* 
coccal  pleurisy,  after  simple  puncture  ;  when  this  occurs  the  virulence  of  the 
streptococcus  is  markedly  attentuated.  I  have  seen  a  case  of  this  nature  at 
the  Necker  Hospital.     It  is  described  by  my  present  colleague  Widal. 

Pleurisy  had  appeared  as  a  late  complication  in  the  puerperium,  and  was 
then  the  only  abnormal  feature.  Examination  and  cultures  of  the  fluid 
showed  the  presence  of  streptococci,  and  inoculation  showed  that  the  pus 
had  lost  in  virulence.  At  each  fresh  puncture  the  fluid  was  less  rich  in 
microbes,  and  the  virulence  diminished,  so  that  the  patient  was  cured  by 
aspiration,  without  operation  for  empyema.  Such  a  result  is  exceptional ; 
the  rule  is  early  rather  than  late  surgical  intervention. 

Purulent  Pneumococcal  Pleurisy. 

Description. — Tliis  form  is  rarer  in  the  adult  than  streptococcal  pleurisy ; 
on  the  other  hand,  it  is  much  more  frequent  in  the  cliild.  The  pneumo- 
coccus  is  usually  present  in  a  pure  state,  other  microbes  being  only  met  with 
in  a  fourth  of  the  cases. 

The  condition  is  commonly  associated  with  pneumoixia,  but  it  may  be 
independent  when  the  pneumococcus  infects  the  pleura  on  its  own  account. 
The  pleura  is  nearly  always  affected  in  the  course  of  pneumonia.  The 
pleurisy  is  often  dry,  and  confines  itself  to  the  production  of  false  membranes 
of  variable  tliickness,  which  line  the  pleura  for  a  certain  extent,  especially  at 
the  interlobar  fissures.  In  other  cases  sero-fibrinous  or  purulent  effusion  is 
also  present.  It  is  a  remarkable  fact  that  the  pneumococcus,  which  does  not 
produce  pus  in  the  lung,  readily  does  so  in  the  serous  membranes  (pleura, 
pericardium,  meninges), 

Maragliano  has  systematically  punctured  the  pleura  in  fifty- eight  cases 
of  pneumonia  ;  in  thirty-eight  of  these,  sero-fibrinous  or  fibrino-purulent 
effusion  was  found. 

The  pus  is  "  laudable,"  according  to  the  expression  of  ancient  writers,     ft 


I 


DISEASES  OF  THE  PLEURA  3H 

is  rich  in  cellular  elements,  and  fibrin — greenish-yellow,  thick,  viscid  and 
creamy,  homogeneous,  and  usually  inodorous.  When  it  is  placed  in  a  glass,  it 
does  not  separate  into  serous  fluid  and  plasma,  Hke  the  pus  due  to  the 
streptococcus. 

Bacteriological  examination  and  cultures  reveal  the  presence  of  the 
pneumococcus.  "  The  pneumococci  are  often  present  in  the  form  of  long 
Hues,  which  might  be  mistaken  for  chains  of  Streptococcus  pyogenes.  The 
pneumococcus,  however,  in  these  cases  usually  presents  stained  capsules  that 
are  very  easy  of  detection,  and  its  elements  have  a  more  marked  lanceolated 
form  than  in  pneumonic  expectoration.  Phagocytosis  is  common,  especially 
in  the  benign  forms  in  process  of  recovery  "  (Xetter). 

The  trouble  usually  supervenes  during  the  decline  of  pneumonia,  or  even 
during  convalescence.  In  many  cases  pneumonia  has  ended  two  or  tliree 
weeks  before  pleurisy  appears.  These  cases  have  also  received  the  name 
metapneumonic  or  postpneumonic.  Metapneumonic  pleurisies  (Gerhardt) 
may  be  sero-fibrinous,  but  I  am  concerned  here  with  the  purulent  form, 
which  is  the  more  frequent. 

Purulent  metapneumonic  pleurisy  may  invade  the  great  pleural  cavity, 
but  is  more  often  confined  to  some  part  of  the  pleura,  being  interlobar, 
mediastinal,  or  diaphragmatic. 

Metapneumonic  pleurisies  are  sometimes  seen  in  series,  as  if  they 
were  tributary  to  an  epidemic. 

Pneumonic  pleurisy  rarely  begins  with  very  acute  symptoms,  and  the 
onset  is  more  usually  insidious,  being  unaccompanied  by  pain  and  by 
recrudescence  of  fever.  (Edema  of  the  chest-walls  is  frequent  in  strepto- 
coccal, but  exceptional  in  pneumococcal,  pleurisy  (Netter). 

In  about  a  fourth  of  the  cases,  especially  in  the  encysted  forms,  the 
termination  is  by  vomica.  It  is  much  more  frequent  than  in  the  other 
varieties  of  purulent  pleurisy,  and  supervenes  from  the  fifteenth  to  the 
thirtieth  day.  In  other  cases  the  pus  is  not  evacuated  by  the  bronchi,  but 
forms  a  swelling  in  an  intercostal  space,  or  towards  Scarpa's  triangle.  Lastly, 
it  may  become  encysted,  hke  an  abscess,  and  be  absorbed,  especially  in 
children. 

Pneumococcal  pleurisy  is  notably  less  grave  than  streptococcal  pleurisy. 
It  may  recover  by  vomica  or  by  absorption  of  the  fluid,  for  the  pneumo- 
coccus is  not  endowed  with  great  vitality.  After  evacuation  of  the  fluid, 
the  lung  quickly  expands  again.  An  attempt  may  be  made  to  cure  these 
cases,  especially  in  children,  by  simple  aspiration  of  the  liquid,  with  or  without 
aseptic  lavage.     The  operation  for  empyema  may  sometimes  be  avoided. 

In  some  cases  metapneumonic  purulent  pleurisy  is  very  grave,  especially 
when  the  pneumococcus  is  associated  with  other  pyogenic  organisms,  such 
as  the  streptococcus  and  the  staphylococcus. 


312  TEXT-BOOK  OF  MEDICINE 

Although  this  holds  good,  it  would  not  do  to  place  too  great  confidence 
in  the  benign  nature  of  the  pneumococcus  ;  there  are  cases  where,  although 
the  pneumococcus  is  quite  isolated,  its  virulence  is  as  great  as  that  of  the 
most  active  pyogenic  germs.  I  treated  a  youth  for  a  most  severe  attack 
of  purulent  pleurisy,  in  which  the  pneumococcus  was  the  only  microbe 
found.  Such  cases  I  have  usually  treated  by  aspiration.  I  performed  a 
first  and  second  puncture,  hoping  to  avoid  an  operation  for  empyema  ; 
but  as  the  fever  remained  high,  and  the  fluid  reformed,  with  severe 
general  symptoms,  it  was  necessary  to  perform  thoracotomy.  I  remember 
especially  two  cases  of  purulent  pleurisy,  due  to  the  pneumococcus  alone. 
I  performed  two  successive  punctures,  without  result,  and,  at  my  request, 
the  patients  were  operated  upon,  with  success. 

All  that  I  have  said  concerning  metapneumonic  purulent  pleurisy 
applies  to  the  primary  cases  which  supervene  without  previous  pneumonia. 

In  addition  to  the  metapneumonic  form,  we  also  see  early  cases  in  which 
the  effusion  appears  at  the  same  time  as  the  pneumonia.  Lemoine  has 
given  them  the  name  of  "  parapneumonic."  We  must  not  forget  the  cases 
of  aseptic  puriform  pleurisy ;  they  must  not  be  confused  with  the  septic 
forms  of  pleurisy. 

Purulent  Pleurisies  due  to  Staphylococci. 

*'  The  Staphylococcus  pyogenes,  which  plays  such  an  important  part 
in  suppuration  of  the  cellular  tissue,  the  glands,  and  the  bones,  has  only 
relatively  a  small  share  in  the  aetiology  of  pleural  suppuration  "  (Netter). 
The  staphylococci  are  more  often  associated  with  other  microbes. 

The  rarity  of  purulent  staphylococcal  pleurisy  does  not  permit  us  to 
give  its  history.  It  is,  however,  important  to  know  that  a  staphylococcus 
has  been  found  in  effusions  which  have  remained  sero-fibrinous  ;  it  has  also 
been  found  in  the  fluid  of  sero-fibrinous  pleurisies  wliich  have  subsequently 
become  purulent  without  the  addition  of  fresh  microbes. 

Wounds  and  injuries  may  cause  purulent  pleurisy,  due  to  the  staphylo- 
coccus. The  Staphylococcus  aureus  may  spring  from  an  osteo-myehtis, 
anthrax,  or  suppurative  tonsilhtis  (Fraenkel).  It  cliiefly  invades  the  pleura 
of  those  who  offer  favourable  soil,  and  are  already  victims  to  typhoid  fever, 
scarlatina,  Bright's  disease,  overwork,  etc.  We  do  not  always  find  its 
point  of  entry  into  the  organism,  and  we  may  ask  if  the  microbe  did  not 
exist  in  a  latent  state,  awaiting  a  favourable  occasion  for  development. 

Tubercular  Purulent  Pleurisy. 

We  have  already  studied  sero-fibrinous  and  haemorrhagic  tubercular 
pleurisy,  and  we  may  therefore  turn  to  the  purulent  form.  Tliis  form  is  due 
to  the  tubercle  bacillus,  without  other  associated  microbes.    If  there  were 


I 


DISEASES  OF  THE  PLEURA  313 

other  bacilli,  the  condition  would  be  purulent  pleurisy  in  a  tubercular  patient, 
but  the  pleurisy  would  not  be  tubercular  in  the  true  sense  of  the  word.  The 
tubercular  form  only  comprises  about  a  tenth  of  the  cases  of  purulent  pleurisy. 

The  fluid  is  sero-purulent,  contains  very  little  fibrin,  and  is  dull  greenish, 
^\^th  a  powdery  sediment.  It  has,  then,  none  of  the  characters  of  the 
laudable  pus  of  pneumococcal  pleurisy.  The  purulent  fluid,  especially  in 
old  effusions,  may  be  fatty  and  chyliform.  Koch's  bacillus  may  be  dis- 
covered in  the  fluid.  If  the  disease  is  not  a  pure  infection,  other  pyogenic 
agents  are  found  in  varying  numbers. 

This  form  is  rarely  purulent  at  first ;  the  fluid  is  often  sero-fibrinous,  but 
is  particularly  rich  in  red  corpuscles  and  in  lymphocytes.  Later  the  fluid 
becomes  turbid  and  sero-purulent.  As  the  effusion  reforms  readily,  and  as 
puncture  has  at  times  to  be  repeated,  the  purulent  change  was  formerly  set 
down  to  thoracentesis,  whereas  the  change  is  really  due  to  the  fact  that  the 
puncture  has  been  made  at  different  stages  of  the  disease. 

The  chief  point  about  this  form  of  pleurisy  is  that  it  may  be  insidious, 
and  pass  through  its  phases  without  acute  symptoms.  It  corresponds  partly 
to  the  varieties  formerly  described  under  the  name  of  chronic  or  latent 
purulent  pleurisy,  which  may  last  for  "several  months  without  notable  change 
in  the  condition  of  the  patient. 

It  is  sometimes  accompanied  by  perforation  of  the  pleura  (pyopneumo- 
thorax), but  is  rarely  followed  by  vomica. 

The  diagnosis  of  tuberculosis,  in  the  case  of  purulent  pleurisy,  is  often 
difficult.  I  do  not  allude  to  those  patients  who  have  pulmonary  tuberculosis, 
with  or  without  pneumothorax,  for  the  nature  of  the  effusion  is  then  evident, 
but  I  refer  to  purulent  pleurisy  due  to  local  tuberculosis  of  the  pleura.  How 
Is  the  pathogenic  diagnosis  to  be  made  ?  The  tubercle  bacillus  is  looked  for 
in  the  fluid,  but  is  rarely  found,  and  we  must  therefore  have  recourse  to  the 
means  which  I  have  indicated  in  the  section  on  Sero-fibrinous  Tubercular 
Pleurisy. 

Inoculation  of  a  small  quantity  of  pus  into  the  mammilla  of  a  suckling 
guinea-pig  has  been  performed  by  Nattan-Larrier  in  six  of  my  cases.  The 
bacilli  pass  into  the  milk  after  five  to  ten  days,  and  show  the  tubercular 
nature  of  these  cases. 

Although  I  am  of  opinion  that  surgical  intervention  is  necessary  in  other 
varieties  of  purulent  pleurisy,  I  agree  with  most  authors  that  the  tubercular 
variety  should  usually  be  respected.  Thoracotomy  often  gives  bad  results. 
The  patient  should  be  treated  medically,  and  we  should  content  ourselves 
by  removing  the  excess  of  fluid  when  necessary  by  aspiratory  punctures. 


314  TEXT-BOOK  OF  MEDICINE 

Other  Purulent  Pleurisies. 

Other  microbes,  such  as  Micrococcus  pyogenes  tenuis  (Rosenbach), 
pneumo-bacillus  of  Friedlander,  Micrococcus  tetragenus  (Netter),  bacillus  of 
typhoid  fever  (Rendu  and  De  Gennes),  the  coli  bacillus,  may  cause  puru- 
lent pleurisy.  Appendicular  pleurisy  will  form  the  subject  of  a  special 
section. 

In  many  conditions  several  pathogenic  agents  are  associated  ;  when  these 
secondary  infections  are  superadded  they  deprive  the  pure  forms  of  their 
proper  appearance — I  might  almost  say  of  their  specific  nature.  The  result 
is  multiple  clinical  types,  without  well-determined  characters  and  course. 


VI.  ASEPTIC  PURIFORM  EFFUSIONS  INTO  THE  PLEURA— 
INTEGRITY  OF  THE  POLYNUCLEAR  CELLS. 

Puriform  effusion  is  not  always  synonymous  with  septic  effusion,  as  we 
see  clinically  that  turbid  liquids  may  remain  sterile  throughout  their  whole 
course.  Aseptic  pus  does  not  involve  the  grave  prognosis  of  microbic  pus  ; 
this  distinction  must  be  carefully  recognized. 

Bacteriology  shows  the  absence  of  micro-organisms  in  aseptic  pus,  but 
Widal  has  emphasized  a  special  characteristic  in  the  puriform  fluid  from 
the  meninges  or  the  pleura  ;  this  characteristic  is  the  integrity  of  the  poly- 
nuclear  cells.  When  the  fluid  is  septic,  the  polynuclear  cells  are  damaged 
in  the  fight  against  the  microbes  and  their  toxines,  the  nucleus  and  the 
protoplasm  being  altered.  This  result  follows  from  Metchnikoff's  laws  of 
phagocytosis.  In  aseptic  puriform  fluids,  on  the  other  hand,  the  polynuclear 
cells  show  no  change  either  in  the  nucleus  or  in  the  protoplasm. 

In  recent  years  we  have  seen  several  cases  at  the  Hotel-Dieu.  I  give  a 
summary : 

1.  Woman  admitted  for  apical  pneumonia.  Defervescence  had  3et  in,  when  a  band 
of  dulhiess  was  foimd  at  the  right  base.  Aseptic  serous  fluid  on  puncture.  Second 
puncture  three  days  later,  as  effusion  had  increased  ;  puriform  fluid  drawn  off.  We 
might  have  thought  of  parapneumonic  empyema,  but  the  fluid  was  sterile.  Numerous 
films  showed  that  the  polynuclear  cells  were  unchanged.  The  fluid  was  absorbed  with 
great  rapidity,  and  four  days  later  we  had  much  difficulty  in  obtaining  a  few  drops  of 
fluid  which  had  not  become  serous. 

2.  Man  admitted  for  bastard  pneumonia  at  the  left  base.  Onset  was  sudden,  with 
rigor  and  temperature  of  105°  F.  Dullness,  increased  vocal  fremitus,  tubular  breathmg, 
and  fine  subcrepitant  rales.  The  disease  stopped  short  on  the  fifth  day,  and  the  tem- 
perature fell  to  normal.  It  rose  again  on  the  seventh  day  to  101°  F.,  but  the  patient 
did  not  appear  worse,  and  his  breathing  was  not  quickened.  The  rales  at  the  left  base 
disappeared,  but  distant  tubular  breathing  was  audible  on  expiration.  Vocal  fremitus 
abolished.  Exploratory  puncture  drew  off  turbid  fluid  like  that  seen  in  acute 
rheumatism.  The  fluid  was  centrifugalized  ;  some  macrophages  and  many  intact 
polynuclear  cells  with  granulations  that  took  the  triacid  stain,  were  found.      The 


DISEASES  OF  THE  PLEURA  315 

glycogenic  reaction  was  very  clear.     Cultures  were  negative.     The  case  was,  therefore, 
one  of  aseptic  puriform  effusion. 

Next  day  the  effusion  had  almost  disappeared,  and  two  days  later  an  explora- 
tory puncture  was  negative. 

Widal  and  Gougerot  have  found  aseptic  puriform  effusions  in  the 
course  of  pneumonia,  or  after  pulmonary  infarcts  of  cardiac  origin.  In  the 
case  of  pneumonia  the  integrity  of  the  polynuclear  cells  prevents  confusion 
between  aseptic  puriform  effusion  and  septic  effusion  due  to  the  pneumo- 
coccus  ;  this  fact  has  an  important  bearing  on  the  course  and  the  prognosis 
of  the  effusion.  Thus,  in  one  of  their  patients  with  pneumonia  4  ounces  of 
turbid  fluid  were  drawn  off  on  the  seventh  day  of  the  disease  ;  the  polynuclear 
cells  were  normal.  The  signs  of  effusion  had  disappeared  by  the  tenth 
day,  and  two  days  later  punctures  were  negative ;  the  puriform  fluid  was 
aseptic.  In  another  case  purulent  fluid,  with  normal  polynuclear  cells,  was 
drawn  off  on  the  fourth  day.  On  the  ninth  day  some  friction  sounds  were 
still  audible,  but  disappeared  a  few  days  later. 

The  pleuritic  fluid  in  cardiac  cases  is  usually  limpid  in  spite  of  the 
presence  of  endothelial  and  polynuclear  cells,  which  indicate  congestion  of 
the  subjacent  lung.  In  asystole,  however,  we  may  find  turbid  fluid  after 
the  appearance  of  a  centre  of  pulmonary  apoplexy,  which  shows  itself 
clinically  by  blood-stained  sputum. 

Aseptic  puriform  fluid  has  sometimes  the  yellowish  colour  of  old  pus,  at 
other  times  the  whitish  tinge  of  recently  formed  pus.  A  fibrinous  clot  nearly 
always  forms  on  standing.  When  the  previous  tinge  was  very  opaque,  the 
clot  gives  the  hquid  a  puriform  tint ;  when  the  tinge  was  simply  whitish,  the 
clot  imprisons  in  its  meshes  nearly  all  the  scattered  cells  ;  it  then  forms  a 
milky-looking  mass,  which  floats  in  clear  fluid. 

The  homogeneous  nature  of  the  protoplasm,  which  is  finely  granular,  and 
the  clear  outline  of  the  nucleus,  wliich  is  rounded  and  punched  out,  show 
clearly  the  integrity  of  the  polynuclear  cells.  Staining  with  hsomatin-eosin, 
after  fixation  with  alooliol  and  drying  in  the  air,  of  the  sediment  smeared 
over  a  slide,  gives  the  diagnosis. 

The  turbid  appearance  is  due  to  the  accumulation  of  polynuclears  which 
have  remained  normal  after  passing  out  of  tlie  bloodvessels  by  diapedesis. 
The  appearance  of  aseptic  puriform  pleurisy  in  cardiac  cases  with  pulmonary 
apoplexy  proves  tliis  congestive  origin.  The  marked  subpleural  congestion 
which  an  infarct  determines,  causes  in  the  bloodvessels  stasis  of  the  red  cor- 
puscles, which,  being  endowed  with  passive  movement,  can  only  pass  out  by 
effraction  through  stoniata  produced  by  the  diapedesis  of  the  white  corpuscles. 
By  reason  of  their  amoeboid  movement  the  polynuclear  cells  pass  through  the 
capillary  walls  and  the  endothelial  barrier,  and  fall  intact  into  the  ])l(Miral 
fluid,  where  they  may  collect  in  such  numbers  as  to  make  the  effusion  ( urhid. 
The  congestion  is  often  so  acute  that  it  induces  exudation  of  numerous  red 


316  TEXT-BOOK  OF  MEDICINE 

corpuscles,  or  even  rupture  of  capillaries  ;  the  colour  of  the  red  corpuscles  then 
effaces  the  white  tinge  given  by  the  polynuclear  cells  when  they  are  alone 
present  in  the  liquid. 

We  see,  in  any  case,  that  a  kind  of  selection  may  be  estabUshed  between 
the  walls  of  the  capillaries  and  the  endothehum  of  the  pleura,  and  that,  in  a 
somewhat  paradoxical  manner,  the  red  congestion  of  the  parenchyma  may 
end  in  a  white  exudate  from  the  serosa. 

Widal  has  thus  explained  the  origin  of  these  puriform  effusions.  The 
asepsis  of  an  effusion  which  has  developed  near  an  infectious  centre  of 
pneumonia  appears  paradoxical  at  first  sight,  but  it  can  be  explained  by  the 
fact  that  the  polynuclear  cell  may  arise  from  the  excessive  hypersemia  of  the 
subjacent  tissues. 

An  aseptic  effusion  which  develops  near  a  patch  of  pneumonia  is  not 
specific,  but  only  correlative  to  a  pulmonary  infection ;  it  is  the  result  of  peri- 
inflammatory  congestion,  and  is  only  an  evidence  of  a  congestive  condition, 
and  must  be  carefully  distinguished  from  the  septic  eSusion  caused  by 
invasion  of  pneumococci,  which  damage  the  polynuclear  cells  of  the  defence. 

We  can  experimentally  produce  aseptic  white  exudates  similar  to  those 
which  develop  spontaneously  in  the  human  serous  membranes.  Amicrobic 
puriform  effusions  may  be  produced  by  injection  of  aseptic  broth  into  the 
peritoneum  of  guinea-pigs.  The  turbidity  of  these  experimental  exudates  is 
due  to  the  accumulation  of  numerous  polynuclear  cells,  which  have  so 
preserved  their  shape  and  functions  that  they  can  perform  in  vitro  their 
usual  phagocytic  action.  This  method  is  used  in  the  laboratory  to  collect 
Hving  leucocytes. 

A  striking  opposition  is  seen  between  the  cause  of  aseptic  puriform  and 
purulent  or  sero-purulent  microbic  effusions.  The  former  are  as  transitory 
as  the  subjacent  congestion  which  causes  them  ;  they  disappear  in  a  few  days. 

The  pubHshed  cases  of  purulent  pleurisy,  which  has  appeared  in  the 
course  of  pneumonia,  and  has  been  cured  by  simple  puncture,  hke  those 
cases  of  cerebro -spinal  meningitis  which  seem  to  recover  after  lumbar 
puncture,  are  most  often  cases  of  aseptic  suppuration  in  which  the  poly- 
nuclears  are  normal. 

When  we  are  studying  the  pus  in  a  case  of  pleurisy,  we  must  make  both  a 

bacteriological  and  also  a  cytological  examination  in  order  to  ascertain  the 

condition  of  the  polynuclear  cells.     If  we  find  intact  leucocytes*  we  know  at 

once  that  the  fluid  is  aseptic  and  the  prognosis  is  benign. 

*  The  integrity  of  the  polynuclears  may  be  shown  by  the  glycogenic  reaction 
which  was  discovered  by  Ehrlich,  and  depends  on  the  mahogany  staining  which  iodine 
vapours  cause  in  certain  cells.  It  is  most  marked,  as  Loeper  has  shown  (Arch,  de  Mede- 
cine  experimentale,  Juillet,  1903),  in  leucocytes  from  cases  of  puriform  pleurisy,  and  much 
less  so  in  the  altered  cells  from  cases  of  empyema.  In  difficult  oases  the  discovery  of 
glycogenesis  by  the  leucocytes  in  the  exudate  may  be  of  service. 


DISEASES  OF  THE  PLEURA  317 

Too  much  attention  cannot  be  paid  to  the  examination  of  turbid 
effusions,  which  are  puriform.  We  have  no  means  of  telUng  at  first  sight 
whether  they  are  septic  or  aseptic.  And  yet  this  fact  is  the  key  of  the 
situation.  If  a  puriform  effusion  is  aseptic,  the  prognosis  is  good — no  risk 
of  vomica  exists,  no  need  arises  for  surgical  intervention,  and  rapid  recovery 
follows. 

On  the  other  hand,  if  the  puriform  effusion  is  septic,  it  is  more  or  less 
serious,  and  surgical  intervention,  instead  of  simple  thoracentesis,  is  most 
often  required. 

VII.  PULSATING  EMPYEMA. 

The  question  of  pulsating  empyema  has  given  rise  to  numerous  works.* 
I  have  devoted  two  lectures  to  it,  and  Comby  in  Ms  writings  has  called 
this  disease  pulsating  empyema,  or  pulsating  pleurisy.  The  former  term 
appears  to  me  preferable,  for  it  indicates  that  the  effusion  is  purulent.  On 
careful  search,  however,  exceptions  might  be  found.  Out  of  about  sixty 
cases  of  pulsating  effusions,  three  or  four  might  be  cited  in  which  the  fluid 
was  not  purulent,  but,  on  closer  scrutiny,  some  of  these  cases  should  be 
revised.  The  case  reported  by  Rummo  is  one  of  hsemorrhagic  pulsating 
pleurisy ;  a  case  reported  by  Comby  is  one  of  pulsating  pleurisy, 
called  serous,  although  the  fluid  on  the  second  puncture  was  purulent. 
In  one  of  Lepine's  cases  the  fluid  was  serous,  but  slightly  turbid.  Piussan 
speaks  of  a  patient  in  whom  pulsations  were  discovered  on  ausculta- 
tion of  the  thorax,  and  admits  the  existence  of  serous  pleurisy  ;  but  "  the 
diagnosis  was  uncertain,  as  thoracentesis  was  rejected."  This  case  is  not 
clear.  It  is  evident,  then,  that  these  exceptional  cases  are  of  very  Uttle  con- 
sequence :  pulsating  pleurisy,  with  serous  fluid,  is  extremely  rare  ;  the  fluid 
is  nearly,  if  not  always,  purulent,  so  that  the  term  **  pulsating  empyema  " 
should  be  retained. 

Another  important  fact  is  that  pulsating  empyema  is  always  found  on 
the  left  side  ;  in  sixty-nine  cases,  I  know  only  one  exception  to  this  rule. 
We  may  therefore  state  that  pulsating  effusions,  with  very  few  exceptions, 
arc  purulent,  and  occupy  the  left  pleura. 

Description. — Every  case  has  two  periods — the  one  of  purulent  pleurisy, 
with  or  without  pneumothorax,  which  lasts  for  weeks  or  months,  and  shows 
no  sign  of  pulsation;  and  the  other, in  which  pulsations  occur,  with  or  without 
an  extrathoracic  pulsating  tumour. 

Every  left-sided  empyema,  whether  it  be  tubercular,  streptococcal, 
pneumococcal,  etc.,  may  finally  pulsate  ;  the  pleurisy  must,  however,  occupy 
the  great  pleural  cavity,  and  be  accompanied  by  much  effusion.     When  the 

*  Diculafoy,  Clinique  Medicare  de  PHdtelDieu,  1898,  p.  118. 


318  TEXT-BOOK  OF  MEDICINE 

effusion  is  scanty  and  encysted,  we  do  not,  as  a  rule,  see  pulsating  empyema. 
In  some  cases  the  pleurisy  has  been  preceded  by  pneumonia  (my  first 
patient) ;  in  others  it  is  primary  (my  second  patient) ;  it  is  often  consecutive 
to  pneumothorax.  Whether  the  pleurisy  is  primary  or  secondary,  and  its 
onset  insidious  or  acute  with  fever  and  pain,  there  is  a  more  or  less  lengthy 
stage,  during  which  we  find  only  the  signs  of  a  left  effusion,  with  or  without 
pneumothorax.  These  signs  vary  according  to  the  quantity  of  fluid,  and 
to  the  presence  or  the  absence  of  pneumothorax.  We  find  here,  as  in  every 
case  of  effusion :  dullness,  diminution  or  aboHtion  of  vocal  fremitus,  absence 
of  vesicular  murmur,  tubular  breatliing,  segophony,  and  sometimes  also 
aphonic  pectoriloquy  and  displacement  of  the  heart  (the  pleurisy  being  on 
the  left  side).  These  signs  are  modified  according  to  the  amount  of  the 
effusion.  If  we  add  oedema  of  the  chest-wall,  which  is  frequent  in  purulent 
effusions,  we  have  the  picture  of  empyema  before  the  appearance  of  pulsation. 

During  the  first  phase  the  general  condition  of  the  patient  varies  to  a 
marked  degree.  In  one  case  fever  persists  without  remission,  perspiration 
is  abundant,  appetite  absent,  and  wasting  rapid.  In  another  case  the 
effusion  behaves  like  a  cold  abscess,  without  pain  or  reaction ;  fever  is 
absent,  or  nearly  so  ;  the  appetite  remains  good  ;  the  patient  attends  to  his 
business,  having  but  httle  distress,  and  only  ceases  doing  so  when  the  efiusion 
is  so  large  as  to  hamper  the  breathing. 

Purulent  pleurisy,  as  I  have  said  above,  is  fairly  often  associated  with 
pneumothorax.  The  latter  may  have  formed  insidiously,  without  dyspncea 
or  pain ;  or  it  may  have  been  sudden,  with  pain  and  dyspnoea.  However 
this  may  be,  we  recognize  pyopneumothorax  by  the  usual  signs,  including 
hippocratic  succussion.  The  duration  of  the  first  stage  is  very  variable, 
and  the  general  condition  of  the  patient  depends  upon  many  causes. 

Let  us  come  to  the  second  phase.  We  find  here  the  characteristic  sign 
of  pulsation.  I  must  divide  the  description  of  pulsating  empyema,  for  an 
extrathoracic  tumour  may  or  may  not  be  present. 

Let  us  first  consider  the  first  condition.  On  examining  a  patient  with 
effusion,  we  are  quite  surprised,  on  auscultation  or  palpation,  to  find  pulsa- 
tions in  some  unusual  area.  Whether  tliis  area  is  behind,  at  the  lower  part 
of  the  chest,  in  front  near  the  sternum,  or  at  the  side,  we  feel  pulsation  Hke 
that  of  a  large  aneurysm.  When  the  hand  is  apphed  over  the  beating 
region,  the  pulsation  shows  itself  by  a  shock,  without  a  thrill.  On  ausculta- 
tion, the  beating  is  transmitted  quite  clearly  to  the  ear,  and  is  isochronous 
with  the  arterial  pulse,  though  blowing  and  smacking  sounds  are  absent. 
On  careful  inspection  of  the  pulsating  area,  we  generally  see  a  movement  of ; 
undulation,  or  of  uplifting. 

Many  cases  of  pulsating  empyema,  without  external  tumour,  have  been 
pubUshed.     I  give  a  resume  of  one  of  Traube's  cases  : 


DISEASES  OF  THE  PLEURA  319 

A  young  man  admitted  for  left  pleurisy.  Costo -sternal  plastron  bulged  ;  chest -wall 
oedematous  ;  dullness  complete,  and  heart  much  displaced  to  the  right  side.  Further, 
the  left  side  of  chest,  from  the  second  to  the  sixth  intercostal  space,  was  raised  up  by 
pulsations  that  were  isochronous  with  the  carotid  pulse.  It  was  a  case,  therefore,  of 
pulsating  empyema,  as  the  autopsy  proved. 

In  this  variety,  I  repeat,  the  beats  of  the  pulsating  empyema  are  percep- 
tible on  inspection,  palpation,  and  auscultation,  and  may  extend  over  a 
very  large  part  of  the  thorax,  but  there  is  no  tumour  in  the  true  sense  of  the 
word. 

In  the  more  common  form  of  pulsating  empyema,  we  find  that  the  pus 
passes  through  an  intercostal  space,  forms  a  prominence  under  the  skin, 
and  gives  rise  to  an  expanded  or  rounded  tumour ;  this  variety  occurred 
in  two  patients  at  the  Hotel-Dieu. 

A  man,  twenty-seven  years  of  age,  admitted  for  pneumonia  of  the  left  lung.  Friction 
sounds  were  also  heard.  The  expected  crisis,  however,  did  not  occur.  The  pneumonic 
phase  was  succeeded  by  a  fresh  subintrant  one,  with  ill-defined  signs.  The  patient 
was  feverish,  had  night-sweats,  and  the  case  began  to  look  Uke  one  of  tuberculosis. 
The  breathing  was  tubular,  and  the  rales  did  not  disappear.  The  idea  of  tubercular 
pneumonia  was  natural,  and  yet  the  expectoration  contained  no  Koch's  bacilli. 

Dullness  gradually  became  marked  at  the  left  base,  and  later  in  the  left  axilla. 
Normal  respiration  and  vocal  fremitus  disappeared  at  these  points.  The  patient  had 
dyspnoea  ;  the  heart  was  displaced  to  the  right ;  fluid  began  to  collect  ;  and,  although 
there  was  no  oedema  of  the  chest-wall,  it  was  probable  that  the  fluid  was  purulent. 
A  new  episode  occurred.  The  patient  felt  sharp  pain  on  the  left  side,  near  the  sternum, 
which  was  increased  by  attacks  of  cough.  Nothing  could  be  seen,  but  on  pressure 
the  ribs  were  as  painful  as  though  affected  by  acute  osteitis.  During  the  next  few  days 
a  swelling  appeared,  and  formed  a  prominent  tumour,  about  as  large  as  the  palm  of 
the  hand.  The  tumour  showed  expansile  pulsation,  and  its  beats  were  synchronous 
with  the  cardiac  systole  ;  it  might  hav^e  been  thouglit  that  a  large  aortic  aneurysm  had 
developed  near  the  sternum.  On  auscultation,  blowing  and  smacking  sounds  were 
not  perceptible. 

While  the  pulsating  tumour  enlarged,  the  effusion  made  progress.  The  whole  diag- 
nosis became  clear  :  we  had  to  deal  with  pulsating  empyema,  consecutive  to  meta- 
pneumonic purulent  pleurisy.  I  punctured  the  tumour,  and  drew  off  homogeneous 
creamy  pus,  due  to  the  pneumococcus.  Bacteriological  examination  showed  pncumo- 
cocci,  without  other  microbes  ;  cultures  gave  the  same  result,  and  inoculation  of  a  mouse 
showed  that  the  pus  was  not  veiy  virulent.  The  case,  therefore,  was  pulsating 
empyema,  with  external  tumour.  The  purulent  collection  in  the  pleura  had  made  ita 
way  through  the  intercostal  space,  and  formed  a  tumour  at  the  upper  part  of  the  thorax. 
The  ribs  were  resected,  and  some  weeks  later  the  patient  was  completely  cured. 

Resume  of  the  second  case  : 

A  man  admitted  to  the  Hdtel-Dieu  for  left  pyopneumothorax,  which  contained 
much  fluid  and  but  little  air.  During  the  next  few  days  the  effusion  increased  in  amount. 
As  the  fluid  in  the  phnira  increased,  the  succussion  sj)lash  became  less  marked  ;  the 
dyspncea  increased  ;  the  dullness  occupied  two-tiiirds  of  the  chest,  but  fedema  of  the 
walls  was  absent  ;  and  as  the  patient  himself  begged  for  puncture,  1  evacuated 
2  pinta  of  fluid.  The  pus  was  thick,  greenish,  liomogeneous,  and  (|uite  odourless  ;  it 
resembled  ])neumococcal  pus,  but  microscopical  examination  and  cultures  showed  the 
absence  of  the  pneumococcus,  and  revealed  the  exclusive  presence  of  the  streptococcus 


320  TEXT-BOOK  OF  MEDICINE 

in  small  numbers.  I  tested  the  virulence  of  this  streptococcus.  A  rabbit,  injected  with 
6  centimetres,  showed  some  reaction,  but  recovered  completely  ;  the  streptococcus, 
therefore,  was  not  virulent.     Inoculation  in  guinea-pigs  did  not  cause  tuberculosis. 

The  patient  improved,  but  the  liquid  gradually  re-formed,  and  enlargement  of  the 
thorax,  dullness,  dyspnosa,  and  loss  of  appetite  reappeared. 

One  morning  he  could  not  lie  down  on  his  left  side  because  his  ribs  were  so  painful. 
We  made  him  sit  up  in  his  bed,  examined  the  left  side,  and,  at  the  level  of  the  ninth 
and  tenth  intercostal  spaces  found  a  small  rounded  swelling,  which  stood  out  like  a 
hernia.  It  was  not  painful  per  se,  but  a  deep  pain,  which  reached  back  as  far  as  the 
shoulder,  was  felt  on  firm  compression.  Our  first  idea  was  that  the  effusion  was  making 
its  way  through  an  intercostal  space.  Next  day  the  tumour  was  more  extensive,  and 
reached  as  high  as  the  eighth  intercostal  space.  When  it  was  examined  by  daylight, 
we  saw  slight  pulsation,  and  also  felt  it  on  placing  the  hand  lightly  upon  the  surface 
of  the  tumour.  There  could  now  be  no  doubt  as  to  the  diagnosis  :  the  patient  was 
suffering  from  pulsating  empyema. 

During  the  next  few  days  the  pulsation  became  very  clear.  The  tumour  pulsated, 
but  was  not  expansile  ;  it  was  not  reducible,  but  since  pressure  was  very  painful,  we 
made  no  great  attempt  at  reduction.  I  performed  aspiration  in  the  sixth  space,  above 
the  tumour,  and,  as  the  pus  was  evacuated,  the  tumour  diminished  in  size,  proving  that 
it  communicated  with  the  pleural  cavity.  Next  day  4  more  pints  of  fluid  were  drawn 
off  ;  the  pus  was  again  homogeneous,  greenish,  and  odourless.  In  consequence  of  this 
fresh  evacuation,  however,  the  pulsating  tumour  disappeared.  After  a  few  days' 
respite,  the  fluid  formed  again,  and  the  pulsating  tumour  reappeared. 

From  the  day  of  admission,  I  had  asked  myself  whether  surgical  intervention  should 
not  be  employed,  because  the  condition  was  not,  in  my  opinion,  curable  by  simple 
puncture.  I  was  afraid,  too,  that  the  great  pleural  cavity,  which  was  so  far  but  httle 
affected,  might  become  a  centre  of  secondary  infection.  The  patient,  however,  would 
not  hear  of  an  operation  ;  the  pimctures  were  enough  for  him,  and  he  would  have  left 
the  hospital  if  I  had  tried  to  bring  further  pressure.  I  may  add,  also,  that  after  mature 
reflection  I  did  not  feel  confident  as  to  the  result  of  an  operation,  which  would  have 
been  performed  under  bad  conditions.  The  disease  was  of  seven  and  a  half  months' 
standing  ;  the  lung  would  be  reduced  to  a  carnified  adherent  stump,  surrounded  by 
adhesions,  and  incapable  of  resuming  its  functions.  How  was  it  possible,  even  by  re- 
moving a  large  number  of  ribs,  for  this  immense  cavity  to  fill  up  ?  and  if  the  patient 
were  tubercular,  as  appeared  very  probable,  how  would  his  economy  stand  such  a  drain 
on  the  system  ?  Evidently,  the  wisest  thing  was  to  hold  one's  hand  ;  and  the  patient 
made  this  decision  easy,  for  he  absolutely  refused  to  hear  of  an  operation.  Palliative 
treatment  was  therefore  resorted  to,  and  aspiration  performed  every  twelve  or  fourteen 
days. 

As  he  wished  to  return  to  Venice,  a  final  puncture  was  made,  in  order  to  put  him  in 
the  best  condition  for  his  journey,  and  4  pints  of  the  same  homogeneous  greenish  pus 
were  drawn  off. 

In  these  cases,  the  interesting  fact,  from  the  pathogenic  point  of  view,  is 
that  the  patient  had  pneumothorax  and  pulsating  empyema.  In  the  one 
the  empyema  was  of  recent  date,  and  associated  with  the  pneumococcus ; 
he  recovered.  In  the  other  the  empyema  was  of  old  date,  and  associated 
with  a  streptococcus  of  slight  virulence.  This  man,  who  was  probably 
tubercular,  would  have  died,  even  if  he  had  decided  to  undergo  an 
operation. 

We  may  now  discuss  the  sahent  features  of  pulsating  empyema.  The 
passage  of  pus  from  the  pleura  into  the  intercostal  space  is  sometimes 


DISEASES  OF  THE  PLEURxl  321 

heralded  by  sharp  pain.  I  am  indeed  surprised  that  this  pain,  which 
announces  the  exteriorization  of  pulsating  empyema,  has  not  attracted 
more  attention.  My  second  patient  had  very  sharp  pain  in  the  seventh 
intercostal  space  before  any  tumour  appeared  externally.  In  my  first 
patient  the  pains  were  still  more  acute,  preceded  the  subclavicular  indura- 
tion by  three  days,  and  were  so  severe  that  they  simulated  acute  osteo- 
periostitis. Injections  of  morphia  and  fomentations  night  and  day  were 
necessary  to  reheve  these  pains.  The  appearance  of  the  purulent  pocket 
shows  itself,  then — at  least,  in  the  cases  which  I  have  seen — by  pain.  The 
tumour  does  not  always  pulsate  as  soon  as  it  forms  :  in  the  second  case  pulsa- 
tions did  not  appear  until  the  third  day,  and  only  became  manifest  on  the 
fourth  day  in  the  first  case. 

The  pulsating  tumour  is  sometimes  spread  out,  at  other  times  rounded  ; 
and,  when  once  formed,  may  be  the  size  of  a  nut,  of  an  orange,  or  larger. 
In  some  cases  it  resembles  an  aneurysm,  and  shows  expansile  pulsation  ; 
on  grasping  it,  it  feels  just  Hke  a  large  aneurysm.  The  expansile  movements 
of  the  tumour,  though  doubted  by  some  authors,  are  nevertheless  marked  in 
most  cases ;  they  were  fairly  clear  in  my  second,  and  undeniable  in  my 
first  patient.  I  am  therefore  of  Bouveret's  opinion  :  "  Though  an  intra- 
pleural pulsating  empyema  presents  scarcely  any  lifting  movements,  an 
extrapleural  one  shows  true  expansile  pulsation.  It  is  quite  comparable  to 
the  pulsation  of  an  aneurysm.  With  each  beat  of  the  heart  the  whole 
surface  of  the  tumour  dilates  suddenly,  and  beats,  not  only  vertically,  but 
also  transversely." 

In  some  cases  the  tumour  is  reducible,  and  we  can  squeeze  the  pus  back 
into  the  pleural  cavity.  Auscultation  reveals  neither  blowing  nor  smacking 
sounds. 

The  tumour  may  develop  at  different  points,  either  behind  or  in  front 
of  the  chest,  but  its  usual  situation  is  to  the  left  of  the  sternum,  at  the  level 
of  the  third  and  fourth  space.  This  was  the  case  in  my  first  patient,  and  the 
same  localization  was  found  in  a  case  reported  by  Berard. 

A  young  man,  after  an  acute  disease,  noticed  a  tumour  developing  rapidly  in  the 
front  of  the  chest,  at  the  left  of  the  sternum.  This  tumour  showed  movements  of 
expansion  and  contraction  synchronous  with  those  of  the  puLse.  The  apex -l)cat  was 
under  the  right  clavicle.  Everyone  thought  of  an  aneurysm,  and  await<^d,  with  dread 
the  moment  when  the  thin  skin  would  burst  and  give  rise  to  fulminant  ha'm(jrrhage. 

The  patient,  who  was  ignorant  of  his  condition,  impatiently  awaited  the  rupture  of 
"  his  abscess,'"  and,  wishing  to  hasten  the  work  of  Nature,  he  plunged  a  pin  into  tht;  apex 
of  the  tumour.  I'us  came  out  in  a  small  quantity  at  lirst,  and  later  in  abundance, 
when  ulceration  had  enlarged  the  wound.  I  have  seen  him  since,  enjoying  the  best  of 
health. 

In  this  case  it  seems  Ukely  that  the  pulsating  empyema  was  consecutive  to 
pneumococcal  pleurisy. 

21 


322  TEXT-BOOK  OF  MEDICINE 

The  tumour  of  pulsating  empyema  may  reach  the  lumbar  region,  as  in 
Courbon's  case  : 

A  young  woman  was  admitted  for  tumour  in  the  left  lumbar  region.  It  was  situated 
just  outside  the  quadratus  lumborum,  immediately  below  the  last  rib.  It  was  elongated, 
fluctuating,  but  not  painful,  and  was  almost  entirely  reducible  ;  there  was  no  change  in 
the  colour  of  the  skin.  The  swelling  had  the  form  of  an  elhpse  with  a  large  axis.  The 
noticeable  feature,  however,  was  the  beats  of  the  tumour,  which  were  expansile  and 
S3Tichronous  with  the  pulse.  The  whole  tumour  showed  alternate  dilatation  and  con- 
traction, perceptible  not  only  to  touch,  but  also  to  sight.  Palpation  revealed  no  thrill, 
and  auscultation  gave  no  blowing  murmur.  The  patient  had  noticed  this  tumour  for 
two  months  ;  for  four  years  her  health  had  been  imperfect,  and  she  had  experienced 
pain  over  the  left  dorsal  vertebrse,  radiating  to  the  left  side  of  the  thorax.  Dyspnoea, 
palpitations,  and  attacks  of  suffocation  came  on  as  soon  as  the  patient  worked  more 
than  usual  or  walked  upstairs. 

Some  months  after  the  onset  of  these  troubles  she  was  in  hospital  at  Blois  for  nearly 
a  year.  When  Courbon  saw  her,  her  heart  was  pushed  over  to  the  right,  and  the 
apex-beat  was  beneath  the  xiphoid  cartilage.  The  left  side  of  the  chest  was  distended, 
absolutely  dull  all  over,  and  silent  on  auscultation.  Courbon  hesitated  between  an 
abscess  of  the  pleura,  pointing  in  the  lumbar  region,  and  an  aneurysm  of  the  descending 
aorta.  He  finally  adopted  the  latter  opinion.  The  tumour  increased  in  size,  and  the 
pulsation  became  so  pronounced  that  those  who  had  hesitated  admitted  the  aneurysm. 
The  thin  skin  finally  burst,  giving  exit  to  a  large  quantity  of  pus  ;  the  tumour  at  once 
diminished  in  size,  the  pulsations  disappeared,  and  the  dullness  on  the  left  side 
diminished.     It  was,  in  short,  a  case  of  pulsating  empyema. 

In  the  following  case,  reported  by  Millard,  a  pulsating  empyema,  which 
simulated  an  aneurysm,  formed  a  tumour  in  the  left  dorsal  region. 

A  man,  thirty-six  years  of  age,  of  tubercular  stock,  and  subject  to  bronchitis,  was 
taken  ill  in  May,  1887,  A\ath  left  pleurisy,  comphcated  by  pneumothorax.  He  made  an  in- 
different recovery.  Some  months  later  dyspncea  and  fresh  signs  of  pneumothorax.  In 
July,  1888,  a  tumour,  which  rapidly  reached  the  size  of  an  orange,  appeared  to  the  left  of 
the  vertebral  column,  at  the  level  of  the  last  rib.  The  swelling  showed  pulsations,  synchro- 
nous with  the  pulse.  His  doctor  diagnosed  an  aneurysm  of  the  descending  aorta.  Millard, 
however,  recognized  the  existence  of  pulsating  empyema,  forming  an  external  tumour. 
He  admitted  the  patient  into  his  ward,  and  punctured  the  tumour,  drawing  off  7  pints 
of  creamy,  inodorous  pus.  The  swelling  became  smaller,  the  pulsations  at  once  disap- 
peared, and  the  patient  gained  much  relief.  Pleurotomy  did  not  appear  to  be  indicated, 
for  the  disease  was  of  fifteen  months'  standing,  and  Millard  preferred  to  resort  to  intra- 
pleural injections  of  tincture  of  iodine.  After  transient  improvement,  the  situation 
became  worse.  Peyrot  resected  the  ninth  rib,  and  drew  off  about  6  pints  of  foetid 
pus.  The  cavity  was  washed  out  several  times  a  day,  but  the  patient  became  rapidly 
feeble,  and  succumbed  to  hectic  fever,  with  colliquative  diarrhoea. 

I  have  just  described  two  varieties  of  pulsating  empyema.  In  the  first 
the  pulsations,  though  felt  externally,  remain  intrathoracic,  and  no  external 
tumour  forms  ;  in  the  second  variety  the  empyema  projects  under  the  skin, 
through  an  intercostal  perforation,  and  forms  a  pulsating  tumour,  which 
usually  appears  at  the  left  of  the  sternum. 

Pulsating  empyema  may  persist  for  a  long  time  without  spontaneous 
opening  of  the  collection ;  vomica  has,  however,  been  noted  in  some  cases. 


DISEASES  OF  THE  PLEURA  323 

The  purulent  collection  opens  into  the  bronchi,  and  the  vomica  differs  in 
no  respect  from  that  consecutive  to  purulent  pleurisies. 

Pathogenesis. — Such  are  the  cUnical  facts.  We  must  now  discuss  the 
pathogenesis,  but  I  shall  be  brief  on  this  question,  wliich  is  not  yet  elucidated. 
I  have  already  said  that  sero-fibrinous  pleurisy,  no  matter  how  abundant  the 
effusion  may  be,  never  pulsates.  I  have  seen  hundreds  of  cases,  and  studied 
them  closely — as  aspiration  has  particularly  attracted  my  attention — for 
nearly  thirty  years,  but  I  have  never  seen  pulsation  at  any  stage  of  sero- 
fibrinous pleurisy.  Purulent  pleurisy  is  practically  the  only  form  which 
shows  pulsation ;  when  it  does,  it  is  not  because  the  fluid  is  purulent,  but 
because  the  lesions  of  neighbouring  organs  favour  the  transmission  of  the 
cardiac  pulsation. 

According  to  Fereol,  pneumothorax  is  the  essential  factor  :  "  Pulsating 
empyema  can  be  produced  only  when  pneumothorax  of  small  extent  and  large 
effusion,  with  displacement  of  the  heart,  are  present.  It  is  the  elasticity  of  a 
compressible  gas  which  allows  this  movement  of  expansion  and  contraction." 
Fereol's  theory  is  shattered  by  the  fact  that  in  many  cases  of  pulsating 
empyema  (as  in  my  first  patient)  pneumothorax  may  be  absent.  Comby 
gives  another  theory  :  "  The  airless  and  compressed  lung  plays  the  part  of  a 
sounding-board  ";  but  the  author  declares  himself  "  ready  to  abandon  this 
theory  for  a  better  one."  Other  authors — Rummo,  Keppler,  Traube — ■ 
invoke  multiple  causes  :  intrapleural  pressure,  adhesions,  paresis  of  the 
intercostal  muscles,  exaggeration  of  the  cardiac  beats,  etc.  ;  but  all  these 
theories  are  so  open  to  criticism  that  we  are  not  absolutely  clear  on  the 
pathogenesis  of  pulsating  empyema. 

Diagnosis. — How  can  pulsating  empyema  be  recognized  and  dis- 
tinguished from  the  diseases  which  may  simulate  it  ?  The  diagnosis  must  be 
made  from  other  pulsating  Rumours  in  the  chest.  When  the  pulsation  is 
in  the  first  intercostal  space  to  the  left  of  the  sternum,  the  case  closely  simu- 
lates aneurysm  of  the  aorta,  causing  an  external  projection  ;  expansile  pulsa- 
tion, perceptible  to  sight  and  touch,  exists  in  both  cases.  Certain  differen- 
tial signs,  however,  exist.  In  empyema  the  pulsating  tumour  appears  in  a 
few  days,  almost  from  one  day  to  the  next ;  e.g.,  in  my  cases  the  tumour 
formed  showed  pulsations  on  the  fourth  day.  In  aortic  aneurysm  tlie 
tumour  takes  twenty  times  as  long  to  appear  ;  it  requires  months  for  the 
rarefying  osteitis  which  eats  away  the  ribs,  to  allow  the  aneurysm  to  project 
externally.  In  the  second  place,  a  patient  suffering  from  pulsating  empyema, 
whatever  be  the  situation  of  the  tumour,  always  has  a  large  left  pleural 
effusion,  with  or  without  ])n(!uni()tlior;ix.  The  signs  of  tliis  large  effusion, 
including  displacement  of  the  heart  to  the  right  side,  are  evident.  In 
the  case  of  aneurysm,  large  pleural  effusion  and  deviation  of  the  heart  to 
the  right  are  not  found.     Lastly,  the  murmurs  which  are  heard  over  the 

21—2 


324  TEXT-BOOK  OF  MEDICINE 

aneurysmal  sac  are  not  found  in  the  case  of  pulsating  empyema.  It  is 
evident,  then,  that  though  the  pulsations  produce  some  analogy  between 
aneurysm  and  pulsating  empyema,  methodical  examination  Avill  clear  up 
the  diagnosis. 

Pulsating  abscesses,  which  have  nothing  in  common  with  pulsating 
empyema,  may  be  met  with  in  the  chest.  Costal  or  costo-sternal  osteitis 
may  give  rise  to  an  ossifluent  abscess,  hke  a  sliirt-button,  which  develops, 
on  the  one  hand,  beneath  the  tissues  which  it  lifts  up,  and,  on  the  other  hand, 
beneath  the  parietal  pleura  which  it  pushes  in.  This  subpleural  collection 
does  not  involve  the  pleural  cavity,  but  it  may  nevertheless  be  placed  in  such 
a  position  that  the  heart-beat  is  transmitted  to  the  external  collection  of  pus 
which  bulges  under  the  skin,  and  the  tumour  acquires  expansile  pulsation, 
comparable  to  that  of  empyema.  We  are  able  to  distinguish  these  pulsating 
abscesses  fiom  empyema,  because  they  are  not  accompanied  by  signs  of 
pleural  effusion.  We  do  not  find  extensive  dullness,  absence  of  thoracic 
vibrations,  deviation  of  the  heart  to  the  right,  and  the  other  signs  of  left 
purulent  pleurisy,  vnih  or  without  pneumothorax. 

It  is  not  sufficient  to  diagnose  pulsating  empyema  ;  we  must  also  ascertain 
the  cause,  since  prognosis  and  treatment  are  equally  concerned.  As  a 
general  rule,  the  recognition  of  pneumothorax  in  a  case  of  pulsating  empyema 
is  a  sure  sign  of  tuberculosis,  excepting,  of  course,  'pneumothorax  consecu- 
tive to  vomica  or  to  operation.  The  search  for  bacilh  in  the  sputum  should 
never  be  neglected ;  their  absence,  however,  does  not  always  ehminate 
tuberculosis.  Recourse  may  be  made  to  injections  of  very  small  doses  of 
tubercuhu  (Grasset's  method)  ;  but  however  carefully  tubercuhn  be  used, 
we  may  sometimes  see  regrettable  incidents,  and  I  would  advise  it  only  in 
case  of  absolute  necessity. 

The  prognosis  of  pulsating  empyema  is  no|;  equally  serious  in  all  cases ; 
the  gravity  chiefly  depends  on  the  cause  of  the  disease.  Pulsating  empyema 
wliich  supervenes  in  a  tubercular  patient,  with  or  without  pneumothorax, 
is  the  more  serious,  because  surgical  intervention  leaves  httle  to  hope  for. 
It  is  often,  indeed,  contraindicated,  and  we  must  be  content  with  repeated 
punctures.  On  the  other  hand,  in  pulsating  empyema  wliich  supervenes  in 
an  individual  suffering  from  pneumococcal  f)leunsy,  the  prognosis  is  less 
grave,  because  surgical  intervention  gives  good  results. 

Treatment. — Pulsating  empyema  demands  surgical  intervention.  Re- 
peated punctures,  with  or  without  injections  of  antiseptic  fluid,  are  purely 
palhative  ;  they  prolong  the  existence  and  reheve  the  patient,  but  they  do 
not  cure  him.  In  some  cases  (pneumococcal  pleurisy)  pleurotomy,  without 
costal  resection,  might  perhaps  effect  a  cure,  but  I  should  have  but  Uttle 
confidence  in  it ;  most  often  it  is  necessary  to  resort  to  thoracotomy,  with , 
free  resection  of  ribs.     Tliis  latter  procedure  saved  my  patient. 


DISEASES  OF  THE  PLEURA  325 

\^II.  INTERLOBAR  PLELTllSY—VOmaE— INTERLOBAR 
HiEMOPTYSES. 

Interlobar  pleurisy  develops,  and  becomes  encysted  between  the  lobes 
of  the  lung.  The  lungs  are  divided  into  five  lobes — two  in  the  left,  three  in 
the  right  lung.  When  the  lung  is  examined,  after  removal  from  the  thorax, 
we  see  that  the  surface  is  furrowed  by  fissures  which  penetrate  deeply,  as  far 
as  the  hilum,  and  di\'ide  it  into  distinct  lobes,  which  are  isolated,  and,  as  it 
were,  suspended  from  the  large  bronchi. 

On  the  left  side  there  is  only  one  interlobar  fissure,  which  begins  belli nd, 
about  3  inches  below  the  apex,  round  which  it  passes,  descending  very 
obhquely  downwards  and  outwards  as  far  as  the  base.  The  left  lung  is  thus 
divided  into  two  lobes — an  upper  and  a  much  larger  lower  one.  On  the 
right  side  the  interlobar  fissure  has  the  same  origin  as  that  on  the  left, 
but  it  soon  bifurcates,  forming  a  kind  of  cross  at  its  bifurcation.  One  branch 
continues  an  almost  horizontal  course,  while  the  other  passes  round  the  lung 
and  descends  obliquely  outwards  as  far  as  the  base.  The  right  lung  is  thus 
divided  into  three  lobes,  the  middle  lobe  being  the  smallest  and  the  lower  one 
the  largest. 

The  visceral  pleura  enters  these  fissures,  and  covers  the  corresponding 
surfaces  of  the  lobes  of  the  lung  ;  for  this  reason,  it  has  been  called  the  inter- 
lobar pleura.  When  adhesions  unite  the  edges  of  a  fissure,  and  the  inter- 
lobar pleura  no  longer  communicates  with  the  pleural  cavity,  we  find  an 
interlobar  sac,  which  favours  the  formation  of  encysted  pleurisy.  The  sac 
nearly  always  contains  pus,  as  Laennec  has  shown,  and  on  section  simulates 
at  first  sight  a  collection  in  the  lung. 

Interlobar  pleurisy  may  be  very  extensive,  and  occupy  the  whole  of  an 
interlobar  space  ;  in  such  a  case  the  neighbouring  lobes  are  much  compressed, 
and  the  encysted  fluid  amounts  to  2  or  more  pints.  In  some  cases,  on  the 
contrary,  adhesions  partition  off  the  interlobar  cavity,  and  the  encysted 
fluid  does  not  exceed  some  6  or  8  ounces.  Indeed,  in  a  recent  autopsy  we 
happened  to  find  several  small  interlobar  abscesses  which  contained  oiijy  a 
few  drachms  of  pus.  It  is  evident,  then,  that  every  intermediate  form  may 
occur  between  interlobar  pleurisy  with  much  effusion  and  small  interlobar 
abscesses. 

The  topography  of  interlobar  pleurisy  is  very  variable.  The  following 
plates  show  the  situation  and  the  relation  of  the  interlobar  fissures  in  the 
normal  state.  The  first  plate- shows  the  lungs  from  their  posterior  aspect — 
the  loft  lung  with  its  single  interlobar  fissure,  and  the  right  one  with  its 
bifurcated  fissure. 

The  second  plate  shows  the  outer  sui'faces :  the  fissure  of  the  left  lung, 
which  is  almost  horizontal  looked  at  from  boliiiid,  now  de-scends  obliquely ; 


326 


TEXT-BOOK  OF  MEDICINE 


and  the  fissure  of  the  right  lung,  which  is  almost  horizontal  seen  from  behind, 
bifurcates,  and  of  its  two  branches,  viewed  laterally,  the  one  is  horizontal, 
the  other  is  oblique. 

Interlobar  pleurisy  is  not  always  locahzed  at  the  back  of  the  chest  to 
the  horizontal  fissure  ;  it  sometimes  occupies  the  axilla  at  the  level  of  the 
oblique  fissure,  and  may  descend  as  far  as  the  diaphragmatic  pleura. 


Fig.   16. — Posterior  View  of  the  Lungs. 

Description. — The  interlobar  form  may  be  primary  or  secondary  to 
pneumonia.  In  the  latter  case,  if  the  pleurisy  follows  the  pneumonic  infec- 
tion closely,  or  if  it  appears  in  the  course  of  pneumonia,  it  is  said  to  be  para- 
pneumonic ;  if  it  does  not  appear  till  some  days  or  weeks  after  pneumonia,  it 
is  said  to  be  post-  or  metapneumonic.  However  paradoxical  the  fact  may 
appear,  I  think  that  interlobar  pleurisy  is  more  often  primary  than  secondary. 
It  develops  on  its  own  account — or,  at  least,  apparently  so — whether 
the  infection  is  due  to  the  pneumococcus  or  to  other  microbes.  In  none  of 
the  eight  cases  which  I  have  quoted  in  my  lectures  at  the  Hotel-Dieu*  did 


Fig.  17. — The  Lobes  and  Fissxtkes  of  the  Lungs. 


interlobar  pleurisy  appear  to  follow  pneumonia,  and,  as  far  as  my  patients  were 
concerned,  I  am  quite  certain  that  there  was  no  pneumonia,  the  condition  of 
the  lung  having  been  verified  at  the  operation.  Moreover,  primary  infection 
of  the  serous  membrane  should  cause  no  surprise,  as  we  know  of  numerous 
examples.     Cases  of  primary  peritonitis,  pleurisy,  and  meningitis  are  at  the 

*  Dieulafoy,    "  La    Pleuresie    Interlobaire "  {Clinique    Medicale    de    V Hotet-Dieu, 
Ireet2™«  lemons,  1899). 


DISEASES  OF  THE  PLEURA  327 

present  day  counted  by  dozens  ;  interlobar  pleurisy  is  of  the  number,  and 
appears  to  me  to  begin  in  most  cases  as  a  primary  infection. 

The  present  description  will  not,  then,  apply  only  to  interlobar  pleurisy 
preceded  by  pneumonia,  but  will  especially  deal  with  primary  interlobar 
pleurisy.  Nothing  is-  more  difficult  to  make  out  than  the  onset  of  inter- 
lobar pleurisy.  Pain  in  the  side,  fever,  and  cough  indicate  that  acute  chest 
trouble  is  in  progress  ;  but  when  we  have  to  decide  the  nature  and  the  seat 
of  this  trouble,  we  have  no  exact  sign  to  guide  us.  Lobar  pneumonia  and 
pleurisy  of  the  great  pleural  cavity  are  very  different.  In  pneumonia,  rigor, 
crepitant  rales,  tubular  breathing,  and  rusty  sputum  indicate  the  diagnosis. 
In  pleurisy,  friction  sounds,  and  signs  of  effusion — i.e.,  dullness,  disappearance 
of  vocal  fremitus,  distant  tubular  breathing,  segophony,  etc. — show  us  the 
evolution  of  pleurisy.  If  the  case  is  one  of  inflammation  of  the  chest, 
the  bilateral  position  of  the  signs  ;  bronchitic  rales,  scattered  over  both  sides 
of  the  chest ;  friction  sounds,  which  bear  witness  to  the  participation  of  the 
pleura  ;  and  tubular  breathing,  which  shows  the  participation  of  the  lung, 
lead  us  to  diagnose  inflammation  of  the  chest. 

The  onset  of  interlobar  pleurisy  is  very  different.  The  infection  in  en- 
cysted pleurisy  is,  to  a  slight  degree,  comparable  to  that  of  a  closed  cavity, 
adhesions  having  cut  of?  all  communication  with  the  great  pleural  cavity. 
The  parts  of  the  lung  near  to  the  infectious  focus  feel  the  effect. 

The  congestion  of  the  lung  shows  itself  by  signs  which  we  shall  study, 
and,  at  the  same  time,  masks  the  nascent  state  of  the  interlobar  lesion. 

During  the  first  days  of  interlobar  pleurisy  examine  your  patient  carefully 
to  see  if  he  has  fever,  cough,  and  pain  in  the  side.  This  is  quite  common- 
place. Percuss  and  auscultate  the  chest.  You  find,  perhaps  behind,  perhaps  in 
the  axilla,  over  a  vaguely  limited  region,  slight  dullness,  riiles,  tubular  breath- 
ing— i.e.,  pulmonary  and  not  pleural  signs  ;  sometimes  also  a  few  erratic 
sounds.  Nothing  is  found  on  the  other  side  of  the  chest — no  tubular  breath- 
ing, no  rales  ;  the  lesion  is  usually  unilateral.  Being  unable,  at  this 
moment,  to  make  an  exact  diagnosis,  you  feel  sure  that  it  is  a  case  neither 
of  true  pneumonia  nor  of  true  pleurisy,  and  you  prescribe  expectant  treat- 
ment such  as  cupping,  antipyrin,  sedative  draughts. 

During  the  next  few  days  the  same  uncertainty  of  the  physical  signs 
persists.  The  lesion  remains  unilateral ;  the  pain  in  the  side  is  persis- 
tent ;  the  cough  is  more  or  less  marked  ;  expectoration  is  absent  or  scanty  ; 
fever  acute,  and  dyspncEa  intense.  Time  passes,  and  tlie  diagnosis  still 
remains  in  doubt.  Whether  the  tubular  breathing  ])e  more  or  less  loud,  the 
rales  more  or  less  extensive,  the  dullnoss  more  or  l(\ss  marked,  matters  little. 
You  have  always  to  consider  the  share  of  the  lung  and  the  share  of  the 
pleura  in  tliis  obscure  disease,  wluch,  for  want  of  a  better  term,  you  name 
"  pleuro-congestion." 


328  TEXT-BOOK  OF  MEDICINE 

As  fever  and  dyspnoea  are  present,  you  have  some  apprehension,  and  ask 
yourself  if  this  lesion,  of  bastard  appearance,  may  not  be  tubercular.  The 
tenth  or  the  twelfth  day  of  the  disease  passes,  and  defervescence  does  not  occur. 

The  picture  then  undergoes  a  change.  If  the  fluid  in  the  interlobar 
fissure  reaches  8  ounces  in  an  adult  or  5  ounces  in  a  child,  percussion  reveals  a 
dull  zone,  suspended,  as  it  were,  between  two  more  resonant  areas, 
either  towards  the  middle  and  posterior  part  of  the  chest  or  in  the  axilla. 
The  idea  of  an  encysted  pleurisy  now  gains  ground  in  your  mind,  and  you 
make  that  diagnosis. 

Anatomical  researches  have  accurately  described  the  normal  topography 
of  the  interlobar  fissures,  and  their  relations  with  the  intercostal  spaces  and 
thoracic  wall  (Rochard).  The  topography  of  the  normal  state  is,  however, 
no  longer  rigorously  true  in  the  pathological  state.  The  situation  and  the 
direction  of  the  fissures  are  modified  by  the  fluid  which  has  accumulated 
between  the  two  lobes  of  the  lung,  and  by  the  pushing  back  of  these  lobes. 

It  is,  however,  not  exactly  at  the  level  of  the  interlobar  fissures  that 
the  suspended  zone  of  dullness  is  found.  Tliis  zone  may  exist  at  different 
parts  of  the  thorax.  If  interlobar  pleurisy  develops  in  the  horizontal  portion 
of  the  fissure,  the  zone  is  situated  behind,  at  the  upper  third  or  the  middle 
part  of  the  chest.  If  interlobar  pleurisy  invades  the  obhque  and  descending 
portion  of  the  fissure,  the  zone  is  found  in  the  axilla,  and  extends  as  far  as 
the  anterior  part  of  the  chest. 

During  the  first  period  of  interlobar  pleurisy  the  chief  points  are  the 
artificial  pulmonary  signs,  rales,  tubular  breathing,  and  dullness  ;  when  the 
effusion  is  fairly  abundant,  the  chief  sign  is  the  existence  of  a  dull  zone, 
suspended  between  more  resonant  areas.  The  diagnosis  is  almost  impos- 
sible in  the  first  phase  of  the  disease.  We  cannot  say  what  the  issue  will  be  ; 
we  may  tliink  of  pneumonia,  pleurisy,  or  congestion,  but  we  remain  in 
doubt.  For  several  days  the  chief  symptoms  are  pain,  cough,  and  dyspnoea  ; 
the  interlobar  effusion,  surrounded  by  the  lung,  does  not  yet  reveal  itself 
by  any  special  sign  ;  on  the  contrary,  the  contiguous  parts  of  the  engorged 
lung  give  rise  to  tubular  breathing  and  rales,  which  attract  attention  to  the 
lung,  while  the  abscess  is  hidden  in  the  interlobar  spaces.  One  sign,  how- 
ever, is  of  great  value — viz.,  the  limitation  of  a  dull  zone,  surrounded  by  more 
resonant  regions  ;  this  zone  of  dullness,  however,  is  only  evident  when  the 
interlobar  fluid  is  sufficiently  abundant. 

In  interlobar  effusion  we  must  not  expect  to  find  the  classical  signs  of 
effusion  into  the  great  pleural  cavity.  In  tlie  latter  case  the  fluid  is  in 
contact  with  the  chest-wall,  and  therefore  the  physical  signs  reach  their 
maximum.  On  the  other  hand,  when  the  effusion  is  hidden  in  the  inter- 
lobar cavity,  the  parts  of  the  lung  interposed  between  the  effusion  and  the 
chest-wall  make  the  signs  feeble,  and  mask  them. 


DISEASES  OF  THE  PLEURA  329 

The  fluid  in  right  interlobar  pleurisy  cannot  push  the  liver  down,  but 
effusion  on  the  left  side,  especially  when  the  mischief  invades  the  descending 
fissure,  may  displace  the  heart  to  the  right. 

Dyspnoea  in  cases  of  interlobar  pleurisy  is  more  marked  than  in  pleurisy 
of  the  great  pleural  cavity.  We  may  have  4  pints  or  more  in  the  pleura, 
without  much  distress.  Interlobar  pleurisy,  though  quite  Hmited,  causes 
early  and  severe  dyspnoea.  The  cUnical  picture,  then,  is  very  different 
between  pleurisy  of  the  great  pleural  cavity  and  interlobar  pleurisy,  and  we 
should  be  liable  to  make  grave  mistakes  if  we  were  to  suppose  that  the  same 
signs  are  applicable  to  both  cases. 

Among  the  possible  symptoms  of  interlobar  pleurisy,  there  are  two  — 
haemoptysis  and  vomica — which  I  wish  to  discuss  in  detail. 

Interlobar  Haemoptysis.— Haemoptysis  has  been  noted  several  times 
in  the  course  of  interlobar  pleurisy,  and  I  saw  two  cases  of  this  during  the 
past  few  years. 

In  Prengrueber  and  Benrmann's  case  a  young  girl  had  repeated  haemoptysis,  although 
she  was  not  tubercular,  in  the  course  of  interlobar  pleiu-isy,  for  -nhich  she  had  been 
operated  upon  and  cured.  A  youth  whose  case  was  reported  by  Letulle  and  Segond 
had  very  abundant  haemoptysis,  which  laH.tcd  a  fortnight,  although  he  was  not  tuber- 
cular. He  was  cured  by  surgical  intervention.  In  one  of  Letulle's  cases,  a  patient 
suflfering  from  interlobar  pleurisy  was  also  attacked  by  haemoptysis,  which  led  to  a 
suspicion  of  caseous  pneumonia.  The  future  proved  that  the  patient  was  not  tuber- 
cular, and  surgical  intervention  eflEected  a  cure. 

The  following  case  has  been  communicated  to  me  by  Dr.  Thahs  : 

A  man,  forty-five  years  of  age,  convalescent  from  left  pneumonia,  was  taken  ill  with 
fever,  pain  in  the  side,  and  acute  dyspnoea.  Some  days  later  a  zone  of  dullness,  sur- 
rounded by  rales,  was  found  at  the  middle  and  posterior  part  of  the  chest.  For  about 
three  weeks  the  chief  symptoms  were  fever,  cough,  dyspncra,  pain,  and  tachycardia. 
One  morning  the  patient,  after  severe  fits  of  coughing,  brought  up  a  quantity  of  pus  ; 
he  had  just  emptied  an  interlobar  pleurisy.  He  continued  every  morning  to  fill  one 
or  two  sputum-glasses  with  purulent  expectoration,  after  which  the  cough  was  less 
severe.  This  condition  lasted  from  four  to  five  weeks,  and  the  fever  disappeared,  but 
the  tachycardia  persisted.  One  day  he  brought  up  some  bloody  sputum,  followed  by 
abundant  liaemoptysis.  Tuberculosis  was  feared,  but  no  bacilli  were  found,  either  in 
the  purulent  expectoration  or  in  the  blood  coughed  up.  Convalescence  was  slow  ; 
the  expectoration  only  dried  up  after  four  months,  yet  the  man  completely  recovered  his 
health. 

Haemoptysis,  then,  is  not  rare  in  the  course  of  interlobar  pleurisy.  This 
fact  has  not  passed  entirely  unnoticed^  for  Pailhas  has  mentioned  it  and 
discussed  its  causes.  When  haemoptysis  supervenes  in  a  case  of  pleurisy,  with 
fever  and  purulent  expectoration,  we  fear  that  the  patient  is  tubercular.  We 
must  be  on  our  guard  against  such  an  interpretation.  The  four  patients 
whose  history  I  have  just  reported  recovered  completely  ;  they  were  not 
tubercular.  I  dwell  on  haemoptysis  in  interlobar  pleurisy  because  it  is  not 
sufficiently  known  ;   we  see,  not  simply  some  blood-stained  sputum,  but 


330  TEXT-BOOK  OF  MEDICINE 

true  and  sometimes  abundant  haemoptysis,  which  may  recur  at  varying 
intervals.  Sometimes  the  spitting  of  blood  supervenes  after  the  vomica, 
as  in  Thahs's  case ;  at  other  times  it  precedes  or  is  contemporaneous  with 
it,  as  in  the  three  other  patients.  I  think  that  this  haemoptysis  is  due 
to  ulceration  of  the  walls  of  the  interlobar  cavity.  Tliis  process,  wliich  causes 
ulceration  of  a  bronchus  and  vomica,  may  also  cause  ulceration  of  a  vessel 
and  haemoptysis.  In  my  httle  patient  who  was  operated  on  by  Tuflier 
(second  case  in  my  chnical  lecture),  it  was  easy  for  us  to  see  the  section  of  the 
bronchiole  by  wliich  the  vomica  had  been  caused  at  the  bottom  of  the  inter- 
lobar cavity.  If  the  accompanying  arteriole  had  participated  in  the  ulcera- 
tion, haemoptysis  would  have  been  the  result.  If  haemoptysis  be  relatively 
frequent  in  interlobar  pleurisy,  and  almost  unknown  in  the  purulent  pleurisy 
of  the  great  pleural  cavity,  it  is  because  the  ulceration,  which  ends  in  vomicae 
and  haemoptysis,  is  more  active  in  interlobar  pleurisy,  which  produces,  as 
regards  the  pleura,  a  "  closed  cavity,"  with  its  consequences. 

Moreover,  whatever  may  be  the  pathogenesis  of  this  haemoptysis,  which 
I  propose  to  call  interlobar,  we  must  be  on  our  guard  against  the  conclu- 
sion that  the  haemorrhage  is  due  to  tuberculosis. 

Interlobar  Vomica. — Let  us  now  deal  with  an  important  symptom  in 
interlobar  pleurisy.  I  refer  to  the  vomica.  Generally  speaking,  the 
opening  of  the  purulent  focus  is  much  more  frequent  in  encysted  effusions 
than  in  pleurisy  of  the  great  pleural  cavity.  The  latter  lasts  months  and 
years,  without  going  on  to  vomica. 

I  was  called  to  see  a  young  girl  who  could  neither  walb  quickly  nor  go  upstairs  with- 
out severe  dyspnoea.  Her  respiration  was  embarrassed  even  during  rest.  The  exam- 
ination of  the  patient  was  neither  complicated  nor  difficult.  I  at  once  discovered  6  or 
7  pints  of  fluid  in  the  left  pleura. 

I  then  learnt  that  she  had  had  pleuro -pneumonia  in  Brazil  a  year  before.  From  that 
time  her  respiration  had  been  panting,  and  she  had  felt  her  heart  beating  on  the  right 
side  ;  but  yet  she  had  travelled  across  Europe,  thinking  that  she  was  "  suffering  from 
anaemia."  Although  I  found  neither  fever  nor  oedema  of  the  chest-wall,  I  thought  that 
pleurisy  of  at  least  a  year's  duration  must  be  purulent.  I  made  several  punctures. 
The  puriform  fluid,  separated  into  two  layers — the  lower  one  thick,  the  upper  one  almost 
serous.  The  fluid  was  absolutely  sterile,  and  very  poor  in  pus  cells.  The  pleurisy  was 
evidently  quiescent.  She  recovered  after  the  fifth  puncture.  This  large  empyema, 
which  had  lasted  for  a  year,  had  not  gone  to  vomica. 

I  saw  an  American  who  for  a  long  while  had  suffered  from  purulent  pleurisy,  and  who, 
in  spite  of  a  large  effusion,  had  several  times  crossed  between  France  and  America. 
After  each  voyage  I  drew  off  a  pint  of  purulent  fluid.  I  do  not  know  what  became  of 
this  patient,  but  I  do  know  that  purulent  fluid  had  remained  several  years  in  the 
pleura  without  giving  rise  to  a  vomica. 

Gueneau  de  Mussy  relates  the  history  of  a  patient  who  suffered  from  left  pleural 
effusion  for  fifteen  years.  The  first  pimcture  brought  away  3|-  pints  of  puriform  fluid, 
which  did  not  contain  a  single  leucocyte,  and  might  have  been  an  emulsion  of  fatty 
matter.  A  fortnight  later  3J  pints  of  similar  fluid  were  drawn  off,  and  the  patient 
experienced  such  reUef  that  he  went  to  Russia.  This  empyema,  which  had  lasted  for 
so  many  years,  had  never  gone  on  to  a  vomica. 


DISEASES  OF  THE  PLEURA  331 

Gueneau  de  Mussy  also  quotes  the  case  of  a  young  man  wlio  suffered  for  eighteen 
months  from  empyema  on  the  left  side.  The  patient  was  punctured,  and  o  pints  of 
purulent  fluid  were  withdrawn.  Two  fresh  punctures  were  made,  some  weeks 
apart,  and  the  improvement  was  such  that  the  patient  was  considered  cured. 
This  empyema  had  not  provoked  a  vomica,  although  it  was  of  eighteen  months' 
duration. 

Some  effusions  of  the  great  pleural  cavity  may  last  months  and  years, 
without  going  on  to  perforation  of  the  lung  and  vomica.  It  is  not  so  in 
encysted  effusions.  Whether  the  case  be  one  of  mediastinal,  interlobar,  or 
diaphragmatic  pleurisy,  encystment,  after  the  fashion  of  closed  cavities, 
favours  ulceration  of  the  walls,  perforation,  and  vomica.  Several  patients 
have  come  under  my  care  at  the  Hotel-Dieu  during  the  past  few  years  with 
encysted  mediastinal  or  interlobar  pleurisy,  which  has  usually  ended  in 
vomica.  Eighteen  cases  of  interlobar  pleurisy,  reported  in  my  chnical 
lectures,  gave  rise  to  vomicae. 

To  sum  up  :  Vomica  is  almost  the  rule  in  purulent  interlobar  pleurisy, 
if  it  is  not  operated  on  in  time  ;  in  that  of  the  great  pleural  cavity  it  is  the 
exception.     Potain  also  holds  this  opinion. 

The  time  at  which  the  interlobar  vomica  supervenes  is  somewhat  vari- 
able. It  appeared  on  the  eighteenth  day  of  the  disease  in  my  second  case, 
and  before  the  fifteenth  day  in  my  first  patient ;  in  other  cases  it  was  later  ; 
but,  speaking  generally,  the  vomica  of  interlobar  pleurisy  is  earher  than  that 
of  empyema  of  the  great  pleural  cavity! 

I  have  several  times  been  able  to  predict  the  vomica  twenty-four  and 
thirty-six  hours  in  advance,  thanks  to  the  sign  which  I  have  long  since 
described,  and  which  depends  on  the  foetor  of  the  breath.  The  fluid 
in  interlobar  pleurisy  is  nearly  always  foetid.  Before  the  opening  into  the 
bronchi  is  large  enough  to  allow  free  passage  of  the  pus,  a  simple  fissure  is 
formed,  and  the  foetid  emanations  of  the  cavity  escape  tlirough  this  narrow 
strait.  Foetor  of  the  breath,  therefore,  may  precede  the  appearance  of  the 
vomica  by  one  or  by  several  days.  Our  patient  in  the  Saint  Cliristophe  ward 
had  foetor  of  the  breath  and  a  "  bad  taste  in  the  mouth  "  several  days  before 
his  vomica  ;  his  wife  had  remarked  that  his  "  breath  smelt  bad."  The 
motlier  of  the  little  girl  in  my  second  case  told  us,  two  days  before  the 
vomica,  "  that  the  child's  breath  had  become  faint  and  bad-smeUing." 
Let  us  not  forget  this  sign,  which  allows  us  to  foresee  the  vomica,  and  aids  us 
in  the  diagnosis  of  interlobar  pleurisy. 

The  vomica  does  not  always  appear  in  the  same  manner.  When  the 
pus  bursts  into  the  bronchi,  the  patient  is  seized  with  fits  of  coughing  and 
acute  dyspnoea,  and  though  so  far  he  has  brought  up  no  sputum,  lie 
now  coughs  up  purulent  sputum,  wjiidi  is  fii'tid  and  scjnictimcs  streaked  with 
blood.  The  quantity  of  pus  varies,  according  as  the  vomica  follows  empyema 
of  the  great  pleural  cavity  or  encysted  pleurisy.     In  the  former  case,  when 


332  TEXT-BOOK  OF  MEDICINE 

the  perforation  is  large  enough,  abundant  pus  is  brought  up ;  the  patient, 
indeed,  appears  to  vomit  pus — whence  the  word  "  vomica  "  {vomere,  to 
vomit).  He  may  bring  up  1  or  2  pints  in  a  few  minutes.  In  encysted  effusion 
which  contains  only  a  few  ounces  (interlobar  pleurisy),  tlie  pus  is  not  brought 
up  in  streams,  but  in  small  mouthfuls,  so  that  the  vomica  might  in  some 
cases  be  taken  for  simple  bronchial  expectoration. 

I  cannot  too  strongly  emphasize  these  little  fragmentary  vomicae 
which  simulate  bronchorrhoea,  and  are  much  more  frequent  than  large 
vomicae  in  partial  pleurisy.  A  patient  tells  you  that  for  some  time  past 
he  has  had  fits  of  coughing,  followed  by  muco-purulent  sputum.  For  want 
of  care,  you  take  the  condition  for  broncliial  catarrh,  foetid  bronchitis,  or 
bronchorrhoea  ;  but  if  you  push  your  investigations  farther,  and  obtain  exact 
answers  from  your  patient,  you  will  learn  that  the  expectoration  in  question 
began  suddenly  after  severe  fits  of  cough  and  dyspnoea,  although  on  the- 
previous  days  expectoration  was  absent.  Push  your  inquiries  farther  still, 
and  the  patient  will  tell  you  that  for  some  weeks  before  the  onset  of  this 
foetid  expectoration  he  had  pain  in  the  side,  fever,  cough,  and  dyspncea ; 
he  had  been  obliged  to  keep  his  bed,  and  had  been  treated  for  an  ill-defined 
thoracic  affection.  In  short,  he  had  interlobar  pleurisy,  and,  in  its  course, 
the  so-called  bronchorrhoea,  which  was  really  a  fragmentary  vomica, 
supervened. 

I  am  convinced  that  many  of  these  interlobar  abscesses  thus  pass 
unnoticed.  The  diagnosis  of  bronchitis,  broncho-pneumonia,  or  of  foetid 
bronchorrhoea  is  made,  when  the  condition  is  really  an  interlobar  abscess 
wliich  opens  into  the  bronchi.  Potain  has  told  me  that  he  has  seen  an 
abscess,  that  was  not  as  large  as  an  egg,  in  the  right  obhque  fissure,  near 
the  diaphragm.  In  a  recent  autopsy  upon  a  case  of  disseminated  pneumo- 
cocci,  we  found  in  the  interlobar  fissure  several  small  abscesses,  which  were 
distinct  from  one  another,  and  only  contained  a  few  drachms  of  pus.  I 
think  that  ulceration  and  perforation  of  such  abscesses  may  produce  ulcera- 
tion of  the  bronchioles  or  of  the  arterioles,  and  give  rise  to  haemoptysis,  the 
cause  of  which  we  ignore,  and  to  small  vomicae,  the  origin  of  which  remains 
unknown. 

Evolution  of  Interlobar  Pleurisy. — We  see,  as  a  rule,  two  phases  in 
interlobar  pleurisy  which  has  not  been  operated  on  in  time — the  one  which 
precedes,  and  the  other  wliich  follows,  the  vomica.  So  far,  we  have  studied 
the  first  phase  ;  let  us  now  see  what  happens  when  the  vomica  has  declared 
itself.  The  cavity  left  by  evacuation  of  the  pus  is  partly  filled  up  by  the 
expansion  of  the  neighbouring  lung  tissue  ;  nevertheless,  where  there  was 
only  a  dull  and  almost  silent  zone,  it  is  not  rare  to  perceive  hollow,  tubular 
breathing,  and  gurgling,  wliich  point  to  a  cavity.  In  favourable  cases,  the 
evacuation  of  an  infectious  focus  by  vomica  is  followed  bv  notable  improve- 


DISEASES  OF  THE  PLEURA  333 

ment.  The  fever  falls  ;  the  dyspnoea  grows  less  ;  the  fits  of  coughing  diminish 
in  intensity ;  the  quantity  of  purulent  sputum  secreted  by  the  walls  of  the 
interlobar  cavity  is  more  or  less  limited  ;  the  foetor  disappears  ;  the  appetite 
returns ;  and,  after  some  weeks  or  months,  the  condition  becomes  normal, 
the  interlobar  cavity  cicatrizes,  and  the  patient  recovers.  I  have  several 
times  seen  this  fortunate  ending  in  interlobar  pleurisy  after  vomica. 

In  other  cases,  however,  the  spontaneous  evolution  is  much  less  favour- 
able, and  multiple  compUcations  may  arise.  The  patient  has  brought  up  a 
quantity  of  pus,  but  although  the  interlobar  focus  is  partly  emptied,  remis- 
sion does  not  occur  ;  iauto-infection  continues  ;  the  fever  remains  high  ;  the 
pulse  is  accelerated ;  sweating  is  abundant,  loss  of  appetite  complete,  and 
wasting  rapid.  The  patient  who  is  not  tubercular,  nevertheless,  appears 
to  be  so  ;  broncho-pulmonary  rales  invade  the  lung,  which  is  infected, 
in  its  turn,  and  the  patient  succumbs  if  a  timely  operation  is  not  per- 
formed. To  this  category  belong  my  first  two  cases.  My  patient  at  the 
Hotel-Dieu  continued  to  infect  himself  after  his  vomica ;  liis  strength  de- 
creased, the  pus  did  not  dry  up,  and  I  am  convinced  the  man  would  have 
died  if  an  immediate  operation  had  not  been  performed.  The  same  remark 
holds  good  in  my  second  case  :  in  spite  of  the  vomica,  the  temperature  kept 
up  at  104°  F. ,  the  pulse-rate  was  140,  and  the  respiration  44 ;  the  com- 
plexion became  sallow;  the  infectioij  made  great  strides,  and,  without 
surgical  intervention,  the  child  was  certainly  doomed. 

Let  these  examples  serve  as  a  lesson ;  they  prove  that  while  there  are 
cases  in  which  the  vomica  is  a  mode  of  cure,  there  are  other  more  frequent 
cases  in  which  complications  come  on  rapidly,  in  spite  of  the  vomica,  and 
which  will  have  a  fatal  termination  if  an  operation  is  not  promptly 
decided  upon. 

These  considerations  are  apphcable  to  gangrenous  interlobar  pleurisy. 

Case  1,  A  young  girl  came  under  Olivier's  care  at  tho  Enfants-Malades.  She 
was  taken  ill  a  fortnight  before  with  chills,  fever,  pain  on  the  right  side,  and  fits  of 
coughing.  Examination  of  the  chest  showed  symptoms  which  were  not  localized. 
Twenty-five  days  after  the  onset  of  the  disease  the  child's  breath  had  a  gangrenous 
odour.  The  expectoration,  which  was  composed  of  grecnish-brovni  masses,  floating  in 
dirty  serous  fluid,  Avas  very  foul-smelling.  The  expectoration  increased  in  amount, 
and  the  cough  was  incessant. 

On  examination  of  the  chest,  a  dull  zone,  with  amphoric  breathing,  was  found  between 
the  middle  and  the  lower  lolx»  :  it  was  evident  that  air  had  pcnetrat(>d  the  empty  focus. 
During  the  next  few  days  pus  was  repeatedly  brought  up  in  large  quantities.  The  fa-tor 
of  the  breath  and  of  the  s()utum  continued,  the  dyspncea  was  very  acute,  the  general 
condition  became  grave,  and  the  patient  died  after  an  illness  of  nearly  three  months. 

A  caN-ity  was  found  between  the  middle  and  lower  lobes  on  the  right  side.  Tho  fluid 
in  it  was  horribly  foetid.  The  walls  of  this  interpleural  cyst  were  irregular,  soft,  and 
covered  with  putrefying  debris  with  a  gangrenous  odour.  A  blackish  slough  wa-s  present. 
Multiple  sections  of  the  lung  tissue  around  the  cavity  showed  very  marked  fibrosis. 
There  was  no  trace  of  tuberculosis. 


334  TEXT-BOOK  OF  MEDICINE 

Case  2.— A  woman,  aged  sixty-three,  had  been  taken  ill  a  month  before  with  pain  in 
the  right  side  and  shivering  fits.  Acute  dyspnoea,  cough,  and  abundant  diarrhoea, 
accompanied  the  onset  of  the  disease.  As  the  situation  did  not  improve  in  spite  of 
treatment,  she  was  admitted  under  Chauffard.  She  had  extreme  dyspnoea,  ^the 
respirations  were  forty-five  a  minute,  and  the  evening  temperature  was  over  103°  F. 
Examination  of  the  thorax  showed  behind,  on  the  right  side,  slight  dullness  over  the 
lower  two -thirds,  abolition  of  the  vesicular  murmur,  and.  faint  tubular  breathing  on 
expiration.  These  signs  somewhat  simulated  those  of  pleural  effusion,  and  yet  punctures 
in  different  intercostal  spaces  gave  no  result.  The  diagnosis  of  pleurisy  was,  therefore, 
abandoned,  and  spleno -pneumonia  was  thought  of.  Some  days  later  cavernous, 
breathmg  was  heard  over  the  middle  of  the  right  lung  ;  mterlobar  pleurisy  was  suspected, 
and  aspiratory  puncture  gave  exit  to  3  ounces  of  foul  sanious  pus.  Bacteriological 
examination  of  the  pus  revealed  micrococci,  streptococci,  and  rods.  Some  days  later 
foul-smelling  pus  was  brought  up.  The  tubular  breathing,  recognized  at  the  level  of  the 
interlobar  space,  took  an  amphoric  timbre.  Antiseptics  were  injected  into  the  focus. 
The  infection  contmued  its  ravages,  and  the  patient  died  in  about  two  months.  At 
the  autopsy  a  gangrenous  pocket  was  found  in  the  interlobar  fissure.  This  primary 
lesion  was  accompanied  by  secondary  foci  of  suppurative  broncho -pneumonia  in  the 
lower  lobe  of  the  lung.  In  these  two  cases  immediate  operation  would  probably  have 
warded  off  these  complications. 

In  another  list  of  complications  I  place  those  of  long  duration  which 
supervene  long  after  the  interlobar  vomica.  In  some  patients  the  improve- 
ment which  follows  the  vomica  is  neither  genuine  nor  lasting  ;  we  try  several 
methods  of  treatment,  and,  fearing  operation,  we  temporize.  The  patient 
continues  to  cough  and  to  spit ;  the  interlobar  cavity  goes  on  secreting  and 
does  not  fill  up ;  the  fever  reappears ;  the  breatliing  is  hampered ;  the  patient, 
who  intoxicates  himself  in  small  doses,  has  no  appetite,  and  wastes ;  the 
fingers  become  clubbed,  and,  although  he  is  not  tubercular,  he  yet  appears 
to  be  so. 

In  this  picture  I  allude  especially  to  a  patient  under  my  care  at  the 
Laennec  Hospital : 

.  A  man,  thirty-five  years  of  age,  was  admitted  into  Leprae's  ward  for  left  inter- 
lobar plem-isy,  which  was  followed  by  vomica.  For  a  long  time  he  had  brought  up 
purulent  and  foetid  expectoration,  accompanied  by  cough  and  dyspnoea.  He  left  the 
hospital  and  came  under  my  care  five  months  later.  At  this  time  he  had  fever,  and 
brought  up  two  spittoons  full  of  foetid  pus  daily.  I  found  a  zone  of  dulhiess,  which 
began  at  the  spme  of  the  left  scapula,  and  extended  obliquely  from  above  downwards, 
and  from  within  outwards,  as  far  as  the  axilla.  The  resonance,  above  and  below,  was 
almost  normal.  Auscultation  of  this  zone  revealed  the  signs  of  cavity — viz.,  cavernous 
breathing  and  gurgling  somids.  I  had  to  content  myself  with  placing  a  trocar  in  the 
cavity,  and  daily  gave  injections  of  alcohol.  The  patient  became  worse  and  succumbed 
four  months  later.  At  the  autopsy  I  found  the  left  interlobar  fissure  converted  into  a 
cavity  filled  with  foetid  pus,  the  walls  being  thickened  and  fibrous.  The  fibrosis  had 
reached  the  adjacent  Imig  tissue,  and  dilated  bronchi  were  present  in  the  fibrous  and 
lardaceous  parenchyma.  No  tuberculosis.  This  case  proves  that  a  cavity,  if  left  to 
itself,  in  interlobar  pleurisy  may  remain  infected  and  cause  fibrosis  of  the  lung  and 
bronchiectasis.  Such  a  gloomy  result  would  not  happen  to-day,  as  immediate  surgical 
treatment  would  lead  to  cure. 


DISEASES  OF  THE  PLEURA  335 

Diagnosis. — Such  may  be  the  results  and  consequences  of  interlobar 
pleurisy  if  left  alone ;  it  is  necessary,  however,  to  diagnose  and  to  treat  the 
condition  in  order  to  avoid  the  catastrophes  of  which  I  have  just  spoken. 
In  my  opinion  the  medical  treatment  of  interlobar  pleurisy  is  futile.  Our 
part  as  physicians  is  to  diagnose  interlobar  pleurisy,  to  follow  out  its  course, 
to  distinguish  the  cases  in  which  it  is  spontaneously  curable,  when  a  vomica 
has  occurred,  to  decide  upon  surgical  intervention,  and,  lastly,  to  point  out 
to  the  surgeon  the  exact  field  of  operation.  Our  part  is  still  considerable, 
for  interlobar  pleurisy  is  one  of  those  numerous  medico-surgical  diseases  in 
wliich  the  hfe  of  the  patient  is  in  our  hands.  It  is  not  sufficient,  during  the 
first  phase  of  the  disease,  to  reUeve  the  pain,  cough,  and  dyspnoea  by  sedative 
draughts,  by  injections  of  morphia,  or  other  appropriate  means  ;  we  must 
endeavour  to  make  a  correct  diagnosis,  and  once  the  disease  is  diagnosed  we 
must  come  to  an  immediate  decision. 

Diagnosis,  however,  is  not  easy  in  these  cases.  The  disease  begins  ^vith 
pain  in  the  right  or  left  side,  accompanied  by  fever,  cough,  and  dyspnoea  ; 
this  onset  is  common  to  pneumonia,  pleurisy,  broncho-pneumonia,  and 
inflammation  of  the  chest.  The  first  few  days  pass,  and  the  diagnosis  is 
uncertain  ;  the  idea  of  lobar  pneumonia  is  put  aside,  because  rusty  sputum, 
crepitant  rales,  and  tubular  breathing  are  absent ;  the  idea  of  pleurisy  is 
practically  ehminated,  because  neither  friction  sounds  nor  the  later  signs  of 
effusion  are  found.  Percussion,  however,  reveals  regions  in  which  the  reson- 
ance is  not  normal.  On  auscultation,  rales,  friction  sounds,  and  sometimes, 
too,  ill-defined  tubular  breathing  are  heard,  and  we  then  fall  back  on  the 
elastic  diagnosis  of  pleuro-congestion.  We  feel,  however,  that  this  is  not 
the  truth,  and  we  always  hope  that  more  definite  signs  will  permit  us  to 
locahze  the  lesion. 

During  the  onset  of  interlobar  pleurisy  this  indecision  is  by  no  means 
wrong,  for,  as  I  said  above,  we  lack  the  exact  elements  for  diagnosis. 
The  pleuritic  focus,  which  is  deeply  hidden  between  the  lobes  of  the  lung, 
cannot  yet  reveal  itself  ;  the  adjacent  lobes  of  the  lung  take  their  part  in  the 
congestive  process,  and  attract  our  attention  by  causing  tubular  breatliing, 
rales,  and  dullness.  It  is  only  about  the  eighth  or  the  tenth  day  that  the 
mterlobar  effusion  becomes  more  abundant,  and  takes  its  share  in  the 
symptoms.  Fresh  signs  are  now  seen  ;  the  dull  zone  is  marked  off  from  more 
resonant  areas.  If  the  disease  occupies  tlie  horizontal  part  of  the  fissure,  it  is 
behind,  towards  the  upper  third  or  middle  of  the  lung,  that  we  find  a  band 
of  dullness,  suspended,  as  it  were,  between  more  resonant  regions.  If  the 
mischief  affects  the  obUque  portion  of  the  fissure,  we  find  the  band  of 
dullness  in  the  axilla,  with  more  resonant  regions  above  and  below  it. 

Theoretically,  exploratory  punctures  should  help  us  in  the  diagnosis.  If 
aspiratory  puncture  in  the  suspected  region  gives  exit  to  purulent  fluid,  the 


336  TEXT-BOOK  OF  MEDICINE 

diagnosis  is  clear.  This  method  has  often  been  put  into  practice  ;  in  several 
cases  it  has  been  performed  six  or  eight  times  in  the  same  subject,  but  most 
frequently  to  no  purpose.  The  conditions  are  quite  different  when  it  is  a 
question  of  puncturing  a  purulent  effusion  in  the  great  pleural  cavity,  or  an 
interlobar  effusion.  In  the  former  case  the  aspirating  needle,  after  passing 
through  the  walls  of  the  chest,  at  once  enters  the  fluid  without  encountering 
the  lung  in  its  passage.  It  is  quite  different  in  interlobar  effusion  ;  the  coUec- 
tion  being  fairly  deeply  situated,  is  surrounded  by  a  more  or  less  considerable 
thickness  of  lung,  and  the  needle  buries  itself  in  the  lung,  when  we  expect  it 
to  enter  the  fluid  collection.  Read  the  cases  again,  and  you  will  see  that, 
in  spite  of  several  punctures  at  different  levels,  the  focus  is  not  found  m  many 
cases.  Aspiratory  punctures,  therefore,  in  the  case  of  interlobar  pleurisy, 
do  not  give  to  the  diagnosis  the  support  which  might  be  expected.  Radio- 
scopic  and  radiographic  (Tufiier)  examination  is  a  method  which  ought  not 
to  be  neglected,  for  it  may  peld  valuable  information. 

In  some  cases  the  diagnosis  of  interlobar  pleurisy  can  be  made  before  the 
vomica  ;  in  others  it  only  becomes  evident  after  the  vomica.  Moreover,  at 
this  time  the  symptoms  given  by  auscultation  change,  and  m  place  of  a 
dull  and  silent  zone  we  now  find  cavernous  breathing,  large  rales,  and 

curclino". 

"     I  have  not  finished  with  the  inherent  difficulties  of  diagnosis  in  interlobar 

pleurisy.     The  following  case  gives  much  information  : 

A  man,  fifty-seven  years  of  age,  was  admitted  for  fever,  cough,  and  pneumonic 
expectoration,  which  was  slightly  fc^tid.  He  said  that,  after  a  chill,  he  had  been  taken 
ill  two  months  ago  .vith  a  violent  rigor,  chattering  of  the  teeth,  and  pam  m  the  right 
side.  Had  he  had  pneumonia  ?  I  am  not  certain,  for  he  had,  so  he  said,  no  rusty 
sputum.  However  this  may  be,  the  disease  went  on,  with  fever,  cough,  pain  in  the 
chest,  and  expectoration.  About  twenty-five  days  after  the  commencement  of  the 
illness,  at  six  o'clock  in  the  morning,  he  felt  something  bui'st  in  1^J^«1^«^*' ^^,^' j\^^'^ 
hours,  brought  up  about  5  ounces  of  foul-smelling,  puinilent  fluid.  He  had  had  a 
vomica.  During  the  next  few  days  the  cough  and  the  expectoration  contmued  and 
three  weeks  after  the  vomica  the  patient,  who  was  feverish  and  wasted,  and  was  still 
bringing  up  5  oimces  of  pus  daily,  came  into  hospital.  ,     .  .,     i      •  ^„+^i 

Examination  showed  the  locahzation  of  the  lesion.  At  the  level  of  the  horizontal 
interlobar  fissure,  on  the  right  side,  we  found  a  zone  of  dulhiess,  limited  above  and 
below  by  more  resonant  regions.  Over  the  dull  zone,  auscultation  ^^^^^^f  .^"^ular 
breathing  and  rales.  We  had  no  doubt  as  to  the  diagnosis,  and  concluded  that  our 
patient  had  emptied  an  interlobar  pleurisy  by  vomica.  As  the  fever  and  the  general 
ill-health  persisted,  I  asked  Cazin  to  open  the  infected  cavity.  The  operation  was 
performed,  and  we  were  then  convinced  that  the  purulent  focus  in  the  interlobar  fissure 
was  but  a  lobar  abscess  of  the  lung,  situated  at  the  upper  part  of  the  middle  lobe,  m 
contact  with  the  interlobar  pleura. 

The  admirable  lecture  of  Trousseau  on  the  diagnosis  of  lobar  and 
interlobar  vomica  helps  us  to  appreciate  the  difficulty  in  diagnosis.  As 
Trousseau  says,  abscesses  of  the  lung  are  extremely  rare,  and  what  some 


DISEASES  OF  THE  PLEUEA  337 

authors  have  taken  for  lobar  are  really  interlobar  abscesses.  In  any  case, 
whether  it  be  a  question  of  vomicae  consecutive  to  lobar  abscess  or  inter- 
lobar pleurisy,  the  indications  for  treatment  are  identical. 

Treatment. — As  I  have  abeady  stated,  medical  treatment  is  purely 
illusory.  There  is  an  infected  cavity  filled  with  fluid,  which  must  be 
evacuated.  In  the  fortunate  but  rare  cases  the  vomica  itself  accomplishes 
the  evacuation  of  tliis  focus,  and  in  a  few  weeks  spontaneous  recovery  occurs. 
It  is,  however,  preferable  not  to  wait  for  the  vomica,  and  in  every  case,  if  the 
fever  persists,  and  the  compUcations  of  infection  continue,  in  spite  of  the 
vomica,  we  should  operate ;  and  if  the  operation  is  performed  at  the  proper 
time,  secundum  arteni,  we  shall  be  on  the  road  to  success.  Moreover,  in  the 
eight  patients  whose  history  I  have  traced  in  my  chnical  lectures,  six  who 
have  been  operated  upon  recovered ;  the  two  who  had  not  been  operated 
upon  succumbed. 

IX.  MEDIASTINAL  PLEURISY— MEDIASTINAL  SYNDROME. 

Discussion. — Under  some  circumstances  false  membranes  and  adhesions 
shut  off  the  pleura  ;  the  pleurisy  is  then  said  to  be  partial  or  encysted. 
Encysted  pleurisy  m.ay  occur  in  the  great  pleural  cavity,  which  is  divided  up 
by  septa  ;  it  is,  however,  in  the  interlobar,  diaphragmatic,  and  mediastinal 
regions  that  pleurisy  finds  conditions  naost  favourable  to  encystment. 

Speaking  generally,  there  is  absolute  difEerence  between  pleurisy  of  the 
great  pleural  cavity  and  encysted  pleurisy.  This  difference  depends  on 
several  causes.  When  pleurisy  develops  freely  in  the  great  pleural  cavity, 
the  liquid  spreads  between  the  chest-wall  and  the  lung.  The  lung  escapes  by 
allo\\ing  itself  to  be  depressed,  thus  averting  the  pressure,  while  the  neigh- 
bouring organs  are  displaced  ;  the  symptoms  are  slight,  and  dyspnoea  only 
becomes  severe  when  the  effusion  is  considerable. 

The  conditions  in  encysted  pleurisy  are  quite  different.  When  pleurisy 
develops  in  an  interlobar  space,  between  the  contiguous  surfaces  of  two 
pulmonary  lobes,  the  latter,  being  in  contact  with  a  closed  cavity,  readily 
become  infected,  and  for  a  time  the  pulmonary  trouble  masks  the  pleural 
miscliief.  Later,  when  the  effusion  has  formed,  it  is  deeply  hidden,  and 
so  partly  escapes  our  means  of  investigation  ;  the  symptoms,  therefore,  are 
not  comparable  with  those  of  pleurisy  of  the  great  pleural  cavity,  in  which 
the  lluid  is  in  direct  contact  with  the  chest-wall. 

When  the  pleurisy  is  diaphragmatic,  the  picture  again  changes,  for  the 
relation  of  the  diaphragm  and  the  endings  of  the  phrenic  nerve  give  rise  to 
>i><''ial  symptonLs. 

Ijastly,  when  pleurisy  is  confined  to  the  mediastinal  region,  the  clinical 
picture  depends  upon  the  importance  of  the  organs  compressed  l)y  the 


338  TEXT-BOOK  OF  MEDICINE 

membranes  and  the  mediastinal  fluid.     In  order  to  grasp  the  cHnical  course 
of  events,  I  will  recall  briefly  the  chief  anatomical  points. 

The  mediastinum  is  the  region  between  the  two  lungs.  It  extends  from 
before  backwards,  from  the  sternum  to  the  vertebral  column,  and  from 
above  downwards,  from  the  sternal  notch  to  the  diaphragm.  This  region, 
which  corresponds  to  the  median  part  of  the  thoracic  cavity,  may  be  divided 
into  an  anterior  and  a  posterior  mediastinum.  This  distinction,  however,  is 
fictitious,  and  this  division  into  two  mediastina  "  holds  good  only  at  the 
root  of  the  lung,  because  above  and  below,  between  the  sternum  and  the 
vertebral  column,  no  such  separation  exists  "  (TiUaux). 

We  find  in  this  region  the  heart  and  the  great  vessels,  the  trachea  and  the 
large  bronchi,  the  oesophagus,  the  pneumogastric,  plirenic,  splanchnic  and 
recurrent  nerves,  the  large  azygos  vein,  the  thoracic  duct,  the  glands,  etc. 
All  these  organs  are  covered  by  a  layer  of  pleura,  which  separates  them  from 
the  lungs.  The  mediastinal  pleura,  like  other  serous  membranes,  is  therefore 
formed  of  two  layers  :  one  of  which  covers  the  organs  in  the  mediastinum, 
whHe  the  other  covers  the  contiguous  surfaces  of  the  lungs.  It  is  in  the  virtual 
space  which  exists  between  these  two  layers  that  the  false  membranes  and 
the  fluid  of  mediastinal  pleurisy  are  encysted.  Mediastinal  pleurisy  may  be 
situated  on  the  right  or  on  the  left  side  ;  it  may  be  divided  into  several 
varieties,  according  as  it  affects  the  anterior  or  the  posterior  mediastinum, 
and  the  upper  or  the  lower  part  of  the  mediastinum.  These  subdivisions  are 
scarcely  apphcable  chnically  ;  in  the  few  cases,  however,  which  I  shall  relate, 
we  shall  see  that  we  are  deahng  chiefly  with  posterior  pleurisy. 

What  happens  when  effusion  and  false  membranes  accumulate  between 
the  layers  of  the  mediastinal  pleura  ?  The  membranes  and  the  fluid  form  a 
tumour,  and  push  back  the  lung  and  the  organs  of  the  mediastinum.  The 
fact  that  the  lung  is  pushed  back  matters  httle— it  is  a  common  condition  m 
all  pleural  effusions— but  if  the  organs  of  the  mediastinum  are  displaced  or 
compressed,  the  condition  is  very  difierent.  The  heart  is  but  httle  affected 
by  mediastinal  pleurisy,  but  tliis  is  not  the  case  with  the  other  organs.  If 
the  trachea  is  displaced  or  flattened,  dyspnoea,  stridor,  and  sucking-in  result. 
In  the  case  of  the  oesophagus  dysphagia  appears,  solid  foods  can  no  longer 
pass,  and  Uquids  can  only  be  swallowed  with  difficulty.  If  the  great  azygos 
vein  is  compressed  as  it  receives  the  small  azygos  and  seven  or  eight  right 
intercostal  veins,  blood-stasis  results,  and  the  collateral  circulation  shows 
itself  by  a  network  of  distended  veins  over  the  chest.  If  the  pneumogastric 
nerve  is  stimulated  by  the  presence  of  fluid  and  of  pleuritic  membrane^ 
the  patient  is  seized  with  fits  of  coughing  and  severe  attacks  of  suffocatio^ 
If  the  recurrent  nerve  is  hampered  by  the  exudate,  laryngeal  troubles, 
such  as  hoarseness,  dysphonia  and  spasms  of  the  glottis,  at  once  supervene. 
I  propose  to  call  this  collection  of  symptoms  the  mediastinal  syndrome, 


DISEASES  OF  THE  PLEURA  339 

which  points  to  the  existence  of  a  tumour  in  the  posterior  mediastinum. 
This  syndrome  is  apphcable  to  mediastinal  pleurisy,  and  existed  in  two 
patients,  whose  history  I  will  now  sketch  : 

Clinical  Cases.— A  young  man  admitted  for  intense  dyspnoea,  with  stridor  and 
8ucking-in.  Inspiration  was  accompanied  by  a  loud  scraping  noise,  while  the  sucking- 
in  was  evident  in  the  supra-  and  substernal  regions. 

Examination  over  the  posterior  mediastinum  gave  valuable  information.  We  found 
pain  on  pressure  and  dulhiess  on  percussion  ;  we  discovered  that  the  stridor  was  most 
marked  m  the  posterior  mediastinum,  from  which  point  it  spread  to  both  lungs 

The  disease  had  begun  suddenly,  five  weeks  before,  with  rigors  and  distress.'  Some 
days  later  attacks  of  suffocation  had  supervened  with  fits  of  coughing,  which  resembled 
whooping-cough  ;  but  expectoration  was  absent. 

The  voice  became  raucous  and  dull,  but  not  aphonic.  About  four  weeks  after  the 
onset  of  the  disease  the  patient  noticed  that  solid  food  passed  with  difficulty  •  he  said 
that  "  it  seemed  to  stop  on  its  way  down.^'  This  dysphagia,  joined  to  the'  stridor 
proved  that  the  trachea  and  the  oesophagus  were  displaced,  or  compressed  by  a  solid 
or  a  fluid  tumour  in  the  mediastinum.  This  hypothesis  was  confirmed  by  the  collateral 
circulation  over  the  upper  thoracic  region,  proving  that  the  great  azyc^os  vein  was 
compressed  in  the  mediastinum.  We  had,  therefore,  to  find  out  what  the  lesion  of  the 
mediastinum  was. 

It  was  not  a  glandular  tumour,  because  enlarged  glands  were  not  present  in  the  neck, 
the  clavicular  hollow,  or  the  axilla  ;  and  the  patient  had  neither  tuberculosis,  syphilis! 
nor  cancer.  It  was  not  an  epithehoma  of  the  oesophagus,  compressing  the  trachea,' 
because  the  dysphagia  had  been  preceded  by  attacks  of  suffocation  and  stridor. 

We  could  eliminate  lymphadenoma,  because  the  onset  was  acute  and  recent,  while 
the  examination  of  the  blood  was  normal,  the  white  corpuscles  being  in  proper  quantity 
and  the  red  corpuscles  as  high  as  4,800,000.  .Alight  it  be  a  purulent  collection  in  the 
mediastinum— /.e.,  abscess  from  congestion,  phlegmon,  or  mediastinal  pleurisy  ?  I 
ought  to  say  that  I  thought  of  mediastinal  pleurisy. 

On  the  night  after  admission  he  was  seized  with  violent  fits  of  coughing,  and  although 
there  had  previously  been  no  expectoration,  he  brought  up  foul-smelling,  purulent 
sputum  ;  and  next  morning  I  found  in  the  sputum-glass  about  2i  ounces  of  greenish 
homogeneous  pus,  such  as  is  caused  by  the  pneumococcus.  Although  the  bacteriological 
examination  did  not  reveal  pneumococci,  Griffon,  with  serum  taken  from  the  patient, 
obtained  a  positive  result :  agglutination  of  the  pneumococci  in  chains  and  in  masses! 
The  pus  in  the  posterior  mediastinum  was  probably  the  result  of  a  pneumococcal 
pleurisy,  going  on  to  vomica.     The  patient  was  cured  six  weeks  later. 

A  woman,  forty-four  years  of  age,  came  under  my  care  for  obstinate  cough.  She 
had  suffered  for  a  week  from  attacks  of  suffocation  and  stridor,  audible  at  a  distance. 
Ilie  cough  was  paroxysmal.  \Vhen  the  cough  came  on  after  a  meal,  it  provoked 
vomiting  of  food  ;  although  it  lasted  only  a  short  while,  the  distress  was  extreme, 
ihe  stridor,  as  well  as  tho  supra-  and  substernal  sucking-in,  were  more  marked 
during  the  cri.ses  of  dyspnoea.     At  times  the  voice  was  raucous  and  muffled. 

The  disease  appeared  to  have  started  from  a  chill.  Cough  and  distress  were  the 
first  signs.  Stridor  and  attacks  of  dyspntea  appeared  later.  Dysphagia  supervened, 
and  the  patient  had  difficulty  in  swallowing  hquids.  '•  Something  shut  up  "  as  soon 
as  she  swallowed  any  food. 

Breathing  was  audible  on  both  sides  ;  no  abnormal  sounds.  Percussion  showed 
aormal  resonance.     Heart  and  aorta  normal.     No  fever.     Temperature,  <J8-5^  F. 

Laryngoscopic  examination  :  Oblitiuity  of  the  larynx ;  deviation  of  tho  trachea  to 
the  right  ;  swelUng  of  the  arytenoid  region  ;  (edema  of  the  superior  vocal  cords,  leaving 
ynly  a  chmk,  and  complcte-ly  hiding  tho  lower  cords.  No  paralysis  of  the  recurrent  nervo. 

22—2 


^^  TEXT-BOOK  OF  MEDICINE 

Wo  found  hevo  tho  ..ediastina,  ^y;;*"--  f ''-J-lXf '/^a:^^^^^^ 
sufocation,  dy^P^S-,  compros.,on  and  d^^™^^^^^^  ^  .  J^^,„^. 

-i:Tz;jror:rroSrr^^^^^^ 
:::rJ;i':^::A:i7o!:orBt:s:?:s-orj.i^^^^ 

cocci,  but  no  other  niicrobes  ^^^-^^^^^^^  syndrome  was  due  to  pneumococcal 

the  hospital  in  good  health.  _ 

I  have  found  some  scattered  cases  of  mediastinal  pleurisy,  and  give  a 

resume  of  them ; 

.nrtraPs  Case  -Carman  mth  signs  of  advanced  phthisis.  The  expectoration 
,vhith  lad  been "hthistal,  suddenly  changed  in  character.  He  woke  up  wrth  v.olenj 
iStf  'Uhh.g,\nd  hrought  up  a  .ar.e^c.uan..^  of  P-*"^  "^^^^  ^^  ^^^ 

""" ilT'wtotv  both  lungs  were  filled  with  tubercular  cavities.    On  opening  the 
Chief hrtcru:T;|U^^^^^^^^^^ 

[:rrt:ri^^.ind  the'^btn^hr  T\is  cavit/was  big  enough  to  adnjit  ajarge  oran^ 
'nrialse  membranes  which  formed  its  walls  were  m  relation  exterr^ally  mth  the  lu^, 

^UL'^rtJ^^tS^e^nttes:^^^^^^^^^ 

°-Src!l-'.rh^atsrJSresTt^^^^^^ 

£ror-i:rth:^t:;t=fa=^^^ 
'«ru';:::rc:L^"i'r:id:i;"rhfdto:gf rxg ».. .  he  lost  aesh,  and 

pros'  Z'l  a'^^trent  signs  of'chronic  phthisis.     At  the  -'"P'^ -/-f,  ^t^ 

i^:r  Tt  :=s  wtNsrb;s==- " 

'•'Zi:o."'ar;Gr,Bon.  Case-A  woman,  <orty.«vc  years  of   ^ge^";^,^": 
i„  si.  days  before  ™th  ^^-ring  fit,  and  ,,.n  m    he  « 

Ce'rfS:S';urrt;T:erhe!;ioTi:Mlide.     Traube'sspace^w.— 
She  heart  did  not  appear  to  be  displaced.     Exploratory  puncture^^^^^^^^^ 
drops  of  yellowish  fluid,  very  rich  in  virulent  pneumococc.     '^  "°"''f  ™  °'^™',  .  ft, 
in  twenty.four  hours.     In  spilB  of  treatment    f'«  dy'^P^r  ''"*  ""'  'X7on  tj» 
disti>3ss  was  extreme,  the  temperature  reached  1M°F.,  and  the  patient  d,ed 

"Ttttfautopsy  mechastinal  pleurisy  was  found.  The  collection  wa.  situate, 
between  tie  irmer'aspect  of  the  I'eft  lung  and  the  left  wall  o  the  -fd-tmum  » 
nmited  by  false  membranes,  which  were  thick,  tibrmous,  -f  ™Yb^dant  hS  2 
two  layer's  of  the  mediastinal  pleura.  The  pus,  wteh  ™''  ""'  f  j""**"'  ^,  ,^„ 
..lassicil  featurc-s  of  pneumococcal  pus,  and  spread  downwards  as  fat  as 


DISEASES  OF  THE  PLEURA  341 

diaphragmatic  sinus,  which  was  filled  with  false  membranes,  while  it  did  not  reach 
higher  than  the  hilum  of  the  lung.  Mediastinal  pleurisy  here  occupied  the  lower  part 
of  the  mediastinal  pleura.  Further,  the  left  interlobar  fissure  was  joined  together, 
and  adhesions  existed  between  the  lower  lobe  and  the  costal  pleura.  The  whole  lower 
lobe  was  increased  in  size  ;  the  cut  section  showed  a  typical  areolar  abscess,  of  a  spongy 
appearance,  the  pockets  of  which  were  full  of  pus.  The  mediastinal  glands  were  hyper- 
trophied.  Bacteriological  examination  showed  that  the  pus  in  the  pleura  and  the  lung 
contained  only  most  virulent  pneumococci. 

Description.— We  may  now  discuss  mediastinal  pleurisy,  which  is  a 
new  chapter  in  pathology.  We  shall  not  consider  pseudo-mediastinal 
pleurisy,  which,  from  its  situation  on  the  left  side,  simulates  pericarditis  with 
large  effusion  (Grancher). 

Mediastinal  pleurisy  may  be  primary  or  secondary — primary  when  the 
pneumococcal  infection  is  present  only  in  the  mediastinal  pleura,  secondary 
when  it  is  consecutive  to  pneumonia.  It  appeared  to  be  primary  in  my  two 
patients,  as  well  as  in  Bouveret's  case  ;  it  was  associated  with  pneumococcal 
suppuration  in  the  lung  in  Thoinet  and  Griffon's  case  ;  Andral's  patient 
was  tubercular. 

Mediastinal  pleurisy  is  unilateral,  and  is  usually  confined  to  the  anterior, 
posterior,  or  inferior  regions  of  the  mediastinal  pleura  ;  it  may  extend  to 
other  regions,  such  as  the  costo-diaphragmatic  sinus,  and  coexist  with 
adhesions  of  the  interlobar  fissure  and, adhesions  of  the  lung  to  the  chest- 
wall. 

The  liquid  was  purulent  in  the  six  cases  quoted  ;  purulence  is,  indeed, 
common  to  encysted  pleurisy  of  the  mediastinum,  the  interlobar  fissure,  or 
the  diaphragm.  In  three  cases  in  wliich  the  infectious  agent  was  looked  for 
the  pneumococcus  was  found.  The  onset  of  mediastinal  pleurisy  is  not 
distinctive  ;  the  pain  in  the  chest,  the  fever,  and  the  cough  give  no  precise 
indication.  When  infection  of  the  mediastinal  pleura  occurs,  the  adjacent 
lung  is  affected  by  the  closed  cavity,  becoming  inflamed  and  congested.  The 
hidden  focus  is  accessible  neither  to  percussion  nor  to  auscultation.  The 
patient  coughs,  breathes  with  difficulty,  has  fever,  and  complains  of  distress  ; 
sputum  is  absent  or  has  no  special  feature,  and  we  think  of  pneumonia  or  of 
pleurisy,  but  we  cannot  localize  the  lesion.  Purulent  fluid  and  false  mem- 
branes accumuhite  in  the  affected  segment  of  the  pleura,  and  form  a  kind 
)f  tumour,  the  localization  and  the  size  of  which  determine  tlie  appearance 
)f  symptoms. 

If  the  encysted  collection  travels  toward  the  lung,  and  affects  the  niediasti- 
lum  to  only  a  slight  extent,  the  signs  ar(>  uncertain,  and  the  diagnosis 
emains  indefinite.  If  the  pleural  collection  travels  towards  the  organs  of  the 
i.iediastinum  and  pushes  them  back,  the  mediastinal  syndrome  then  ajipears. 
pyspiiffia,  attacks  of  opjm'ssion,  suck-ing-in  and  stridor,  dyspiiagia,  whoup- 
|iig-cough,   displacement   of  the   larynx  and   the   trachea,   recognized  on 


342  TEXT-BOOK  OF  MEDICINE 

laryngoscopic  examination,  vocal  troubles,  collateral  circulation  in  the 
thorax,  are  the  symptoms  and  signs  which  help  us  in  diagnosis. 

Let  me  emphasize  the  value  of  stridor,  which  occupies  the  chief  place  in 
lesions  of  the  mediastinum.  What  must  be  understood  clinically  by  this 
word  "  wheezing "  (cornage)  ?  It  is  a  term  employed  in  veterinary 
medicine.  Some  horses,  whose  breathing  is  almost  normal  as  long  as  they 
are  at  rest,  are  seized  while  trotting  or  cantering  with  laboured  breathing, 
accompanied  by  a  rasping  noise,  which  constitutes  the  "  bruit  de  cornage  " 
(roaring).  A  healthy  man  breathes  silently  both  during  inspiration  and 
expiration,  and  we  cannot,  so  to  say,  hear  him  breathe,  because  the  air 
traverses  the  glottis,  larynx,  and  trachea  freely.  If  the  air  meets  any 
obstacle  to  its  passage,  sonorous  vibrations  are  at  once  produced,  and  the 
"  bruit  de  cornage  "  becomes  audible.  The  tone  of  this  bruit  varies  some- 
what according  to  circumstances  ;  it  may  have  a  snoring,  rasping,  or  sawing 
character. 

The  lesion  may  be  situated  in  the  larynx  or  in  the  trachea,  so  that  we 
find  laryngeal  and  tracheal  stridor.  The  former  stridor  is  far  from  rare  • 
oedema  of  the  larynx,  spasm  of  the  glottis,  paralysis  of  the  posterior  crico- 
arytenoid muscles,  and  cancerous  lesions  of  the  larynx — in  short,  any  lesion 
which  produces  stenosis  of  the  larynx — may  determine  stridor.  When  the 
stridor  is  of  laryngeal  origin,  the  vocal  troubles  and  examination  with  the 
laryngoscope  indicate  the  site  of  the  lesion. 

The  tracheal  lesions  that  may  cause  stridor  are  intrinsic  when  they  arise 
in  the  walls  of  the  trachea  (syphihtic  gumma,  polyjjoid  excrescences,  and 
stenosis),  and  extrinsic  when  they  arise  in  the  mediastinum  (solid  and  fluid 
tumours) ;  mediastinal  pleurisy  is  of  this  nature. 

While  the  injury  to  the  organs  of  the  mediastinum  caused  by  pleurisy 
shows  itself  by  the  symptoms  just  enumerated,  the  examination  of  the 
dorsal  region,  which  corresponds  to  the  posterior  mediastinum,  furnishes 
valuable  signs.  Pressure  on  the  upper  dorsal  vertebrae  and  the  corre- 
sponding costo-vertebral  grooves  is  painful.  In  the  same  region  more 
marked  dullness  is  found  on  the  right  or  left  of  the  vertebral  column, 
according  to  the  side  affected.  The  stridor  is  most  marked  at  this  spot,  and 
diminishes  as  the  distance  from  the  mediastinum  increases.  Sonorous  and 
moist  rales  may  be  heard  in  the  lung  near  the  mediastinum.  They  indicate 
congestion  of  the  lung,  are  present  in  front  and  behind,  and  are  more 
numerous  on  the  affected  side.  Radiography  may  give  useful  information, 
as  in  one  of  my  patients. 

Mediastinal  pleurisy,  like  most  encysted  empyemata,  tends  to  vomica. 
The  vomica  generally  supervenes  some  weeks  after  the  onset  of  the  disease, 
and  is  scanty,  as  the  pus,  encysted  in  the  mediastinal  pleura,  never  reaches 
a  large  amount.     The  vomica  of  my  patient  at  the  Necker  Hospital  might 


DISEASES  OF  THE  PLEUKA  343 

be  put  down  at  6  ounces  ;  in  my  patient  at  the  Hotel-Dieu  it  did  not  exceed 
3  ounces  :  it  was  fcBtid  in  both  cases.  Andral's  patient  had  an  abundant 
vomica,  but  the  approximate  quantity  is  not  given. 

Diagnosis. — The  diagnosis  of  mediastinal  pleurisy  is  very  difficult. 
The  signs  are  insufficient  and  indefinite  until  the  mediastinal  syndrome 
appears.  When  this  syndrome  appears,  percussion  and  auscultation  of  the 
dorsal  region  (which  corresponds  to  the  posterior  mediastinum)  give  informa- 
tion as  to  the  locahzation  of  the  lesions.  We  can  then  by  these  signs  and 
symptoms,  aided  by  radiography,  arrive  at  the  topographic  diagnosis  ;  the 
knowledge  that  the  lesion  occupies  the  mediastinum  is  the  first  step  in  the 
diagnosis.  The  nature  of  the  lesion  has  then  to  be  ascertained.  Is  it 
tuberculous,  cancerous,  or  syphihtic  adenopathy  ?  is  it  a  lymphadenoma,  or 
is  it  an  aneurysm  of  the  aorta  ?  is  it  an  abscess  or  pleurisy  ? 

As  I  have  said,  the  onset  and  the  course  of  the  symptoms  may  give  a 
clue  to  the  diagnosis.  Mediastinal  adenopathies  and  tumours  do  not  begin 
suddenly  \Nith  fever  :  the  onset  is  insidious,  and  the  course  slowly  pro- 
gressive ;  moreover,  the  swelHng  in  the  neighbouring  glands  (neck,  axilla) 
aids  in  the  diagnosis.  Mediastinal  pleurisy,  on  the  contrary,  arises  suddenly, 
like  an  acute  febrile  disease  ;  fever,  paiii,  and  cough  mark  the  onset,  dyspnoea 
is  early,  and  vomica  supervenes  in  at  least  half  the  cases.  Furthermore,  in 
the  three  cases  in  which  laboratory  researches  have  been  made,  bacteriological 
examination  and  sero-diagnosis  iave  demonstrated  the  pneumococcus ; 
sero-diagnosis  would  therefore  be  useful  before  the  appearance  of  the 
vomica  in  order  to  ascertain  the  nature  of  the  disease. 

Treatment. — The  prognosis  is  not  free  from  gravity.  The  disease  is 
serious  in  itself,  and  also  from  the  secondary  infections  which  may  reach  the 
bronchi  and  the  lungs.  We  must,  then,  be  ready  to  operate  if  occasion 
arise.  Thanks  to  the  marvellous  progress  of  surgery,  the  posterior  mediasti- 
num has  become  fairly  accessible  to  surgical  investigations.  Dr.  Potarca 
(of  Bucharest),  in  a  work  entitled  "  La  Chirurgie  Intramediastinale  Pos- 
terieure,"  has  collected  several  cases  of  operations  for  purulent  collections  in 
tlie  posterior  mediastinum,  phlegmon,  mediastinitis,  suppuration  from  bony 
or  from  glandular  lesions,  and  foreign  bodies.  Although  in  the  memoir  in 
question  purulent  mediastinal  pleurisy  is  not  studied  (apart  from  Zimbicld's 
doubtful  case),  it  is  still  true  that  the  posterior  mediastinum  should  be 
opened  in  mediastinal  pleurisy  if  occasion  arise. 

X.  DIAPHRAGMATIC  PLEURISY. 

Pleurisy  of  the  diaphragmatic  portion  of  the  pleura  may  be  primary  or 
secondary,  and  dry  or  accompanied  by  effusion,  which  may  be  fibrinous  or 
purulent,  free  or  encysted.     The  dry  form  is  the  more  frequent.     Cirrhosis 


344  TEXT-BOOK  OF  MEDICINE 

of  the  liver,  peritonitis,  nepliritis,  the  puerperal  state,  tuberculosis,  and 
pneumonia  are  the  common  causes  of  diaphragmatic  pleurisy.  In  pelvic 
peritonitis  the  inflammation  is  transmitted  from  the  peritoneum  to  the 
pleura  by  the  lymphatic  vessels,  especially  by  those  which  accompany  the 
utero-ovarian  vessels,  and  pass  along  the  pillars  of  the  diaphragm.  As 
regards  metapneumonic  pleurisy  of  the  diaphragm,  the  considerations 
enumerated  in  the  case  of  interlobar  pleurisy  remain  the  same. 

The  effusion  is  usually  scanty,  and  sometimes  encysted,  wliile  the  lung 
is  often  the  seat  of  acute  congestion,  which  enters  largely  into  the  clinical 
picture  of  the  disease. 

The  symptoms  of  diaphragmatic  pleurisy  vary  in  severity ;  they  are 
sometimes  moderate,  but  in  acute  cases  the  disease  shows  itself  by  sharp 
pain  at  the  middle  of  the  diaphragm  (neuralgia  of  the  phrenic  nerve).  The 
pain  reaches  as  high  as  the  shoulder,  and  can  be  provoked  by  compressing 
the  insertions  of  the  diaphragm  into  the  tenth  rib  (diaphragmatic  point)  two 
fingers'  breadth  from  the  linea  alba  (Gueneau  de  Mussy),  or  by  pressing  on 
the  phrenic  nerve  in  its  passage  between  the  lower  heads  of  the  sterno- 
cleido-mastoid  muscle.  The  inferior  costal  region  is  immobilized  because  of 
the  paresis  of  the  diaphragm  (Andral),  and  the  usual  signs  of  pleurisy — viz. 
friction  rub,  dullness,  tubular  breathing,  and  segophony — only  appear  when 
the  great  pleural  cavity  is  also  affected.  In  the  grave  cases — which  are, 
moreover,  rarer  than  Andral's  description  would  lead  us  to  suppose— the 
symptoms  are  acute,  and  recall  the  crises  of  angina  pectoris  ;  the  breathing 
is  short,  and  interrupted  by  hiccough ;  the  voice  is  "broken  ;  dyspnoea  is 
excessive  ;  one-half  of  the  diaphragm  is  immobiUzed,  and  if  the  other  half 
is  affected,  the  patient's  life  is  in  danger.  Suppurative  diaphragmatic 
pleurisy  has  no  special  symptoms,  but  behaves  like  the  pleurisy  which  we 
have  just  described  ;  it  is  encysted,  like  partial  pleurisies,  and  in  some  cases, 
especially  in  elderly  people,  it  remains  latent,  being  only  found  at  the 
autopsy.  It  ends  fairly  frequently  by  vomica.  The  agonizing  pains  of 
diaphragmatic  pleurisy  may  be  reUeved  by  means  of  dry-cupping,  fifteen  or 
twenty  leeches,  or  injections  of  morphia ;  antipyrin  may  be  prescribed, 
and  an  ointment  of  methylate  of  salicylate  may  be  applied  to  the  painful 
region. 

XI.  LOCULATED,  AREOLAE,  OR  POLYMORPHOUS  PLEURISY. 

Pleurisy  arising  in  the  great  pleural  cavity  may  be  loculated.  Some- 
times it  occupies  a  large  pocket,  which  may  contain  several  ounces  of  sero- 
fibrinous or  purulent  fluid  (unilocular) ;  at  other  times  a  series  of  small  ones, 
when  we  speak  of  multilocular  pleurisy. 

Unilocular  Pleurisy. — I  have  recently  had  a  case  under  ray  care  at  the 


DISEASES  OF  THE  PLEUKA  345 

Hotel-Dieu.     The  pocket  was  encysted  in  the  middle  portion  of  the  right 
pleural  cavity  behind. 

A  woman,  twenty-one  years  of  age,  had  her  first  attack  of  pneumonia  in  1898. 
The  disease  was  situated  on  the  left  side.  On  May  21,  1900,  pneumonia  of  the  right 
apex,  after  a  chill.  Temperature  was  over  10-t°  F.  ;  acute  pain  in  the  side  ;  tongue  dry 
and  red  ;  vomiting  and  diarrhoea  ;  condition  of  the  patient  very  grave.  On  May  28  the 
temperature,  which  had  varied  from  103°  F.  to  10-4-5°  F.,  showed  some  tendency  to  fall ; 
the  vomiting  and  the  pain  in  the  side  became  less.  Two  days  after,  pain  reappeared, 
but  was  now  lower  down  ;  and  while  auscultation  revealed  the  existence  of  redux 
crepitation  at  the  apex,  very  harsh  breathing,  accompanied  by  friction  soimds  and 
some  crepitant  rales,  was  already  perceptible  over  the  middle  of  the  lung.  From 
June  1  to  5,  the  temperature  varied  from  101°  to  103°  F.,  patient's  condition  was  satis- 
factory, and  pain  in  the  side  disappeared.  On  the  5th,  examination  showed  dullness 
at  the  angle  of  the  scapula,  over  an  area  of  2  inches  in  the  vertical  and  4  inches  in  the 
horizontal  direction.  This  dullness  was  clearly  limited  above,  where  the  apex  had  re- 
gained its  resonance,  while  it  gradually  becami!  less  marked  below.  Vocal  fremitus 
abolished  only  in  the  region  where  the  dullness  was  absolute.  Auscultation  showed 
distant  tubular  breathing  and  very  clear  a^gophony  over  the  dull  zone,  with  slight 
aphonic  pectoriloquy.  Exploratory  puncture  blank,  1  inch  above  and  2  inches  below 
the  dullness.  At  the  focus  itself  a  green  sero -purulent  fluid,  rich  in  leucocytes,  and 
containing  numerous  pneumococci,  mostly  in  chains  of  from  five  to  ten  elements,  as 
well  as  some  diplococci,  was  drawn  off.  The  pneumococcus  was  inoculated  into  a  mouse, 
and  showed  itself  virulent,  while  it  grew  well  on  the  different  culture  media,  and  preserved 
its  chain-like  form  on  agar.  From  the  31st  to  the  7th  the  condition  remained  stationary, 
and  the  pleurisy  made  slow  progress,  diffusing  in  a  circle,  and  invading  the  base  and  the 
apex  at  the  same  time,  the  dullness  being  propagated  towards  them.  The  pleurisy 
remained,  however,  clearly  "  suspended,"  and  on  Jime  11  punctures  yielded  pus  neither 
at  the  apex  nor  at  the  base.  In  the  centre  of  the  dull  zone,  however,  the  pus  was 
greenish,  thick,  creamy,  and  rich  in  pus  corpuscles  and  fatty  granules.  The  pneumo- 
cocci in  chains  had  become  rare.  On  the  12th,  operation  for  empyema  was  performed 
at  the  level  of  the  angle  of  the  scapula,  with  resection  of  a  rib,  and  we  found  10  ounces 
of  pus,  forming  a  focus  limited  above  and  below  by  false  membranes. 

The  patient  recovered.  This  was  veiy  clearly  a  case  of  loculated  pleurisy,  with  a 
large  pocket,  which  had  developed  in  the  great  pleural  cavity,  and  not  a  case  of 
interlobar  pleurisy.  Moreover,  in  interlobar  pleurisy  the  signs  (iegophony,  souffle, 
and  pectoriloquy)  have  never  the  clearness  fovmd  in  the  present  case. 

Areolar  and  Polymorphous  Pleurisy. — Loculated  pleurisy  may  be 
chronic  from  the  first,  or  be  due  to  acute  attacks  affecting  the  pleura,  which 
is  already  partitioned  off  by  the  false  membranes  of  former  inflammation. 
Loculated  pleurisy  may  be  sero-fibrinous,  hsemorrhagic,  or  purulent ; 
indeed,  it  is  not  rare  on  performing  thoracentesis  to  meet  with  serous  fluid  in 
some  pockets  and  pus  in  others.  Sometimes  the  loculation  is  simple,  and 
the  false  membrane  divides  the  efEusion  into  two  pockets  only ;  more  often 
the  loculation  is  multiple,  and  the  pockets  are  numerous  ;  lastly,  in  some 
cases  the  pleurisy  is  areolar,  as  if  the  false  memljranes  were  themselves 
infiltrated  with  serous  fluid. 

Areolar  and  polymorphous  pleurisy  usually  present  the  following  forms : 
W(^  find  in  a  patient  the  signs  of  considerable  effusion,  and  diagnose  the 


346  TEXT-BOOK  OF  MEDICINE 

presence  of  4  or  5  pints  of  fluid  in  the  pleura  ;  puncture  is  performed,  and 
we  are  astonished  at  withdrawing  very  Uttle  fluid,  wliich  is  not  in  proportion 
to  the  signs  present ;  further,  we  note  the  persistence  of  the  signs  of  effusion 
at  the  other  parts  of  the  thorax,  either  above  or  below  the  point  of  puncture. 
The  exploratory  needle  shows  that  fluid  is  still  present  at  these  points,  and 
we  conclude  that  a  membranous  septum  is  interposed  between  two  or  more 
pockets  of  fluid.     This  form  has  been  called  "  partitioned  pleurisy." 

Sometimes  the  fluid  is  identical  in  the  different  pockets  ;  at  other  times 
it  is  serous  in  some  and  hsemorrhagic  or  purulent  in  others.  In  this  case 
the  pleurisy  is  called  "  polymorphous  "  (Galliard). 

The  disposition  of  the  false  membranes  wliich  partition  the  pleura  is, 
however,  very  variable.  Sometimes  a  single  horizontal,  oblique,  or  vertical 
pseudo-membranous  partition,  which  divides  the  pleura  into  two  (bilobed 
pleurisy),  exists  ;  at  other  times  multiple  and  irregular  adhesions  divide  the 
pleural  cavity  into  numerous  small  and  distinct  cavities  (multilocular  or 
areolar  pleurisy).  In  the  latter  case  we  often  see  pockets  occupied  by  a 
gelatinous  quivering  mass  that  is  formed  of  a  fibrinous  network  impregnated 
with  serous  fluid,  while  the  neighbouring  pockets  contain  sero-fibrinous, 
sero-hsemorrhagic,  or  sero-purulent  fluid. 

The  partitioning  has  been  attributed  to  the  false  membranes  of  ante- 
cedent pleurisies  ;  relapsing  pleurisy  is  said  to  be  more  easily  partitioned  than 
pleurisy  which  affects  an  intact  serosa.  In  these  cases  the  pleurisy  is  said 
to  be  multilocular  from  the  start.  We  may  also  observe  the  following  varieties : 
encysted  serous  pleurisy,  followed  by  adjacent  empyema,  or  encysted  em- 
pyema, complicated  by  adjacent  sero-pleurisy.  The  latter  cases  are  more 
common,  because  empyema  is  much  more  often  encysted  than  serous  pleurisy. 

Save  in  exceptional  cases  (Jaccoud),  the  diagnosis  of  loculated  pleurisy 
can  only  be  made  after  puncture.  The  attention  is  arousejd  by  the  in- 
sufiicient  quantity  of  fluid  evacuated.  Sometimes,  also,  the  puncture  may 
be  blank,  if  the  needle  penetrate  the  septum.  The  diagnosis  will  be 
confirmed  by  methodical  exploration  of  the  pleural  cavity,  by  means  of  an 
aspirator,  which  is  provided  with  a  long  needle. 

The  prognosis  is  especially  serious  when  encysted  suppurations  escape 
notice,  because  this  fact  prevents  treatment  by  free  incision ;  we  only  find 
them  at  the  autopsy.  We  must  remember  that  polymorphous  pleurisy  may 
be  symptomatic  of  tuberculosis  or  of  pleuro-pulmonary  cancer. 

XII.  SYPHILITIC  PLEURISIES. 

Early  syphihtic  pleurisy  occurs  in  the  secondary  stage,  while  late  syphi  • 
litic  pleurisy  is  seen  during  the  tertiary  period. 

The  early  form  has  been  well  described  by  Chantemes^e  and  Widal,  who 


DISEASES  OF  THE  PLEURA  347 

quote  several  conclusive  cases.     At  the  Hotel- Dieu  I  have  seen  a  very  clear 
example : 

A  man,  twenty  years  of  age,  came  into  the  hospital  with  pain  at  the  lower  angle 
of  the  left  scapula.  Pleurisy  without  effusion  was  found.  Friction  sounds  were  heard, 
which  extended  behind  and  laterally  as  far  as  the  axillary  region.  Other  ortrans 
healthy.  Auscultation  of  the  lung  showed  no  lesions,  and  we  had  to  deal  with  apyi-etic, 
painful  pleurisy  of  four  days'  duration. 

We  could  not  incriminate  tuberculosis,  influenza,  or  rheumatism.  This  boy,  how- 
ever, showed  a  well-marked  syphilitic  roseola.  The  syphilis  was  two  months  old. 
The  cicatrix  of  a  chancre  was  visible  on  the  dorsal  surface  of  the  penis,  and  enlarged 
glands  were  present  in  the  groins.  He  complained  of  headache  and  sore -throat,  and 
we  found  syphilitic  angina,  with  mucous  patches.  As  pleurisy  had  appeared  in  a 
youth,  who  had  for  two  months  been  infected  with  sj'philis,  it  seemed  natural  to 
consider  the  pleurisy  as  a  secondary  complication  of  syphilis,  and  I  placed  the  patient 
on  mercurial  treatment.  The  pleurisy  remained  dry,  and  I  found  no  effusion.  The 
pain  and  friction  sounds  disappeared  in  ten  days. 

Similar  cases  have  been  published,  and  the  occurrence  of  syphilitic 
pleurisy  in  the  secondary  stage  is  therefore  well  proved.  Why  should  we  not 
see  early  syphiUtic  pleurisy  when  we  see  nephritis,  arteritis,  icterus,  and 
]>ronchitis  appear  among  the  early  manifestations  of  syphilitic  infection  ? 
Early  syphiUtic  pleurisy  may  be  dry,  or  be  accompanied  by  effusion.  I  do 
not  beUeve  that  the  efiusion  is  ever  so  abundant  as  to  necessitate  thora- 
centesis. An  important  difference  between  early  and  late  syphilitic  pleurisy 
is  that  the  former  is  not  associated  with  pulmonary  lesions,  while  the  latter, 
with  which  I  am  now  dealing,  forms  part  of  the  broncho-pulmonary  syphi- 
loma discussed  in  the  chapter  on  Syphihs  of  the  Lung. 

I  have  been  able  to  find  only  a  small  number  of  cases  of  tertiary  syphihtic 
pleurisy.  According  to  Mauriac,  "  this  pleurisy  is  often  seen,  and  is 
accompanied  by  effusion."  Tertiary  lesions  of  the  pleura  may  be  placed 
in  one  of  the  following  categories  :  Either  the  pleural  lesion  is  an  unimportant 
complication  of  the  pulmonary  lesion,  or  the  effusion  is  abundant ;  the 
pleurisy  is  the  chief  feature,  and  the  condition  well  merits  the  name  of 
syphilitic  pleurisy.  As  an  epiphenomenon,  mention  must  be  made  of  this 
pleurisy  in  some  cases  of  tertiary  sypliihs  of  the  lung ;  it  has  been  referred 
to  by  Carlier.  In  one,  he  says  without  further  amplification,  that  the 
pleura  on  one  side  contained  300  grammes  of  a  clear  yellow  fluid,  and  the 
visceral  layer  presented  recent  false  membranes,  which  were  very  easily  torn, 
while  the  parietal  and  diaphragmatic  layer  was  also  inflamed. 

In  Jacquin's  thesis  Balzer's  case  of  syphiUtic  pleurisy  with  large  effusion 
is  described : 

A  man,  thirty-two  years  of  ago,  came  to  hospital  with  functional  troubles  and 
physical  signs  which  led  to  the  diagnosis  of  caseous  pneumonia  on  the  right  side.  A 
month  later  abundant  effusion  appeared  on  the  right  side.  Ple\irisy,  complicating  f  i]l)or- 
culosis  of  the  lung,  was  then  diagnosed  ;  but  after  four  days  the  patient  died,  and  the 
autopsy  revealed  a  syphilitic  liver  liiat  M'as  studded  with  gummata  and  segmented  by 


348  TEXT-BOOK  OF  MEDICINE 

scars.  The  right  lung  was  also  full  of  gummata,  the  largest  of  which  just  involved  the 
pleura.  These  gummata  did  not  contain  a  single  Koch's  bacillus.  The  lesions  in  the 
right  pleura  were  so  characteristic  that  I  give  them  in  detail.  "  In  the  right  pleura  a 
much  more  considerable  effusion  exists  than  physical  examination  would  have  led  me 
to  suppose.  There  are  about  4  pints  of  turbid  blood-stained  serum.  The  parietal 
and  visceral  layers  of  the  pleura  are  considerably  thickened  over  the  whole  extent  of 
the  effusion.  They  show  a  continuous  fibrous  covering,  1  or  2  millimetres  in  thickness, 
attaining  at  the  base  of  the  lung  a  thickness  of  nearly  1  centfmetre.  This  fibrous  cap  is  sur- 
rounded by  false  membranes  at  several  spots.  At  the  points  where  the  fibrous  thicken- 
ing is  most  considerable  we  find,  on  section  of  the  pleura,  hard  yellowish  caseous  masses 
as  large  as  a  pea  or  as  a  millet-seed."  This  case  of  tertiary  syphilitic  pleurisy,  in  which 
the  effusion  amounted  to  4  pints,  is  most  conclusive. 

I  saw  the  following  case  : 

I  was  called  to  treat  a  man  with  terrible  dyspnoea,  which  had  recurred  in  more 
or  less  acute  attacks  for  the  past  year.  Tubercular  broncho -pneumonia  had  been 
diagnosed.  On  my  first  examination  I  found  signs  of  an  effusion,  which  I  estimated 
at  1^  pints.  Although  this  quantity  of  fluid  did  not  explain  the  patient's  dyspnoea,  I 
performed  thoracentesis,  but  drew  off  only  21  ounces  of  slightly  rose-coloured  fluid. 
The  patient  experienced,  however,  no  relief.  I  searched,  wthout  success,  for  the  cause 
of  the  disease,  when  he  finally  confided  to  me  that  he  had  had  syphilis.  This  avowal 
guided  my  treatment.  I  at  once  gave  mercury  and  iodide  of  potash  in  large  doses,  and 
the  dyspnoea  improved  so  rapidly  that  at  the  end  of  a  few  weeks  the  breathing  was 
almost  normal.  At  my  last  visits  no  trace  of  pleurisy  remained,  though  the  broncho- 
pulmonary lesions  were  slower  to  improve.  In  this  case,  again,  the  syphilitic  nature  of 
the  trouble  was  shown  by  the  beneficial  action  of  specific  treatment. 

There  exists,  then,  tertiary  pleurisy,  which  is  associated  with  syphilitic 
lesions  of  the  lung,  and  the  true  means  of  diagnosing  it  is  to  think  of 
syphilis. 


XIII.  APPENDICULAR  PLEURISIES— PYOPNEUMOTHORAX  AND 
SUBPHRENIC  EMPYEMA. 

In  1890  I  read  a  paper  before  the  Academic  de  Medecine*  on  "Appen- 
dicular Pleurisy,"  a  name  which  is  generally  accepted  at  the  present 
day.  Later,  in  my  clinical  lectures  at  the  H6tel-Dieu,f  as  I  had  seen  how 
frequently  appendicular  subphrenic  empyema  precedes  or  accompanies 
infection  of  the  pleura,  I  have  united  appendicular  pleurisy  and  sub- 
phrenic empyema  in  a  single  description,  and  I  shall  do  so  in  this  chapter. 

I  think  that  it  will  be  useful  to  give  a  resume  of  some  cases  : 

Clinical  Cases. — A  man,  twenty-six  years  of  age,  admitted  to  the  Hotel-Dieu.  He 
suffered  from  shortness  of  breath,  was  pale,  had  an  anxious  look,  with  simken  eyes,  and 
a  wretched  pulse  ;  he  appeared  moribund.  He  complained  of  a  pain  in  the  right  side 
of  the  chest,  and  was  so  feeble  that  he  could  not  raise  himself  on  the  stretcher.     On 

*  Dieulafoy,  "  La  Pleuresie  Appendiculaire  "  (commimication  a  1' Academic  de 
Medecine,  seance  du  Mardi,  10  Avril,  1900). 

t  Dieulafoy,  "  Pleuresie  Appendiculaire  et  Empyeme  Sous-phrenique  "  (C'linique 
Medicate  de  V Hotel-Dieu,  1903,  vol.  iv.,  15""^  et  16™*  letons). 


DISEASES  OF  THE  PLEURA  349 

the  right  side  I  found  a  large  eflfusion,  with  absolute  dullness,  except  at  the  apex,  where 
the  resonance  was  exaggerated. 

It  is  not  common  for  pleural  effusion,  however  abundant,  to  show  such  general 
symptoms.  In  this  case  it  was  not  simply,  dyspnoea,  but  adynamia,  bordering  on 
collapse,  which  dominated  the  scene.  What,  then,  did  this  efEusion  conceal  ?  Apert 
at  once  performed  exploratory  puncture,  in  order  to  ascertain  the  nature  of  this  pleurisy, 
and  drew  ofi  turbid  fluid,  which  was  of  nauseous  odour  and  not  homogeneous. 

The  case  was  therefore  one  of  foetid,  perhaps  of  putrid  or  of  gangrenous,  pleurisy. 
There  was  not  time  to  make  a  pathogenic  diagnosis,  and  the  imperative  indication  was 
immediate  surgical  intervention.  Marion  therefore  came  to  see  the  patient,  but 
found  him  in  his  death  agony,  with  thready  pulse  and  cold,  cyanosed  limbs.  Death 
occurred  soon  afterwards. 

Prom  the  information  given  by  the  family,  it  was  possible  to  reconstruct  the  case. 

He  was  taken  ill  on  November  10  Anth  abdominal  pains,  which  increased  in  severity 
during  the  night,  chiefly  on  the  right  side.  Next  morning,  as  he  felt  easier,  he  went  to 
his  office.  In  the  evening  he  passed  a  motion.  The  next  night  was  more  comfortable, 
but  on  Sunday  evening  (the  third  day)  he  was  seized  ^rith  such  severe  pain  on  the 
right  side  of  the  belly  "  that  he  twisted  and  groaned  in  agony." 

During  the  exammation  his  wife  remarked  that  the  belly  was  particularly  painful 
on  the  right  side.  An  enema  and  poultices,  with  laudanum,  were  prescribed.  Next 
day  vomiting  came  on.  Patient  had  fever  and  rigors  ;  he  was  constipated,  and  the 
abdominal  pains  were  as  severe  as  ever.  During  the  next  few  days  the  situation  did 
not  improve.     The  hepatic  region  became  painful,  and  a  blister  was  ordered. 

Meanwhile  the  patient  began  to  cough,  and  complained  of  pain  in  the  right  side  of 
the  chest.  Pleuro -pneumonia  was  diagnosed.  Fever  retmrned  ;  violent  pain  in  the 
chest,  M-ith  extreme  dyspnoea,  cold  sweats,  and  tachycardia,  supervened.  On  the 
morning  of  the  29th  hydropneumothorax  was  found.  He  was  then  brought  to  the 
Hotel-Dieu. 

To  sum  up  :  The  disease,  which  lasted  nineteen  days,  was  divisible  into  two  stages  : 
the  first  or  abdominal  stage  was  characterized  by  acute  appendicitis,  and  treated  by 
medical  means;  while  the  second  or  thoracic  stage  terminated  with  symptoms  of  pneumo- 
thorax and  death.     Let  us  now  see  what  the  autopsy  revealed. 

Thoracic  cavity  first  examined.  Intercostal  space  perforated  under  water.  As 
soon  as  the  pleura  was  opened,  a  nauseous  odour  was  noticed,  and  bubbles  of  gas  came 
up  through  the  water,  showing  the  presence  of  foetid  gases  in  the  pleura,  and  confirming 
the  diagnosis  of  pneumothorax,  made  during  life  by  the  physician  who  had  sent  up  the 
patient.     The  case  was  one  of  j)neumothorax  by  putrefaction,  and  not  by  perforation. 

In  the  pleural  cavity,  were  7  pints  of  very  foul  greyish  fluid.  The  left  lung,  which 
was  pushed  back  against  the  spine,  was  reduced  to  a  fifth  of  its  normal  size,  airless,  and 
no  longer  crepitant.  No  adhesions  bound  it  down  to  the  costal  wall,  but  its  base  was 
adherent  to  the  diaphragm.  Pus  was  present  between  the  two  layers  of  the  thickened 
diaphragmatic  pleura.  No  sign  of  perforation  or  of  gangrene  found.  The  pleurisy 
was  putrid,  but  not  gangrenous  ;  putrefaction  and  formation  of  gas,  but  no  mortifica- 
tion of  the  tissues,  existed. 

Let  us  now  pass  on  to  the  abdominal  cavity.  On  the  left  side,  nothing  to  notice  ; 
no  trace  of  peritonitis.  On  the  right  side,  numerous  adhesions  from  the  abdominal 
wall  to  the  organs,  and,  on  tearing  them  through,  5  ounces  of  pus,  quite  as  fa-tid  as  the 
pleural  fluid,  flowed  out.  The  abdominal  cavity  was  explored,  j)us  and  membranes 
found  ;  some  were  spread  out  over  the  intestine  and  the  liver,  while  others  reached 
up  b<'iiind  the  caicum  and  the  colon.  I'osterior  surface  of  tiie  ciecum  bound  down  by 
membranes  to  the  [)arietal  peritoneum.  The  appendix  was  included  in  this  mass.  It 
was  very  long,  of  the  vertical  type,  and  passed  up  on  the  posterior  surface  of  the  c;eiuin  ; 
it  was  free  at  its  caical  origin,  but  higher  up  it  wits  surrounded  by  adhesions  and  bathed 


350  TEXT-BOOK  OF  MEDICINE 

in  pus.  Its  walls,  which  were  double  their  proper  size,  were  becoming  gangrenous, 
but  liad  not  perforated.  It  was  in  this  part  of  the  apiaendix,  wliich  had  been  trans- 
formed into  a  closed  cavity,  that  the  acute  toxi-infection  was  elaborated.  The  jiurulent 
track  continued  behind  the  colon,  turned  round  the  hepatic  flexure,  and  spread  out  in 
front  of  the  right  lobe  of  the  hver,  setting  up  abscesses  in  its  course. 

The  liver  was  partly  hidden  by  perihepatitis.  The  diaphragm  was  examined  for 
a  perforation ;  as  none  was  found,  the  infection  had  evidently  been  carried  to  the 
pleura  by  the  lymphatic  vessels. 

Other  organs — i.e.,  liver,  spleen,  kidney,  and  heart — were  healthy.  The  left  lung, 
however,  had  been  infected.  The  apex  showed  a  splenized  region  as  large  as  an  egg, 
with  several  infarcts  in  different  stages  of  evolution.     The  left  pleura  was  healthy. 

Bacteriological  and  experimental  researches  were  made  by  Apert  with  the  jjua 
dra^\^l  oiT  by  aspiratory  puncture,  and  also  the  peritoneal  pus  removed  at  the  autopsy. 
The  result  was  as  follows  : 

Some  of  the  micro-organisms  were  aerobic,  while  others  were  anaerobic.  They  had 
caused  putrid  pleurisy,  as  shown  by  the  formation  of  gas  within  the  pleura. 

With  guinea-pigs  and  rabbits,  inoculation  of  pus  into  the  cellular  tissue  and  in- 
jection of  pus  into  the  vein  of  the  ear  produced  abscesses  and  infarcts,  containing  the 
same  micro-organisms  that  were  found  in  the  specimens  of  pus. 

The  patient  had  been  taken  ill  with  classical  appendicitis.  I  do  not  know  what  the 
original  diagnosis  was,  but  I  do  know  that  the  treatment  was  medical  when  it  should 
have  been  surgical.  The  man  would  have  been  saved  by  early  operation,  just  as  we 
save  all  the  patients  who  are  operated  on  in  good  time,  when  no  precious  time  is  lost 
in  medical  treatment  which  is  based  on  erroneous  pathogenic  concejjtions.  This  treat- 
ment is  Avrong,  for  it  apjjears  to  be  doing  something  when  it  does  nothing  but  give  the 
toxi-infection  time  to  strike  a  fatal  blow.  Enemata,  sedatives,  and  rest  were  ordered, 
while  infection  of  unusual  \'irulence  was  brewing  in  the  closed  cavity  of  the  appendix. 
Aerobic  and  anaerobic  microbes  then  made  their  way  through  the  walls  of  the  appendix, 
and  provoked  the  formation  of  purulent  tracks,  which  took  an  ascending  course,  and 
in  a  few  days  reached  up  behind  the  caecum  and  colon,  and  spread  to  the  anterior  and 
upper  surface  of  the  Hver. 

The  phrenico-pleural  phase  now  appeared ;  cough,  dyspnoea,  and  pain  were  its 
signs.  The  diaphragm  was  not  perforated,  but,  thanks  to  the  lymphatic  channels, 
was  traversed  by  microbes  of  undiminished  virulence.  It  might  well  be  said  of  this 
process,  Vires  acquirit  eundo.  The  pleural  infection  was  so  acute  that  the  effusion 
rapidly  reached  7  pints.  Putrefaction  was  shown  by  the  appearance  of  the  pneumo- 
thorax. The  lesions  were  so  severe  that  events  hurried  on,  and  the  patient  died  nine- 
teen days  after  the  onset  of  appendicitis. 

The  infection,  which  started  from  the  appendix,  had  followed  two  courses — the  one 
by  the  lymphatics,  and  the  other  by  the  blood.  The  lymphatic  infection  took  place  by 
extension  ;  though  it  started  so  far  down  and  reached  so  high  up,  yet  in  a  few  days 
it  spread  across  the  abdominal  cavity  and  invaded  the  pleura.  The  infection  of  the 
left  lung  was  due  to  microbic  emboli. 

But,  it  will  be  asked,  is  pleurisy  a  frequent  complication  of  appendicitis  ? 
It  is  certainly  far  from  rare,  and  in  proof  I  can  quote  many  cases. 

I  saw  a  very  remarkable  case.  The  patient  was  a  lady,  in  whom  I  diagnosed 
appendicular  jileurisy  and  subphrenic  empyema.  The  double  operation  was  j^erformed 
by  Segond :  he  operated  first  on  the  pleura,  and  a  fortnight  later  he  attacked  the 
subphrenic  empyema.     The  patient  recovered. 

In  consultation  with  Brun  and  Jalaguier,  I  saw  a  youth  with  appenchcular 
pleurisy.  On  May  20  he  was  attacked  mth  appendicitis.  Three  days  later  Brun  found 
severe  peritonitis.     Operation  performed  next  morning.     Appendix  was  gangrenous ; 


DISEASES  OF  THE  PLEURA  351 

peritoneal  fluid  was  sero-purulent  and  foetid.  Free  drainage  established.  During  the 
next  few  days,  in  spite  of  improvement  in  the  peritoneal  condition,  situation  was  grave, 
and  temperature  very  high.  No  cause  could  be  found  for  the  persistence  of  these 
alarming  symptoms.  On  June  2  symptoms  of  right  pleurisy  were  discovered,  and 
exploratory  puncture  drew  oil  turbid  fluid.  On  June  -i  operation  for  emjjyema  ;  a 
large  quantity  of  dirty,  horribly  foetid  fluid  dra^mi  off.  Free  drainage  established. 
Next  day  diffuse  inflammation  at  the  edges  of  the  thoracic  wound,  but  no  gaseous 
crepitation.  During  the  following  days  the  inflammation  stopped  ;  the  antiseptic 
irrigations  of  the  pleura  seemed  to  indicate  that  the  pleural  focus  had  been  effectively 
treated,  but  yet  fever  persisted  and  the  situation  became  worse. 

I  then  saw  the  patient,  with  Brun  and  Jalaguier.  Minute  examination  revealed 
no  fresh  lesions  in  any  organ.  We  were  of  opinion  that  the  patient  was  suffering  from 
a  profound  intoxication,  and  prescribed  accordingly.  About  June  11  cerebral  symp- 
toms (intoxication,  or  perhaps  meningeal  infection)  of  photophobia,  strabismus,  irregu- 
larity of  the  pulse,  and  stiffness  of  the  neck  supervened,  and  the  patient  died. 

Resume  of  two  cases  of  appendicular  pleurisy  described  by  Terillon  : 

A  young  man,  seventeen  years  of  age,  had  suffered  from  appendicitis.  Belly  dis- 
tended and  painful ;  on  the  right  side  a  jjainful  swelling,  reaching  from  the  ihac  crest 
to  the  false  ribs.  Affection  was  of  six  days'  duration.  Temperature,  103°  F.,  and 
pulse  rapid.  Intervention  decided  on.  On  opening  the  abdomen,  caecum  was 
adherent  to  the  abdominal  wall ;  sharp  gush  of  pus  occurred.  The  abscess  occupied 
the  iliac  fossa  behind  the  caecum,  and  reached  up  towards  the  kidney.  On  the  next 
day  the  temperature  as  high  and  the  pulse  as  rapid  as  before  operation  ;  general  condi- 
tion worse.  Two  days  later  it  was  noticed  that  the  respiration  was  embarrassed,  and 
existence  of  a  large  right  effusion  was  made  out.  Puncture  yielded  pus.  After  opera- 
tion for  empyema,  fever  fell  at  once,  improvement  followed,  and  the  patient  was 
completely  cured. 

Boy,  fourteen  years  old,  had  suffered  for  five  days  from  right  iliac  peritonitis.  The 
temperature  was  10-t^  F.,  and  the  gravity  of  the  situation  was  e\adent.  Terrillon  pro- 
posed immediate  operation,  which  was  not  agreed  to.  Ten  days  later  he  was  sent  for 
in  a  hurry.  The  child  was  sitting  up  in  bed,  having  shown  symptoms  of  asphyxia 
since  the  morning.  Large  effusion  present  on  right  side.  About  a  pint  of  fcetid  pus 
was  dra-n-n  off  by  puncture,  but  syncope  came  on  suddenly,  and  the  patient  died.  It  is 
probable  that  in  this  case,  as  in  the  preceding  one,  prompt  operation  would  have  brought 
about  a  cure. 

The  pleural  complications  of  appendicitis  have  been  studied  in  Germany 
since  1891.  Here  is  a  series  of  cases.  Wolbrecht,  in  his  thesis  (Berhn,  1891) 
entitled  "  Pleural  Complications  in  TyphUtis  and  Perityphhtis,"  quotes  a 
few  cases,  two  of  wliich  are  personal. 

Case  1. — A  joiner,  twenty-four  years  of  age,  who  some  days  before  had  experienced 
the  symptoms  of  perityphlitis,  came  into  his  clinic.  Signs  of  subphrenic  abscess  and  of 
right  pleurisy.  Exploratory  puncture  drew  off  fujtid  pus.  Operation  for  empyema 
perforimd  ;  lifth  rib  resected  ;  5  pints  of  nauseous  fluid  withdrawn.  Two  months  later 
patient  was  cured. 

Case  2. — .\  num  suffering  from  ])erityphlitis,  with  circumscribed  peritonitis.  Ten 
days  later  right  pleurisy,  witli  rederaa  of  tlie  chest-wall.  Exploratory  pum^ture  showed 
turbid  blood-stained  cflusion.  Three  days  later  patient  seized  with  violent  coiigli, 
and  brought  up  abundant  foul-smelling  pus.  lie  finally  recovered,  after  a  convalescence 
of  three  mouths. 


352  TEXT-BOOK  OF  MEDICINE 

Larsen  and  Winge  relate  a  case  of  appendicitis,  with  retrogression  of  the 
peritoneal  symptoms  at  the  end  of  the  first  week : 

Pain  in  the  right  hypochondrium  appeared,  and  right  pleurisy  developed  rapidly. 
The  dyspnoea  became  very  intense,  and  death  followed.  Post-mortem  :  pyopneumo- 
thorax on  the  right  side  ;  perforated  appendix  buried  in  an  abscess  ;  narrow  purulent 
track  ran  up  behind  the  Uver,  and  had  perforated  the  diaphragm  in  two  places. 

Grawitz,  under  the  title  of  "  Perforation  of  a  Perityphlitic  Abscess  into 
the  Pleural  Cavity,"  has  pubHshed  the  following  case  : 

A  woman  was  taken  ill  a  fortnight  before,  with  pain  in  the  right  side  of  the  belly, 
constipation,  fever,  and  vomiting.  Later  the  symptoms  of  right  pleurisy  supervened, 
and  the  patient  died  three  weeks  after  admission  to  hospital.  Post-mortem  :  the  whole 
appendix  was  converted  into  a  sac,  and  had  perforated  ;  near  its  base  was  a  calculus, 
the  size  of  a  haricot  bean.  The  intestinal  coils  were  adlierent  in  the  right  iliac  fossa, 
and  the  pelvis  contained  pus.  From  the  gangrenous  appendix  a  sinuous  cavity  extended 
upwards  behind  the  right  kidney  and  the  duodenum.  A  perforation,  as  large  as  a 
sixpence,  was  present  in  the  posterior  part  of  the  diaphragm,  and  established  com- 
munication between  the  subdiaphragmatic  region  and  the  right  pleura.  Three  pints  of 
foetid  pus  in  the  pleural  cavity. 

Wollert  has  pubUshed  similar  cases  : 

A  young  man,  sixteen  years  of  age,  was  taken  ill  with  appendicitis.  Thirteen  days 
later  sharp  pains  at  the  right  base,  and  intense  dyspnoea.  Right  pyopneumothorax, 
with  metallic  tinliling,  found.  Post-mortem  :  iDcritonitis,  consecutive  to  appenchcitis. 
Sheet  of  pus  over  the  ascending  colon,  the  diaphragm,  and  the  hver.  The  diaphragm 
was  perforated,  and  the  right  pleura  contained  8  pints  of  j)urulent  Huid,  with,  foetid  gas. 

Appendicular  pleurisy  is  sometimes  serous ;  the  infection  is  reduced  to  a 
minimum,  and  recovers  with  or  without  operation. 
Case  seen  with  Larcher  and  Monod  : 

Young  girl  suffering  from  appendicitis,  diagnosed  by  Larcher,  and  operated  upon  by 
Monod  on  May  9.  Everything  went  well  until  May  18,  when  pain  appeared  in  the  right 
hypochondrium  and  at  the  base  of  the  chest.  The  temperature  now  rose  to  103°  F. 
Cough  was  frequent,  though  expectoration  absent.  This  condition  lasted  for  several 
days,  without  appreciable  change.  I  was  then  called  to  see  the  patient,  and  found 
friction  sounds  and  fluid  on  the  right  side.  In  this  case  we  had  to  discuss  the  projjriety 
of  surgical  intervention.  As  the  general  condition  was  not  bad,  we  agreed  to  see 
patient  again  before  we  decided.  We  had  the  satisfaction  of  witnessing  the  successive 
disappearance  of  the  tubular  breathing  and  the  friction  sounds,  while  the  fever  yielded 
and  recovery  ensued  at  the  end  of  four  weeks. 

A  child,  fourteen  years  of  age,  who  had  had  several  previous  attacks,  was  again 
taken  ill  with  appendicitis  and  pericsecal  abscess.  He  was  operated  on  by  Jala- 
guier.  The  appendix,  of  the  vertical  t3rpe,  had  a  bent  extremity,  which  was  adherent 
and  communicated  with  the  cfecum.  Some  days  later  dyspnoea  came  on  ;  dullness, 
with  tvibular  breathing  on  expiration,  and  aphonic  pectoriloquy,  were  cUscovered  at 
the  right  base.     Some  effusion  formed,  but  was  absorbed  eight  days  later. 

Korte  reports  the  case  of  a  woman  suffering  from  retrocsecal  inflammation.  In 
spite  of  incision,  the  infiammation  passed  through  the  diaphragm  and  reached  the 
pleura.  Resection  of  the  eighth  and  ninth  ribs  ;  patient  recovered  from  the  effusion, 
which,  the  author  states,  was  serous.  Another  case  of  Korte's  is  that  of  a  man,  twenty- 
eight  years  of  age,  who  was  taken  ill  with  sharp  abdominal  pains  on  the  right  side, 


DISEASES  OF  THE  PLEUKA  353 

fever,  and  shivering.  A  purulent  collection  necessitated  surgical  intervention,  and  a 
putrid  phlegmon,  which  reached  from  the  csecum  to  the  diaphragm,  was  opened.  An 
effusion,  which  was  punctured,  formed  on  the  right  side.  The  author  describes  it  as 
serous.     The  patient  finally  recovered. 

Description. — The  first  point  to  note  is  the  manner  in  which  the  appen- 
dicular infection  reaches  the  pleura.  How  does  a  remote  lesion  like  appen- 
dicitis attack  the  pleural  cavity  ?  Why  does  appendicitis,  which  is  a  very 
small  lesion,  succeed  in  a  few  days  in  producing  putrid  pleurisy,  with 
several  pints  of  fluid  ?     Let  us  try  to  answer  these  questions. 

The  infection,  wliich  becomes  more  virulent  in  the  closed  cavity  of  the 
appendix,  causes  the  pathogenic  microbes,  Bacillus  coli,  and  other  aerobic 
or  anaerobic  germs  to  spread  to  the  peritoneum.  Sometimes  perforation  or 
gangrene  of  the  walls  of  the  appendix  occurs,  and  the  microbic  pulp  spreads 
widely  over  the  peritoneum  ;  at  other  times  the  migration  of  microbes  takes 
place  through  the  imperforated  wall,  as  we  may  see  from  specimens.* 

The  infection,  after  reaching  the  peritoneum,  behaves  in  different  w^ays. 
It  may  only  spread  a  short  way  from  its  seat  of  origin,  being  hmited  or  not 
by  adhesions,  or  it  may  excite  remote  foci,  wliich  show  no  apparent  relation 
to  the  original  focus.  These  remote  abscesses  are  due  to  microbes  carried  to 
a  distance,  but  in  what  way  we  do  not  always  know.  Can  these  remote 
abscesses  arise  in  the  pleural,  as  in  the  peritoneal,  cavity  ?  In  other  words, 
can  remote  pleurisy  occur  in  the  course  of  appendicitis  ?  Certainly ;  but 
most  often  it  is  by  proximity,  through  the  peritoneal  track,  by  way  of  the 
adhesions  and  of  the  lymphatics  that  extension  to  the  pleura  takes  place. 
Under  such  circumstances  the  appendicitis  is  nearly  always  of  the  ascending 
type.  The  direction  of  the  appendix  is  an  essential  factor.  In  appendicitis 
of  the  descending  type  the  purulent  collections  and  adhesions  often  form 
in  the  pelvis  near  the  bladder  and  rectum,  but  in  the  ascending  type  the  pus 
and  membranes  pass  up  towards  the  hver.  The  infection  takes  place  from 
below  upwards,  because  the  initial  focus,  or  'primum  movens,  gives  it  this 
direction.  It  reaches  the  hypochondrium,  passes  through  the  diaphragm, 
and  invades  the  pleural  cavity,  having  marked  its  route  by  purulent  tracts, 
so  that  it  is  possible  to  follow  the  infection  from  its  small  origin  in  the 
appendix  to  its  full  maturity  in  the  thorax.  Appendicular  pleurisy  nearly 
always  occurs  on  the  right  side;  there  are  very  few  exceptions  to  this 
rule. 

Let  us  now  turn  to  the  cUnical  side  of  the  question.  At  what  moment 
may  pleural  com})lications  ensue  in  appendicitis  ?  They  appear  about  a 
week  or  a  fortnight  after  the  on.set  of  appendicitis.  The  infection,  which 
starts  from  the  appendix,  does  not  begin  its  migration  before  the  third  or 
fourth  day.  Surgery  has,  therefore,  time  to  intervene.  By  suppressing 
*  Diculafoy,  Clinique  Mcdicalc  del' Hutd-lJicu,  18'J7,  pp.  345,  .'>l(">,  347. 


354  TEXT-BOOK  OF  MEDICINE 

the  infecting  focus  at  its  commencement,  the  disease  is  cut  off  at  the  root. 
Let  us  not  forget  that  appendicitis,  whether  slight  or  severe,  may  be  fol- 
lowed by  pleurisy,  just  as  it  may  be  followed  by  abscess  of  the  liver  ;  in  the 
case  of  appendicitis  the  benign  nature  is  only  apparent.  Pleural  com- 
pUcations  are  hardly  hkely  when  the  active  process  of  appendicitis  is 
extinct. 

The  appearance  of  appendicular  pleurisy  is  usually  heralded  by  the 
symptoms  which  I  have  called  abdomino-phrenic — viz.,  pain  in  the  right 
hypochondrium  radiating  to  the  shoulder,  dyspnoea,  and  apparent  increase 
in  the  size  of  the  liver.  These  symptoms  are  explained  by  the  perihepatitis 
and  the  subphrenic  empyema  which  often  precede  the  stage  of  pleurisy. 
Pleural  symptoms,  pain  in  the  side,  and  cough  appear  in  their  turn,  and 
blend  with  the  abdomino-phrenic  ones. 

The  abdomino-phrenic  symptoms,  which  usually  precede  those  of  pleurisy, 
may  themselves  be  preceded  by  abdominal  symptoms  of  pain  in  the  right 
flank,  puffiness,  and  dullness  ;  they  indicate  the  passage  of  purulent  infection 
from  the  right  iHac  fossa  to  the  hypochondrium. 

As  appendicular  pleurisy  has  not  always  the  same  course,  we  must  study 
its  various  forms.  As  a  rule,  the  pleurisy  is  putrid,  with  much  effusion  ; 
the  fluid  forms  rapidly.  The  fever  is  variable  ;  dyspnoea,  anxiety,  loss  of 
strength,  weak  pulse,  sallow  and  earthy  tint  of  the  skin,  bear  witness  to  the 
gravity  of  the  situation.  It  is  true  that  the  pleural  infection  is  not  the 
only  cause :  the  peritoneal  infection  is  responsible  for  its  share.  (Edema  of 
the  wall  is  not  rare. 

We  frequently  find  amphoric  breathing  and  hippocratic  succussion,  which 
point  to  pneumothorax.  At  first  we  tliink  of  pleuro-pulmonary  perforation, 
and  do  not  admit  the  possibility  of  pneumothorax  from  putrefaction. 

In  considering  putrid  right  pleurisy,  we  must  always  think  of  appendi- 
citis, even  though  it  has  been  so  slight  as  to  attract  but  Httle  attention. 
We  must  reconstruct  the  appendicular  and  abdominal  stages,  which  have 
preceded  the  phrenic-pleural  stage  by  six  or  eight  days. 

Whether  there  be  pneumothorax  or  not,  as  soon  as  pleurisy  develops 
suddenly,  with  grave  symptoms,  we  should  without  delay  investigate  the 
nature  of  the  fluid.  Exploratory  puncture  is  performed  at  once,  and  turbid, 
non-homogeneous,  greyish  or  brownish  foetid  fluid  is  drawn  off.  In  such 
a  case,  without  waiting  for  the  result  of  aerobic  or  of  anaerobic  cultures, 
operation  for  empyema  must  be  performed  immediately.  The  fluid,  in  a 
test-tube,  divides  into  two  layers  ;  the  lower  one  forms  a  dense,  dark- 
coloured  deposit ;  the  upper  has  a  serous  or  turbid  appearance. 

Appendicular  pleurisy  has  httle  tendency  to  vomica;  its  course  is  so  rapid 
and  compUcations  occur  so  quickly  that  the  vomica  has,  doubtless,  no  time 
to  occur.     I  know  of  only  two  cases  : 


DISEASES  OF  THE  PLEURA  355 

One  (Krokne)  concerns  a  young  girl  with  appendicitis  and  jjeripaecal  peritonitis. 
Some  weeks  later  subphrenic  empj^ema  occuri'ed,  and  was  followed  by  fits  of  coughing 
and  fcetid  vomica.  Laparotomy,  performed  forty-eight  hours  later,  revealed  a  large 
subdiaphragmatic  abscess,  opening  into  the  thoracic  cavity.  The  condition  might, 
perhaps,  have  been  due  to  the  opening  of  a  subphrenic  abscess  without  concomitant 
pleurisy. 

I  would  say  as  much  conceriiiiig  the  following  case,  reijorted  by  Andre 
and  Michel : 

A  yoimg  woman  had  appendicitis  and  peritonitis.  Laparotomy  evacuated  a 
quantity  of  fcetid  pus  ;  pleuro -pulmonary  signs  appeared  later  ;  exploratory  punctures 
made,  in  order  to  ascertain  the  nature  of  the  fluid,  gave  no  result,  and  an  exploratory 
incision  had  no  better  success.  The  patient  was  seized  with  vomica  and  died.  No 
autopsy  was  allowed. 

Such  is  the  history  of  putrid  appendicular  pleurisy  in  its  most  common 
form.  In  some  cases  the  fluid,  as  I  have  said,  is  serous,  the  infection  is 
reduced  to  a  minimum,  and  the  condition  resembles  serous  pleurisy,  which 
absorbs  spontaneously  or  yields  to  puncture.  These  benign  cases  of  appen- 
dicular pleurisy  are  not  accompanied  by  the  grave  symptoms  of  the  preceding 
variety. 

Appendicular  Subphrenic  Empyema. — I  have  mentioned  above  how  the 
infection  ascends  from  the  appendix  to  the  pleura.  In  its  course  this 
infection  marks  its  route  by  puridcnt  collections,  of  wliich  one  is  subphrenic 
empyema.  The  collection  may  be  of  Uttle  or  of  serious  import  ;  we  may 
find  from  1  to  3  pints  of  fluid.  If  the  collection  is  small  in  amount 
the  signs  are  difficult  to  recognize,  but  yet  the  subphrenic  pain  is  a  good 
guide.  If  the  collection  is  abundant,  we  find,  besides  the  pain,  which  may 
be  made  worse  by  pressure  in  the  subphrenic  region,  deformity  and  bulging 
in  the  epigastric  and  right  hypochondriac  regions  ;  the  Hver,  which  is  pushed 
down  by  the  effusion,  appears  enlarged,  though  it  is  only  displaced,  and,  on 
the  other  hand,  the  dullness,  wliich  ascends  towards  the  thoracic  cavity, 
simulates  a  non-existent  effusion  in  the  pleura. 

Although  the  liver  is  surrounded  by  pus  it  remains  free,  and  tliis  point 
distinguishes  it  radically  from  appendicular  infection  of  the  organ,  which 
is  then  riddled  with  abscesses.  The  reason  is  that  the  mode  of  infection  is 
quite  different  in  the  two  cases.  In  the  former  case  the  infection  spreads  by 
the  peritoneum,  and  has  nothing  to  do  with  tlie  liver,  while  in  the  latter 
case,  the  infection  is  carried  to  the  liver  tissue  by  the  portal  vein. 

The  infection,  in  its  upward  course,  does  not  always  reach  the 
j)l<'ura,  but  is  arrested  in  its  progress  and  causes  subplirenic  empyema 
without  consecutive  pleurisy.  Cases  of  tliis  nature  are  not  immerous ; 
they  have  been  described  by  Leyden,  by  Mayal,  Lang,  and  Greig  Smith ; 
and  in  France  have  been  treated  in  works  which  are  reviewed  in  Lape}-re's 
monograph.     Spillman  has  pubUshed  the  following  case  : 

23—2 


356  TEXT-BOOK  OF  MEDICINE      ' 

A  youth  with  appendicitis  Avas,  on  the  seventh  day,  seized  with  dyspnoea  and  very 
sharp  pain  between  the  nipple  and  the  false  ribs  on  the  right  side  ;  absolute  dullness  in  the 
axilla  and  at  the  right  base  ;  punctures  were  negative  ;  acute  dyspnoea  and  death  some 
days  later.  Post-mortem :  purulent  tracts  and  subphrenic  collection,  estimated  at 
4  pints,  in  addition  to  appendicitis  ;  the  lungs  were  oedematous,  but  the  pleura  was  free. 

Subphrenic  empyema  does,  therefore,  occur  without  concomitant 
pleurisy,  but  most  often  both  lesions  are  present. 

Cases  in  which  the  abscess  contains  gas  have  been  quoted,  and  deserve 
therefore  the  name  of  appendicular  subphrenic  pyopneumothorax. 
Speaking  generally,  pyopneumothorax  is  consecutive  to  perforation  of  a 
neighbouring  organ,  to  ulcerations  of  the  stomach  and  duodenum,  to  per- 
foration of  the  diaphragm,  and  communication  with  the  thoracic  cavity,  etc. 
These  cases  of  pyoj)neumotliorax  are  very  rare,  and  when  gas  is  found  in 
the  subphrenic  focus  it  nearly  always  comes  from  perforation  of  a  neigh- 
bouring organ,  such  as  the  stomach,  intestine,  but  especially  the  diaphragm 
and  air-passages. 

In  a  case  published  by  Starcke,  subphrenic  pyopneumothorax  was  consecutive  to 
appendicitis,  but  the  presence  of  gas  was  explained  by  perforation  of  the  diaphragm 
and  communication  with  the  bronchi.  Greig  Smith  speaks  of  subphrenic  pyopneumo- 
thorax following  appendicitis.  Here  also  the  presence  of  gas  was  due  to  perforation 
of  the  diaphragm.  Vanlair  says  a  child  presented  an  epigastric  tumour  (probably 
subphrenic  empyema)  after  appendicitis.  Three  days  later  pneumothorax  suddenly 
appeared  on  the  right  side  ;  the  skin  over  the  epigastric  tumour  became  thin.  An  incision 
was  made,  letting  out  foetid  fluid  and  gas.  We  may  suppose  that  the  gases  in  the  sub- 
phrenic collection  came  from  the  concomitant  pneumothorax. 

Case  1  (reported  by  Sallet). — A  child  had  a  swelling  in  the  -epigastric  angle,  following 
appendicitis.  At  the  same  time  abolition  of  vocal  fremitus,  segophony,  and  dullness 
were  found  at  the  base  of  the  right  side  of  the  chest.  Below  the  dull  area  amphoric 
resonance  and  bruit  d'airain.  Thoracentesis  yielded  foul  pus.  Next  day  lower  ribs 
resected  and  the  diaphragm  incised.  Pus  and  gas  came  out,  and  death  supervened 
three  weeks  later.  Post-mortem,  the  subphrenic  pocket  contained  no  pus,  and  the 
pleura  only  some  serous  fluid. 

Case  2. — A  child  had  appendicitis  ;  eight  days  later  painful  swelling  in  the  right 
hypochondrium  ;  diagnosis  of  subphrenic  abscess,  verified  by  operation  ;  death  next 
day ;  no  autopsy. 

Eisenlohr  writes  :  A  youth  had  appendicitis  ;  symptoms  of  peritonitis  supervened  a 
week  later.  Some  days  afterwards  tubular  breathing  at  the  right  base,  marked  tym- 
panites and  bulging  of  the  hypochondrium.  Patient  died,  and  post-mortem,  mild 
appendicitis,  causing  all  these  troubles,  was  found.  Right  side  of  the  peritoneal  cavity 
invaded  by  pus  and  adhesions.  Between  the  liver  and  the  diaphragm  a  pocket  full  of 
pus  and  gas.  This  pocket  communicated  through  a  perforation  in  the  diaphragm  with 
the  right  pleura,  which  also  contained  pus  and  gas. 

Appendicular  subphrenic  pyopneumothorax,  therefore,  exists.  It  is 
ushered  in  by  the  symptoms  of  subphrenic  abscess,  given  above,  with  bulging, 
tympanites  of  the  epigastrium  or  hypochondrium  and  acute  dyspnoea. 
It  may,  therefore,  be  difficult  to  know  whether  pyopneumothorax  is  supra- 
or  subdiaphragmatic.     Does  the  gas  in  the  subphrenic  pocket  come  from  a 


DISEASES  OF  THE  PLEURA  357 

communication  with  the  air-passages,  or  can  a  putrid  collection,  as  in 
putrid  pleurisy,  produce  the  gas  ?  The  analysis  of  the  cases  which  I  have 
just  quoted  nearly  always  shows  production  of  gas  by  effraction,  perforation 
of  the  diaphragm,  and  communication  of  the  subphrenic  focus  with  the 
pleura  or  with  a  bronchus.  In  two  cases  only,  tliis  production  by  effraction 
has  not  been  noted.  It  is  possible  that  in  subphrenic  pyopneumothorax, 
as  in  putrid  pleurisy,  gas  may  result  from  putrefaction. 

Surgical  intervention  is  the  only  treatment  in  subplirenic  empyema.  It 
must  be  early,  and  is  often  double  ;  it  may  be  triple,  and  comprise  the 
empyema,  the  pleurisy,  and  the  appendicitis. 

In  a  case  reported  by  Margery  tliree  successive  operations  were  performed : 
first,  laparotomy,  to  open  the  abscess  in  the  ihac  region  and  resect  the 
appendix  ;  secondly,  ten  days  later,  opening  of  the  subphrenic  abscess  ;  and, 
lastly,  operation  for  empyema  some  days  afterwards.  Remarkable  to  relate, 
the  case  terminated  in  recovery. 


XIV.  FCETID,  PUTRID,  AND  GANGRENOUS  PLEURISY. 

This  section  is  devoted  to  the  pleurisy  in  which  foid-smelling  fluid  is 
present.  I  propose  to  unite  them  under  the  general  term  of  ozsenous 
pleurisies  {S^eiv,  to  smell  badly).  The  symptom  which  first  attracts  attention 
is  the  foul  smell  of  the  pleural  fluid,  whether  it  is  evacuated  by  puncture, 
incision,  or  by  vomica.  A  few  drops  drawn  off  by  exploratory  puncture 
are  often  sufflcient  to  exhale  a  foul  odour. 

I,  for  my  part,  have  seen  several  instructive  cases  Avhich  I  have  described 
in  my  lectures  at  the  Hotel-Dieu.*  We  have,  therefore,  material  for  clearing 
up  the  question  of  ozsenous  pleurisy,  which  I  shall  divide  into  three  groups 
— foetid,  putrid,  and  gangrenous. 

Foetid  Pleurisy. 

This  name  must  be  reserved  for  pleurisy  in  which  the  fluid  is  foul-smelling, 
while  the  stench  is  not  due  to  putrefaction  or  gangrene.  The  term  "  foetid  " 
implies  that  the  pleurisy  is  neither  putrid  nor  gangrenous.  It  is  not  putrid, 
for  it  has  none  of  the  characters  of  putrefaction  and  does  not  give  off  gas  in 
the  pleural  cavity  (the  patient,  therefore,  has  not  pneumothorax)  ;  inocula- 
tion of  the  fluid  does  not  cause  gaseous  inflammation,  and  the  liquid,  placed 
on  a  culture  medium,  produces  neither  fermentation  nor  l>ul)bles  of  gas  in 
the  test-tube.  The  pleurisy  is  not  gangrenous,  for  we  find  neither  sloughs 
in  tlie  fluid  nor  any  trace  of  gangrene  in  the  walls. 

This  proves  that  the  odour  of  the  fhiid  is  not  an  index  ftf  pu<  refaction 

*  Dieulafoy,  "  Pleuresies  Fetides,  Putricles,  Gangr^neusea  "  {Clinique  Medicale  de 
I'Hi'M-lJieu,  \W:i,  vol.  iv..  IJ'""  et  4"'"'  If9()ns). 


358  TEXT-BOOK  OF  MEDICINE 

or  of  gangrene,  in  the  same  way  as  fcstor  of  the  breath  and  of  the  expectora- 
tion does  not  always  mean  gangrene  of  the  lung.  Tliis  important  distinction 
had  not  escaped  the  notice  of  Laennec  and  Trousseau. 

The  cases  of  sero-purulent  or  purulent  pleurisy  that  are  simply  foetid, 
without  putrefaction  and  gangrene,  are  so  frequent  that  it  would  be  common- 
place to  publish  them.  The  fluid  was  foetid  in  several  of  the  cases  reported 
in  my  lectures  on  interlobar  pleurisy. 

It  is  to  be  noted  that  encysted  pleurisy  is  more  often  foetid  than  putrid 
or  gangrenous,  while  putridity  and  gangrene  are  common  in  pleurisy  of  the 
great  pleural  cavity.  Pleurisy  of  the  great  pleural  cavity  may  not  be  foetid, 
as  is  proved  by  the  following  case,  which  is,  I  believe,  the  only  one  of  foetid 
pleurisy  that  has  been  closely  examined  by  cy to- diagnosis  and  cultures,  and 
confirmed  by  experimental  research : 

A  man,  twenty-seven  years  of  age,  admitted  for  pain  in  right  side,  obstinate  cough, 
and  foetid  expectoration.  Disease  began  six  weeks  before.  He  was  taken  ill  with 
shivering  fits,  fever,  and  sharp  pain  in  the  right  side  of  the  chest.  Fits  of  coughing 
soon  supervened,  and  he  brought  up  much  yellow  but  odourless  expectoration.  The  pain, 
which  extended  all  over  the  right  side,  had  its  maximum  behind,  below  the  scapula, 
and  the  expectoration  became  foetid.  The  man  looked  ill ;  respiration  rate  increased, 
and  his  temperature  was  103°  F.  The  sputum  glass  was  filled  with  diffluent  fcetid 
expectoration  of  a  greyish-yellow  colour.  It  had  never  been  blood-stained.  The  breath 
was  also  fcetid.  The  foetor  was,  however,  not  like  that  of  gangrene.  Examination  of 
the  sputum  revealed  neither  blood,  elastic  fibres,  nor  Koch's  bacilli,  but  numerous 
microbes.     Thi'eads,  bacilli,  cocci,  diplococci,  and  streptococci  ;  no  pneumococci. 

Dullness  behind  most  marked  over  middle  and  inferior  part  of  chest.  On  ausculta- 
tion, subcrepitant  rales  above  this  zone,  and  at  the  level  of  the  eighth  intercostal 
space,  4  inches  from  the  median  line,  cavernous  breathing,  but  no  gurgling — a  fact  which 
proves  that  the  condition  was  due  to  consolidation  of  the  lung,  and  not  to  cavity. 
Below  this  zone,  on  expiration,  tubular  breathing  of  a  pleuritic  tone. 

Exploratory  puncture  gave  exit  to  a  serous  fluid,  which  was  for  the  time  being  odour- 
less. Cy  to -diagnosis  showed  polynuclear  cells  ;  no  lymphocytosis,  no  endothelial 
plaques.  The  absence  of  lymphocytosis  ehminated  acute  tubercular  pleurisy.  The 
absence  of  endothelial  plaques  put  mechanical  pleurisy  out  of  the  question.  We  had 
to  do  with  an  acute  infectious  pleurisy,  consecutive  to  a  similar  lesion  of  the  lung. 
However,  one  thing  puzzled  us  :  the  pulmonary  lesion  was  foetid  and  the  pleurisy  was 
not.  The  lesion  of  the  lung  resembled  neither  pneumonia  nor  broncho -pneumonia. 
We  might  have  considered  hepatization  of  the  lung,  resembling  somewhat  the  infarcts 
consecutive  to  septic  emboli,  but  we  found  no  suspicion  of  such  an  origin. 

The  left  side  of  the  chest  was  healthy  and  the  heart  was  normal,  while  the  urine 
contained  neither  sugar  nor  albumin. 

During  the  next  few  days  the  situation  changed.  The  patient  looked  ill,  was  pros- 
trated, and  had  an  earthy  tint.  The  cavernous  breathing  diminished  and  the  foetid 
expectoration  was  less  abundant,  but  the  pleural  effusion  made  rapid  progress.  The 
dyspnoea  increased,  the  temperature  rose  to  103°  F.,  and  exploratory  puncture  yielded 
turbid  fluid,  like  dirty  water,  and  horribly  foetid,  although  some  days  before  it  Avas 
yellowish  and  odourless.  The  absence  of  pneumothorax  eliminated  putrid  pleurisy. 
The  fluid  was  placed  on  culture  medium  and  inoculated  into  a  guinea-pig.  As  the  case 
demanded  immediate  surgical  intervention,  Legueu  resected  the  ribs. 

The  incision  let  out  4  pints  of  fluid,  which  resembled  muddy  water,  and  had  a  very 


DISEASES  OF  THE  PLEURA  359 

marked  fcetor.  No  gas,  no  membranes,  no  shreds  of  slough.  The  finger  could  only 
just  reach  the  retracted  lung.     No  adhesions. 

Result  of  operation  excellent.  In  a  ie^v  days  the  sputum  became  less  abundant  and 
lost  its  foetid  odour.     Recovery  complete  in  six  weeks. 

Examination  of  the  foetid  fluid  from  the  second  puncture  (Apert).  The  fluid  was 
not  purulent  in  the  true  sense  of  the  word,  but  turbid  and  analogous  to  dirty  water. 
On  direct  examination  with  the  microscope,  this  fluid,  which  at  the  first  puncture  was 
rich  in  polynuclear  cells,  now  contained  only  cellular  elements  in  the  form  of  granular 
masses,  which  stained  badly  and  did  not  show  nuclei.  They  were  dead  leucocytes, 
showing  granular  degeneration.  Further,  many  different  microbes  were  found,  in- 
cluding long  thin  threads,  thin  and  short  bacilli,  and  small  micrococci.  All  these 
microbes,  except  some  micrococci,  did  not  stain  by  Gram. 

On  aerobic  cultures  (agar  and  broth),  colonies  of  Staphylococcus  cdbus. 

On  anaerobic  cultures  (thick  agar),  colonies  having  the  appearance  of  white  lenticular 
points.  No  development  of  gas  among  these  colonies,  either  upon  glucose  agar  or  on 
ordinary  agar  ;  the  cultures  remained  odourless.  Microscopical  examination  of  these 
colonies  showed  that  they  were  composed  of  masses  of  a  small  micrococcus,  which  did 
not  stain  with  Gram,  and  resembled  Veillon  and  Zuber's  Staphylococcus  parvulus. 

A  cubic  centimetre  of  freshly-drawn  fluid,  inoculated  under  the  skin  of  a  guinea- 
pig,  produced  neither  pus  nor  gas,  and  the  animal  remained  in  good  health. 

Such  was  the  history  of  tliis  case.  Let  us  discuss  it.  The  patient 
showed  two  stages  of  infection — the  one  puhnonary,  the  other  pleural. 
Although  the  expectoration  and  the  fluid  were  foetid,  there  was  no  resem- 
blance to  gangrene. 

Was  this  a  case  of  putrid  pleur-isy  ?*  At  first  sight  it  might  have  been 
thought  so,  but  proof  is  absent.  All  the  signs  of  putridity  were  wanting  : 
no  formation  of  gas  in  the  pleura,  no  pneumothorax,  no  gaseous  inflammation 
along  the  track  of  the  aspirating  needle,  no  bubbles  of  gas  in  the  test-tubes, 
and  no  gaseous  lesions  in  the  tissues  of  the  inoculated  animal. 

Foetid  pleurisy  remained.  This  man  evidently  had  had  foetid  pleurisy, 
set  up  by  a  similar  lesion  in  the  right  lung.  There  is  nothing  to  show  that, 
had  the  pleurisy  been  left  to  itself,  it  would  have  become  putrid. 

The  fluid  in  footid'pleurisy  is  turbid  or  sero- purulent,  and  we  find  aerobic 
or  anaerobic  microbes  in  great  variety,  which,  though  little  apt  to  produce 
putrefaction  or  gangrene,  may  give  off  a  foul  odour  (that  of  asafcetida), 
just  as  other  microbes  (chromogenes)  give  off  colouring  substances. 

This  variety  is  the  least  formidable  of  the  group  of  ozsenoas  pleurisy ; 
it  does  not  rapidly  cause  grave  symptoms  (adynamia,  tendency  to  collapse, 
and  syncope),  but  it  must  be  discovered  as  quickly  as  possible  by  exploratory 
puncture  and  operated  on  without  delay. 

The  differentiation  of  foetid  from  putrid  and  gangrenous  pleurisy  is  not 
always  easy  at  first,  and  the  degree  of  foetor  is  not  sufficient  to  make  a 
diagnosis  ;  la])oratory  experiments  and  operation  are  sometimes  necessary 
to  confinn  it. 

*  "  La  IMeuresie  Medinstine  "  (('llni<inp  Mi;dicale  de  VIIotelDiru,  1800,  1""  lecon). 


360  TEXT-BOOK  OF  MEDICINE 

Putrid  Pleurisy. 

Putrid  pleurisy  is  distinguislied  from  the  simply  foetid  variety  by  the 
fact  that  we  find  the  signs  of  putrefaction — i.e.,  formation  of  gas  in  the 
pleural  cavity  (pneumothorax)  and  in  the  test-tube  ;  formation  of  gaseous 
inflammation  along  the  track  of  an  exploratory  puncture  in  the  walls  of  the 
chest ;  appearance  of  gaseous  inflammation  in  the  tissues  of  an  inoculated 
animal ;  rapid  prostration  of  the  patient ;  extreme  gravity  of  the  illness ; 
quick,  compressible  pulse,  with  tendency  to  collapse  and  syncope.  Before 
describing  putrid  pleurisy,  I  will  present  some  cases  which  give  an  exact 
idea  of  its  course. 

On  October  24  a  woman  who  was  very  ill  came  under  my  care.  My  first  impression  of 
her  was  bad  :  ghastly  colour,  marked  fever,  acute  dyspnoea,  profound  weakness,  immi- 
nent collapse,  and  considerable  wasting,  showed  the  gravity  of  the  case.  I  was  struck 
with  the  fcetor  of  her  breath  ;  the  cough  was  frequent,  and  the  sputum-glass  contained 
diffluent,  sanious,  greyish  expectoration,  which  was  very  foetid.  It  was  neither  the 
purulent  fluid  from  a  vomica  nor  the  expectoration  of  bronchiectasis.  This  quasi- 
adynamic  state,  associated  with  foetor  of  the  breath  and  sputum,  led  me  to  think  of 
pulmonary  gangrene.     We  shall  see  that  the  condition  was  not  so. 

We  examined  the  patient.  Nothing  on  the  left  side  of  the  chest,  but  on  the  right  an 
effusion  of  about  20  ounces,  with  moist  rales  above.  Pleuritic  effusion  and  a  pulmonary 
lesion  were  therefore  present.  The  onset  had  been  very  clear.  On  September  15 
sudden  acute  pain  on  the  right  side  of  the  chest.  At  this  time  the  patient  was  at  home, 
convalescent  from  an  operation,  performed  on  August  19,  for  double  salpingitis  and 
utei'ine  fibroma.  The  uterus  and  ovaries  had  been  removed.  On  the  day  of  the 
operation  she  had  such  profuse  haemorrhage  that  vaginal  plugging  was  at  once  per- 
formed. The  loss  of  blood  caused  syncope,  and  for  some  days  she  was  very  weak. 
Her  strength  returned  slowly,  and  on  September  10,  as  the  wound  had  healed,  she  re- 
turned home.  On  September  16,  six  days  after  leaving  hospital  and  four  weeks  after 
the  operation,  rigors,  fever,  and  sharp  pain  in  the  right  side  appeared.  The  cough 
became  very  jiainful,  and,  some  days  later,  she  brought  up  diffluent  and  foetid  sputum. 
Apert  found  effusion  in  the  right  pleura,  and  drew  off  a  pint  of  dirty,  odourless  fluid. 
No  benefit  followed.  Fever  and  dyspnoea  persisted,  expectoration  continued  to  be 
foetid,  and  the  patient  therefore  came  into  the  Hotel-Dieu.  I  have  described  her 
condition  on  admission.  Puncture  with  a  Pravaz  syi-inge  yielded  sanious,  greyish 
fluid,  which  was  so  foetid  that  we  could  not  but  think  of  gangrene.  Yet  the  diagnosis 
was  not  easy.  We  knew  that  she  had  a  lesion  in  the  lung,  with  foetid  expectora- 
tion, and  also  pleural  effusion  that  was  foetid ;  we  knew  that  the  limg  lesion  was 
the  older,  because  the  fcetor  of  the  sputum  preceded  that  of  the  effusion ;  but 
it  remained  to  find  out  the  nature  and  the  origin  of  the  lesions.  We  had  to  discover 
whether  the  lesions  were  gangrenous,  or  whether,  under  the  aspect  of  gangrene,  we  had 
to  do  with  putrid  infection,  ^^^thout  mortification  of  the  tissues,  which  gives  a  very 
different  prognosis.  And,  in  any  case,  what  was  the  entrance  gateway  of  this  infection  ? 
Had  the  germs  been  carried  by  the  blood  or  by  the  air  ?  These  questions  were  of  the 
utmost  importance,  and  it  was  necessary  to  attempt  to  answer  them. 

Let  us  not  forget  that  she  had  undergone  an  operation  four  weeks  before  the  appear- 
ance of  the  thoracic  complications  ;  we  might  therefore  think  of  embolic  infection  of 
abdominal  origin.  To  this  hypothesis  it  might  truly  be  objected  that  the  thoracic 
trouble  had  supervened  four  weeks  after  the  operation,  and,  further,  that  the  result  of 
the  operation  had  been  so  satisfactory  as  to  dismiss  all  idea  of  infection.     These  objec- 


DISEASES  OF  THE  PLEURA  361 

tions  carry  weight,  but  they  are  not  sufficient,  for  I  could  quote  examples  of  remote 
embolic  infection  weeks  after  the  extinction  of  the  original  focus — viz.,  appendicitis 
and  otitis.  Indeed,  the  history  of  appendicitis  teaches  us  that  remote  infections  of 
the  liver,  the  lung,  and  the  pleura  may  supervene  when  the  appendicular  focus  is 
extinct,  because  the  migration  of  the  pathogenic  agents  takes  place  silently,  during 
the  active  phase  of  the  process  in  a  closed  cavity.  I  have  discussed  this  question  at 
length  under  Appendicitis. 

The  history  of  otitis  also  teaches  that  such  remote  infections  as  abscess  of  the  cere- 
brum and  cerebellum,  and  gangrene  of  the  lung  may  supervene,  although  the  otitis 
appears  to  be  extinct.  I  have  given  full  details  in  the  sections  on  Abscesses  of  the 
Cerebellum  and  on  Gangrene  of  the  Lung. 

In  the  same  manner  the  course  of  events  after  a  confinement  gives  material  for 
careful  reflection.  The  confinement  has  been  quite  normal,  the  most  rigid  asepsis  has 
been  observed,  no  apparent  infection  has  been  discovered,  and  yet  microbic  emboli 
may  produce  septic  infarcts  in  the  hmg,  with  or  without  purulent  pleurisy.  I  insist, 
therefore,  on  the  fact  that  an  ill-extinct  infecting  focus,  whether  it  be  abdominal,  appen- 
dicular, aural,  uterine,  or  elsewhere,  may  be  the  origin  of  severe  infections. 

It  miglit  therefore  be  asked  if  the  thoracic  lesions  in  my  patient  had  originated 
from  some  abdominal  focus.     We  shall  see  that  nothing  of  the  kind  had  occurred. 

In  the  course  of  our  interrogation  she  had  spoken  of  a  fcetid  vaginal  discharge  which 
had  lasted  for  a  month,  in  spite  of  daily  injections.  Digital  examination  was  made, 
and  a  large  mass,  enclosed,  as  it  were,  in  a  funnel,  was  felt  at  the  fundus  vaginap. 
Examination  with  the  speculum  revealed  a  gre3'ish  mass,  surrounded  by  ondematous 
mucous  membrane.  The  parts  were  bathed  in  sanious  fluid,  which  was  horribly  ftetid. 
After  repeated  douches,  the  mass,  which  proved  to  be  the  forgotten  plug,  was  seized 
\vith  a  pair  of  forceps  and  with-drawn. 

After  the  extraction  of  this  foreign  body,  which  had  remained  so  long  in  situ,  about 
3  ounces  of  feet  id  fluid  came  away.  After  copious  douches  the  mucosa  of  the  fundus 
vaginae  showed  shallow  ulcerations,  with  sanious  base  and  red  edges,  which  were  clean 
cut.  The  ulcerations  bled  readily,  when  the  speculum  was  opened.  We  now  held  the 
offending  body,  and  could  understand  the  chain  of  events.  The  fundus  vaginae  had  been 
transformed  into  a  closed  cavity  by  the  forgotten  tampon.  In  this  culture  medium 
ulceratioas  occurred.  The  microbes,  in  the  form  of  septic  emboli,  entered  the  venous 
system,  and  set  up  foci  in  the  lung  and  the  pleura. 

The  removal  of  the  tampon  was  followed  by  a  fall  of  temperature,  as  was  natural, 
since  we  liad  just  removed  the  infective  focus  ;  but  the  condition  of  the  patient  remained 
just  as  bad,  and  the  fever  reappeared,  because  the  thoracic  lesions  continued  their 
course. 

Were  these  lesions  putrid  but  not  gangrenous  ?  This  question  had  to  be  elucidated, 
1)ut  for  the  moment  the  urgent  indication  was  to  suppress  the  pleural  focus,  and  to  see 
what  could  Ijc  done  for  tlie  pulmonary  one. 

1  asked  Marion  to  operate.  A  pint  of  extroiiicly  Uvild  fluid  giisiied  out,  but  tlie 
pus  contained  no  trace  of  sloughs. 

Their  absence  eliminated  the  hypothesis  of  ])leural  gangrene,  just  as  the  absence 
of  clastic  fibres  and  sloughy  elements  in  the  sputum  excluded  gangrene  of  the  lung. 

After  the  operation  tlio  fever  fell,  and  the  general  condition  raj)iflly  improved. 
Tlio  ft£'tid  expectoration  ceased  in  ten  days.  Tlireo  weeks  later  the  j)alient  was  com- 
phitely  cured.     See  temperature  cliart  on  p.  .3()2. 

Apert  examined  the  fa-tid  fluid  from  the  vagina,  the  sputum,  and  the  fluid  from 
the  pleura.  These  three  foci  contained  identical  microbes,  whidi  were  botii  iirrobic 
and  anaerobic,  though  tlie  latter  were  tlic  moii-  iiiijjortaiit. 

Ciilliircs  ;.';i\f  tin-  following  results  : 

Aerobic  Cultures.     Those  made  witii  the  pus  from  the  vagina  and  the  pleura  woro 


362 


TEXT-BOOK  OF  MEDICINE 


very  small.  About  a  dozen  tiny  colonies  were  visible,  and.  were  formed  by  a  strepto- 
coccus, with  irregular  granules  which  stained  with  Gram.  Those  made  with  the  sputum 
yielded  the  same  streptococcus,  some  colonies  of  Stapliylococcus  aureus,  and  a  large  white 
yeast  fungus. 

Anaerobic  Cultures. — Anaerobic  cultures  were  made  with  samples  from  the  vagina, 
the  pleura  and  the  sputa  :  (1)  on  broth,  in  Pasteur's  pipettes  ;  (2)  on  agar  in  Liborius- 
Veillon's  tubes.  The  broth  rapidly  became  cloudy,  a  foetid  odour  developed,  and 
bubbles  of  gas  rose  to  the  surface,  when  the  tube  was  shaken.  No  streptococci  were 
found  on  microscopical  examination,  though  a  large  number  of  bacilli  and  fine  cocci 
were  visible. 

Liborius'  tubes  were  sown  with  successive  dilutions  (a  drop  of  fluid  put  in  the 
first  tube,  a  drop  of  this  diluted  fluid  placed  in  the  second  tube,  and  so  on).  In  the 
first  dilutions  the  colonies  were  too  close  together  to  be  isolated.  On  the  third  or  fourth 
day  gas  was  generated,  which  split  up  the  agar. 

In  further  dilutions  it  was  easy  to  study  the  two  species  in  tubes  sown  with  pus  from 
the  vagina,  the  pleura,  and  the  sputum.  One  of  these  species  presented  the  form  of 
white,  opaque,  lenticular  colonies,  due  to  a  large  slightly  elongated  coccus  (coccus- 


Ocfober 


DATEi 


November 


J6' 


2^'  £5   ee    £7  ea    es  30    SI     i      e     j     a     s     6     7     a     9 

tI 

\  X          \t^ 

^JX            fi|l 

I J  ^    .         t  §-  0 

Y       A 

I  -i   t       -\    v-h 

__     v±±     ]  5^                       . 

■^     I    t^i-     V    ^     ^K                  A                  D 

'^^^       J[    V               \/%         *-.*t-      K-Tv- 

i-s       iV              ^  \        ^J   ^      \  \  \ 

§1                             u   -T^      \zi   J   X 

II                                                         Ca^                        >/       »   '    ^^&      A 

It                                         V    ^                                   'v'^*'°V 

($;                                                                                  ^ 

:::x 


■ss- 


Fig.  18. — Temperature  Chart. 


bacillus),  which  was  isolated  or  disposed  in  pairs  and  masses,  and  stained  with  Gram. 
The  other  species  showed  itself  in  the  form  of  yellowish  muriform  colonies,  due  to  fine 
cocci  in  mass.  Experiments  were  made  upon  animals.  One  guinea-pig  received 
under  the  skin  ^  c.c.  of  vaginal  pus,  and  another  ^  c.c.  of  pleural  pus,  without  result. 
A  rabbit  received  i  c.c.  of  pleural  pus  in  the  veins,  without  any  other  result  than  serious 
indisposition,  which  yielded  after  two  days.  These  researches  allowed  us  to  recon- 
struct the  nature  and  the  course  of  the  infection.  The  disease  occurred  in  two  stages. 
The  toxi-infection  started  from  the  fundus  vagina?.  Halle  has  shown  that  the 
vagina  normally  contains  aerobic  microbes  in  the  form  of  a  streptococcus,  differing  from 
the  Streptococcus  pyogenes,  and  strictly  anaerobic  microbes,  which,  after  inoculation  of 
animals  in  pure  culture,  cause  abscesses  and  gangrene.  The  aero-anaerobic  toxi- 
infection  had  therefore  arisen  in  the  plugged  vaginal  cloaca.  The  infectious  germs  had 
been  carried  by  the  veins  to  the  right  heart,  thence  to  the  lung,  and  had  passed  into  the 
pleura.  Infection  of  the  lung  showed  itself  by  rigors,  fever,  and  i^ain  in  the  side.  An 
ill-defined  area  of  lung  had  been  embohzed  and  converted  into  a  putrid,  but  not  gan- 
grenous, infarct.  The  pleural  fluid,  which  was  odourless  at  the  first  puncture,  was 
putrid  at  the  second  one.  We  thus  built  up  the  vaginal,  pulmonary,  and  pleural  stages 
of  the  infectious  process. 

In  tliis  series  of  infections  tlie  infection  was  putrid,  but  not  gangrenous.     It  was 


DISEASES  OF  THE  PLEUKA  363 

putrid,  as  proved  by  the  production  of  gas  in  the  anaerobic  cultures.  It  Tvas  not  gan- 
grenous, for  we  drew  off  from  the  pleura  no  sloughing  shreds.  An  analysis  of  the  sputum 
revealed  neither  fibres  nor  sloughs.  Here  the  process  of  putrefaction  was  not  associated 
with  mortlGcation. 

The  history  of  appendicitis  furnishes  us  with  many  cases  of  putrid  and 
of  gangrenous  pleurisy.  I  have  discussed  appendicular  pleurisy  in  a  pre- 
ceding section.  It  may,  indeed,  be  said  that  appendicitis  is  one  of  the 
most  frec^uent  sources  of  purulent  pleurisy.  As  a  model  let  me  mention  the 
following  case  : 

A  man  came  to  us  moribund,  with  extensive  right  pleurisy,  complicated  by 
pneumothorax,  and  died  some  hours  before  the  operation.  His  history  and  the  autopsy 
enabled  us  to  reconstruct  the  morbid  picture.  The  pleura  contained  7  pints  of  foul- 
ameUing  pus  and  gas.  Pleurisy  and  pneiimothorax  were  the  result  of  appendicular 
infection.  The  lesions,  which  started  from  the  appendix,  began  in  the  right  part  of  the 
abdomen,  and  reached  the  right  thoracic  cavity.  The  putrid  infection  here  was  not  of 
embolic  origin,  as  in  the  preceding  case,  but  the  lesions  spread  by  continuity. 

I  think  it  useful  to  quote  cases  of  putrid  pleurisy  : 

Widal's  Case. — Man  suddenly  taken  ill  with  acute  pain  on  the  right  side  of  the  chest 
and  violent  dyspnora.  Tiie  pain,  after  rehef  from  an  injection  of  morj^hia,  reappeared. 
The  dyspnoea  increased,  the  cough  became  paroxysmal,  the  general  condition  grew  worse, 
and  the  patient  was  admitted  under  Widal.  At  the  left  base,  dullness  and  tubular 
breathing  (effusion)  ;  above,  tympanites  and  amphoric  breathing  (pneumothorax). 
The  dyspncea  was  so  acute  that  a  puncture  was  at  once  made,  and  gave  exit  to  2  pints 
of  puriform  fluid  of  extremely  foetid  odour. 

No  improvement.  Next  day  the  signs  of  hydropneumothorax  were  complete. 
Around  the  puncture  a  bright  red  swelling  developed,  which  on  pressure  yielded 
gaseous  crepitation.  The  gaseous  inflammation  commenced  some  hours  after  the 
puncture.     Ojieration  decided  upon,  but  the  patient  died  before  the  surgeon's  arrival. 

Post-mortem  :  On  opening  the  thorax,  greyish,  sanious,  and  extremely  foetid  fluid, 
mixed  with  gas,  escaped  from  the  left  pleura.  The  pleur?e,  after  removal  of  the  false 
membranes,  were  carefully  examined.  These  membranes  were  fibrinous  and  not  ad- 
herent. No  trace  of  gangrene  found  on  the  serosa.  The  left  lung  was  also  examined 
with  the  greatest  care  :  no  tubercules,  no  foci  of  broncho-pneumonia,  no  gangrene. 

This  case,  then,  is  one  of  putrid  pleurisy  without  gangrene.  The  pathogenic  agent 
was  the  Proteus  vulgaris.  A  guinea-pig  was  inoculated  under  the  skin  with  1  e.c. 
of  pleural  fluid.  Next  day  a  large  pocket  developed  at  the  point  of  inoculation,  and 
gave  very  evident  gaseous  crepitation  on  palpation.  On  the  skin  which  covered 
tin's  gaseous  aliscess  an  ulcer  soon  formed,  and  gave  exit  to  sanious  and  fcrtid  fluid 
containing  various  microbes,  chiefly  tlie  Proteus  vuk/aris. 

Courtois-SufTlfs  Case.— A  man,  twenty-three  years  of  ago,  who  had  had  chills  and 
pail)  in  tlic  sifle  at  tlio  right  base,  came  into  the  Beaujeon  Hospital.  Kight  pleurisy  with 
eflusion,  estimated  at  2  pints.  In  a  few  days  the  dyspnoea  was  marked,  the  patient 
])ecame  cyanosed,  and  thoracentesis  was  necessary.  The  puncture  gave  exit  to  about 
1 J  l)ints  of  puriil(!nt  fluid,  which  was  extremely  feet  id.  Next  day,  at  the  seat  of  puncture, 
an  (edematous  and  reddish  swelling  appeared,  which  had  the  appearance  of  a  phlegmon, 
and  oxttmded  as  far  as  the  base  of  the  thorax.  On  paljiation,  fine  crepitation,  due  to 
gaseous  inflltration.  During  the  next  few  days  the  situation  grew  wor.sc:  the  temperature 
\\as  about  lO.T  F.,  sweats  were  abundant  and  fcrtid,  the  face  was  bloated  and  earthy, 
and  the  dyspno'a  acute.  Thoracotomy  gave  exit  to  fluid  pus,  whicli  was  extremely 
fu'tid  and  of  a  brownish  tint.     Tiio  pleural  cavity  was  then  washed  out  with  a  very 


364  TEXT-BOOK  OF  MEDICINE 

weak  solution  of  permanganate  of  potash.  After  some  nps  and  downs  the  patient 
died. 

The  results  of  the  autopsy  were  :  In  the  chest -wall  a  gaseous  inflammation  around 
the  seat  of  the  puncture,  pleural  cavity  contained  a  little  fluid,  pleura  thickened,  but 
no  trace  of  gangrene  in  the  lung  or  the  pleura. 

Boinet's  Case. — Well-built  man,  twenty-four  years  of  age,  seized  with  rigors, 
cough,  and  acute  pain  at  the  lower  part  of  the  left  side  of  the  chest.  Left  pleural 
effusion,  with  amphoric  breathing  and  metalhc  tinkling  (pyopneumothorax).  The 
situation  rapidly  became  worse.  Puncture  yielded  sanious  pus  of  extremely  foetid 
odour.  Next  day  operation  for  empyema  gave  exit  to  4  pints  of  stinking  pus  and  gas. 
"Patient  died  twelve  days  later.  Post-mortem,  Boinet  found  three  pockets  in 
the  pleura,  containing  putrid  fluid  mixed  with  gas.  No  communication  with  the  lung, 
no  tubercular  lesions,  and  no  gangrene  in  the  lung  or  the  pleura. 

Netter's  Case. — Child  with  pyopneumothorax.  Puncture  gave  exit  to  foetid  pus 
and  gas.  Subcutaneous  emphysema  then  developed.  Broca  operated  for  empyema, 
and  the  child  made  excellent  progress.  With  regard  to  these  cases  of  putrid  pleurisy, 
Netter  says  that  he  has  found  an  anaerobic  bacillus  in  the  form  of  long,  thin  filaments, 
mixed  with  other  micro-organisms. 

Description. — These  cases  give  a  clear  idea  of  putrid  pleurisies.  They 
chiefly  affect  the  great  pleural  cavity,  unlike  foetid  pleurisy,  which  is  usually 
encysted.  The  fluid  is  sero-purulent,  turbid,  greyish,  and  not  homogeneous  ; 
when  placed  in  a  test-tube,  it  divides  into  two  layers — the  lower  dense  and 
opaque,  the  upper  more  transparent. 

These  cases  frequently  have  an  embohc  origin  ;  the  original  focus  may  be 
in  the  vagina  or  the  appendix,  as  was  the  case  with  our  patients,  in  otitis, 
in  osteomyehtis,  in  phlebitis,  etc.  In  some  cases  putrid  pleurisy  results 
from  neighbouring  lesions  (lung  or  mediastinum).  It  may  be  set  up  by 
abdominal  mischief,  renal  or  hepatic  suppurations,  subphrenic  empyema, 
with  or  without  perforation  of  the  diaphragm.  In  other  cases  the  cause 
and  the  origin  remain  unknown. 

The  microbes,  which  are  chiefly  anaerobic,  lead  to  the  formation  of  gas 
(putrefaction)  in  putrid  pleurisy.  The  appearance  of  pneumothorax  without 
perforation  of  the  pleural  cavity  is  thus  explained.  This  pneumothorax, 
formerly  called  essential,  is  quite  different  to  pneumothorax  by  perforation. 
The  latter  is  due  to  the  introduction  of  air  into  the  pleura,  while  the  former 
arises  without  the  presence  of  air. 

From  the  clinical  point  of  view  we  find  in  both  forms  the  same  physical 
signs — viz.,  tympanites,  amphoric  breathing,  metallic  tinkling,  and  liippo- 
cratic  succussion. 

Gas  may  form  in  the  walls  of  the  thorax  and  produce  gaseous  phlegmon. 
Simple  aspiratory  puncture  sows  the  germs  in  the  chest-wall,  and  a  gaseous 
phlegmon  with  oedema  follows  in  a  few  hours. 

Experimental  research  yields  analogous  results.  The  inoculation  of  a 
drop  of  pleural  fluid  in  the  cellular  tissue  of  an  animal  provokes  gaseous 
phlegmon  (Widal). 


DISEASES  OF  THE  PLEURA  365 

Lastly,  the  development  of  gas  may  be  abundant  in  anaerobic  cultures  ol 
the  pathogenic  agents  of  putrid  pleurisy. 

The  diagnosis  of  putrid  pleurisy  is  impossible  before  puncture.  Every 
case  is  accompanied  by  general  symptoms,  which  rapidly  becom,e  grave,  and 
comprise  small,  quick  pulse,  dyspnoea,  prostration,  and  collapse — symptoms 
which  are  rarely  found  in  other  varieties  of  pleurisy.  In  such  a  case  the 
additional  presence  of  pneumothorax  is  in  favour  of  putridity,  but  yet  the 
putrid  nature  of  the  effusion  can  only  be  established  by  exploratory  puncture. 
Accordingly,  if  we  are  in  doubt,  even  though  the  effusion  is  scanty,  we 
must  confirm  the  diagnosis  by  early  puncture.  Furthermore,  puncture 
should  immediately  be  followed  by  thoracotomy,  with  or  without  resection 
of  ribs,  for  the  needle  track  may  rapidly  become  infected,  and  diffuse  gaseous 
inflammation  may  develop  in  a  few  hours. 

But  it  will  be  said  puncture  only  shows  us  the  foetor  of  the  fluid  ;  it 
does  not  at  once  reveal  putridity.  To  this  I  would  reply  that  it  matters 
Httle  whether  the  pleurisy  be  foetid  or  putrid :  every  foul-smelling  pleurisy 
should  be  operated  on  without  delay. 

Gangrenous  Pleurisy. 

The  phenomena  of  putrefaction  just  described  are  common  to  putrid 
and  to  gangrenous  pleurisy.  These  two  varieties  are  distinguished,  not  by 
the  foetor  of  the  fluid,  but  by  the  shreds  of  slough  which  float  in  the  effusion 
or  are  adherent  to  the  walls. 

The  description  of  putrid  and  gangrenous  pleurisy  present  many  similar 
points,  yet  the  latter  may  assume  two  forms  which  are  of  importance : 
sometimes  the  lung  is  not  involved;  at  other  times  the  gangrene  is  pleuro- 
pulmonary,  and  is  then  far  more  grave.  I  shall  here  quote  cases  of  the 
former  variety  : 

Comby  and  Vogt's  Case. — Young  girl,  eleven  years  of  age,  taken  ill  with  left  pleurisy. 
Some  days  later  she  woke  up  with  true  orthopnooa.  Next  day  Comby  and  Vogt  found 
extreme  dyspnoea,  temperature  104 ""  F.,  signs  of  effusion  at  the  base  of  the  left  chest, 
and  above  those  of  pneumothorax.  First  diagnosis  was  pneumothorax  from  tubercular 
perforation  of  the  lung.  Four  days  later  puncture  gave  exit  to  a  pint  of  very  foetid 
pus.  The  first  diagnosis  was  then  changed  to  gangrenous  pyopneumothorax.  Comby 
incised  the  seventh  intercostal  space,  and  came  on  a  mass  of  false  membranes,  which 
he  Ijroke  up  with  the  hnger.  Four  or  five  pints  of  horribly  fcetid  pus  came  out.  The 
child  finally  recovered. 

Rendus  Case.* — A  man  who  looked  phthisical  was  admitted  for  pncurao- 
thorux.  He  was  wasted,  cyanosed,  and  much  distressed;  cough  frequent,  breath  had 
no  odour,  and  temperature  was  normal.  Pleural  eftusion  at  the  right  base  and  above 
j)neumothorax.  Succussion  splash  and  metallic  tinkling.  This  condition  was  said  to 
have  begun  with  violent  pain  in  the  right  side.     On  the  day  after  admission  his  condition 

*  Meeting  of  February  3,  181)9.  Althoiigli  the  author  has  entitled  his  papi  r  "  Putrid 
Pleurisy,"  the  putrid  pleurisy  was  in  reality  gangrenous,  because  he  found  "  a  large 
lihrecl  of  sloughing  tissue, in  which  elastic  fibres  were  discovered  under  tlio  niiiroscope. 


366  TEXT-BOOK  OF  MEDICINE 

was  alarming.  Dyspnoea  was  acute,  cyanosis  was  marked,  and  the  heart  was  dis- 
placed ;  puncture  yielded  extremely  foetid  pus.  Rist  at  once  operated.  One  and  a 
half  jjints  of  foetid  pus  came  out,  and  the  cavity  was  washed  out  with  a  solution  of 
permanganate  of  potash.  Two  days  later  painful  oedema  -with  emphysematous  crack- 
ling was  found  at  the  right  base.  An  incision  was  made,  and  very  foetid  serous  fluid, 
mixed  with  bubbles  of  gas,  let  out.  Later  a  phlegmonous  patch  of  the  same  nature 
appeared  on  the  left  arm,  at  a  spot  which  had  been  vaccinated  some  days  before.  The 
condition  of  the  patient  became  very  alarming.  Restlessness  and  dehrium  were  acute  ; 
the  pus  from  the  empyema  again  became  very  foetid,  and  washing-out  of  the  pleura 
brought  away  a  large  slough  of  blackish  gangrenous  tissue,  which  was  extremely  foetid, 
and  showed  elastic  fibres  under  the  microscope.  Patient  finally  recovered.  Bacterio- 
logical examination  showed  the  presence  of  anaerobes. 

Let  us  now  turn  to  those  cases  in  which  we  find  gangrene  of  the  lung  and 
of  the  pleura ;  it  is  usual  for  grangrene  of  the  lung  to  precede  that  of  the 
pleura.  To  avoid  repetition,  I  would  ask  the  reader  to  turn  to  the  section 
on  Gangrene  of  the  Lung. 

Pleuro-pulmonary  gangrene,  hke  that  of  the  lung,  may  have  an  emboUc 
(otitis,  appendicitis,  etc.)  or  an  aerial  origin.  As  the  points  have  been 
discussed  under  Gangrene  of  the  Lung,  I  shall  not  repeat  them. 

The  descriptions  of  gangrenous  and  of  putrid  pleurisy  in  part  blend. 
Acute  pain  in  the  side,  fever,  bad  pulse,  earthy  tint  of  the  skin,  dyspnoea, 
prostration,  and  tendency  to  collapse,  show  the  extreme  gravity  of  gan- 
grenous pleurisy ;  fcetor  of  the  breath,  stinking  and  blood-stained  sputum, 
show  the  participation  of  the  lung  in  the  gangrenous  process. 

As  regards  prognosis,  the  addition  of  gangrene  marks  a  further  step  in 
the  gravity  of  putrid  pleurisy  ;  but  in  reahty  these  two  varieties  are  so  closely 
alhed  that  they  almost  come  under  one  description.  The  same  aero-anae- 
robic agents  which  produce  pleurisy — that  is  simply  putrid — may  cause 
gangrene  either  in  the  patient  or  in  animals  used  for  experimental  research. 
In  Widal's  case  the  gangrene  was  absent,  but  yet  inoculation  of  the 
pleural  fluid  in  a  guinea-pig  "  produced  a  gaseous  and  gangrenous  abscess 
in  the  animal,  which  died  after  extensive  sloughing  of  the  skin  of  the  abdo- 
men and  thorax."  In  Rendu's  case  the  pleurisy  was  labelled  putrid, 
but  yet  a  gangrenous  shred  was  found  later  in  the  thoracic  cavity.  The 
line  of  cUnical  demarcation  between  putrid  and  gangrenous  pleurisy  is, 
therefore,  not  absolute  ;  putrefaction  and  mortification  may  appear  together 
or  in  succession. 

The  spread  of  gangrene  from  the  pleura  to  the  lung  can  only  be  recog- 
nized by  foetor  of  the  breath  and  of  the  expectoration,  and  by  the 
presence  of  elastic  fibres  and  sloughs  in  the  sputum.  Such  is  the  history  of 
stinking  pleurisies  and  their  tliree  groups — foetid,  putrid,  and  gangrenous  : 
the  foul  smell  of  the  effusion,  which  is  the  first  step  in  diagnosis  can  only  be 
revealed  by  early  puncture,  and  immediate  surgical  intervention  is  the  only 
method  of  treatment. 


DISEASES  OF  THE  PLEURA  367 


XV.  VOMICA. 


Definition. — Considering  only  its  etymology,  the  word  vomica  (from 
vomere,  to  vomit)  is  improperly  applied  to  the  symptom  which  we  are  about 
to  describe  ;  custom,  however,  has  consecrated  it,  and  the  word  vomica 
serves  to  describe  the  rejection  of  pus  by  the  respiratory  channels,  just  as 
haemoptysis  denotes  the  rejection  of  blood  from  the  same  passages.  Custom 
has  even  gone  farther,  and,  by  an  abuse  of  language,  has  finally  included 
under  one  term  the  symptom  and  the  lesion,  so  that  we  speak  of  pulmonary, 
pleural,  or  hepatic  vomica — that  is  to  say,  a  purulent  collection  in  the  lung, 
pleura,  or  in  the  liver,  which  has  burst  into  the  bronchi  and  has  been 
coughed  up. 

Description. — The  complete  study  of  vomicse  comprises  the  diagnosis 
both  of  the  symptoms  and  of  the  lesion.  I  shall  here  outhne  the  chief 
varieties. 

1.  Pulmonary  Vomica. — Pneumonia  suppurates  fairly  often  (grey 
hepatization),  but  the  pus  very  rarely  collects  in  the  form  of  an  abscess. 
The  works  of  Laennec,  Graves,  and  Trousseau,  show  how  rarely  pulmonary 
abscesses  occur  in  the  course  of  pneumonia  ;  they  are  so  rare,  indeed,  that 
Grisolle  has  only  collected  twenty-three  proved  cases.  These  abscesses 
sometimes  form  very  rapidly,  on  the  fifth  day  of  pneumonia  (Woillez),  or  on 
the  twelfth,  and  are  never  rejected  later  than  the  twentieth  day. 

The  pus  from  the  pulmonary  vomica  is  scanty,  phlegmonous,  sometimes 
mixed  with  blood,  and  of  a  brownish  colour.  The  pneumococcus  is  the 
pathogenic  agent.  Directly  after  the  evacuation  of  the  abscess  the  physical 
signs  change,  and  where  the  signs  of  pneumonia  have  been  present  we  now 
find  cavernous  breathing  and  splashing  sounds. 

2.  Pleural  Vomicae. — These  vomicse  are  much  more  frequent  and  follow 
interlobar,  mediastinal,  or  diaphragmatic  pleurisy,  or  pleurisy  of  the  great 
pleural  cavdty.  The  vomica  of  interlobar  pleurisy  is  the  most  frequent  of  all. 
Speaking  generally,  vomicse  of  the  pleura  appear  much  more  slowly  than 
those  of  the  lung.  Purulent  collections  in  the  pleura  open  into  the  bronclii 
after  three  to  six  weeks,  and  later  still  when  the  great  pleural  cavity  is 
affected.  As  an  exception  to  this  rule,  when  purulent  pleurisy  develops  in 
a  child,  or  in  a  woman  during  the  puerperal  state,  the  vomica  may  appear 
from  the  second  to  the  third  week  (Trousseau). 

The  symptoms  are  different,  according  as  the  vomica  is  provoked  by 
partial  pleurisy,  which  only  contains  some  ounces  of  pus,  or  by  pleurisy 
of  the  great  pleural  cavity,  wliich  may  contain  several  pints. 

In  encysted  dia[)iiriigniatic  or  interlobar  pleurisy  the  quantity  of  usually 
fcEtid  pus  brought  up  at  the  moment  of  the  vomica  does  not  exceed  some 
ounces  ;  it  then  gradually  diminishes,  and,  in  fortunate  cases,  the  pleuro- 


368  TEXT-BOOK  OF  MEDICINE 

bronchial  fistula  closes.  This  mode  of  cure  is  possible  in  metapneumonic 
interlobar  pleurisy.  I  would  refer  the  reader  to  the  section  on  Interlobar 
Pleurisy. 

In  the  case  of  the  great  pleural  cavity,  when  the  pleura  contains  4  or  5 
pints  of  pus,  the  course  is  less  simple.  The  bursting  of  pus  into  the  bronchi 
often  determines  dyspnoea,  bordering  on  asphyxia.  Fatal  cases  have  been 
quoted,  and  the  patient,  who  has  extreme  distress,  brings  up  streams  of 
purulent  fluid  through  the  mouth  and  the  nose.  The  first  evacuation  is 
generally  followed  by  improvement,  and  then  the  patient,  while  changing 
his  position  or  coughing,  continues  to  bring  up  some  ounces  of  pus.  He  no 
longer  appears  to  vomit,  but  only  to  cough  up  the  pus.  As  soon  as  a  certain 
quantity  of  pus  has  accumulated  in  the  pleura,  the  patient  is  seized  with 
fits  of  coughing,  and  voids  the  pleuritic  fluid  five,  six,  or  ten  times  a  day. 
Sometimes  the  evacuation  of  pus  stops,  but  is  repeated  one  or  more  days 
later,  and  in  some  cases  the  breath  and  the  fluid  evacuated  become  horribly 
foetid. 

Unless  the  fistula  is  so  constituted  as  to  form  a  valve  (Chomel),  the 
inspired  air  enters  the  pleural  cavity,  and  the  signs  of  pyopneumothorax 
are  found. 

Does  pleurisy  become  purulent  when  the  vomica  has  once  formed  ? 
Several  modes  of  termination  may  occur  ;  one  is  recovery,  which  is  rare  in 
general  but  possible  in  interlobar  pleurisy,  especially  in  the  metapneumonic 
variety. 

In  some  patients  the  improvement  consecutive  to  the  vomica  is  only 
transient ;  the  cavity  becomes  infected,  and  the  fever  does  not  cease,  while 
the  patient  loses  appetite,  becomes  cachectic,  and  finally  succumbs.  In 
other  patients  the  cavity  shrinks,  but  the  pleura  and  the  lung  are  invaded 
by  fibrosis,  with  or  without  dilatation  of  the  bronchi,  which,  sooner  or  later, 
compromises  the  individual's  life. 

The  preceding  description  will  have  made  it  apparent  that  the  pleural 
vomica  only  occurs  in  empyema.  There  are,  however,  some  extremely 
rare  cases  in  which  sero-fibrinous  pleurisy  is  terminated  by  vomica. 

3.  Vomica  with  Hydatid  of  the  Lung.— The  pleural  vomicae  which  I 
have  just  described  are  the  most  frequent ;  there  are,  however,  some  rarer 
varieties,  which  I  shall  now  review.  Suppurating  hydatids  of  the  lung  may 
cause  vomicae  which  simulate  pleural  vomica,  with  this  difference,  however — 
that  we  find  fragments  of  hydatid  membranes  and  booklets  in  the  rejected 
matter. 

4.  Vomica  in  Congestion  Abscesses. — Chenieux's  paper  contains  nine 
cases  of  vomicae,  consecutive  to  congestion  abscess,  following  Pott's  disease. 
The  pus  often  contains  bony  sequestrse. 

5.  Vomica  from  Suppuration  of  the  Liver. — Abscesses  and  suppurating 


DISEASES  OF  THE  PLEURA  369 

hydatid  cysts  of  the  hver  may  result  in  vomica  ;  adhesions  are  estabUshed 
by  the  intermediary  of  the  diapliragm,  perforation  follows,  and  the  patient 
voids  the  Uver  abscess  through  the  bronchi.  When  the  vomica  has  its 
origin  in  an  abscess  of  the  liver  the  pus  is  reddish,  tliick,  and  sometimes 
fcEtid ;  when  the  vomica  is  consecutive  to  a  suppurating  hydatid  of  the  Uver, 
the  purulent  fluid  is  mixed  with  hydatid  membranes. 

6.  Vomica  with  Suppuration  of  the  Kidney. — Suppurating  cysts  of  the 
kidney  and  pyonephrosis  may  terminate  by  vomica. 

It  is  not  customary  to  consider  as  a  true  vomica  the  quantity  of  pus 
which  may  be  brought  up  at  one  time  by  a  patient  with  dilatation  of  the 
bronchi ;  it  is,  however,  a  pseudo-vomica  of  which  the  distinctive  characters 
should  be  well  known. 

The  treatment  of  vomica  varies  with  its  causes,  and  surgery  gives  the 
best  results. 


XVI.  CHYLIFORM  AND  CHYLOUS  EFFUSIONS  OF  THE 

PLEURA. 

The  pleura,  Kke  the  peritoneum,  may  contain  milky  effusions  which  have 
the  appearance  of  an  emulsion.  On  thoracentesis  we  expect  to  find  a  sero- 
fibrinous or  purulent  effusion,  but  we  draw  off  chyliform  fluid.  This  fluid 
is  odourless,  and  has  no  tendency  to  coagulate,  because  it  is  not  fibrinous  ; 
in  a  test-tube  it  forms  no  deposit  in  its  lower  part,  and  will  keep  for  days  or 
weeks  without  putrefaction  ;  under  the  microscope  it  shows  some  leucocytes, 
and  in  most  cases  contains  a  large  number  of  fine  fatty  granules,  soluble 
in  ether,  while  chnical  analysis  reveals  a  large  increase  of  fatty  matter. 

The  onset  may  be  ushered  in  by  acute  pain  in  the  side,  but  is  more  often 
unnoticed.  The  collection  increases  insidiously,  Uke  a  subacute  pleurisy. 
This  latent  period  may  last  eighteen  months.  The  effusion  at  length  causes 
distress,  displaces  organs,  especially  the  heart,  and  flattens  the  lung.  It 
may  become  a  cause  of  dyspnoea,  but  is  not  accompanied  by  the  general 
symptoms  of  fever  which  are  so  frequent  in  purulent  effusions. 

Chyliform  effusion  shows  no  tendency  to  absorption.  After  it  has  been 
evacuated,  it  recurs  obstinately.  Punctures  relieve  the  patient,  who  thinks 
iiimself  cured ;  but  the  fluid  slowly  reforms,  and  fresh  evacuation  becomes 
necessary  after  a  more  or  less  extended  period,  during  which  every  morbid 
symptom  has  apparently  disappeared. 

ChyUform  effusion  at  times  gives  way  to  empyema,  in  wliich  case  the 
staphylococcus  is  usually  in  evidence.  Fever  appears,  with  pain  in  the  .'^idc  ; 
the  chest- wall  becomes  cedematous  ;  the  effu.sion  rapidly  increases ;  tiic  fluid 
makes  its  exit  by  vomica,  and  death  soon  follows.  More  rarely  chyliform 
effusion  recovers  after  first  becoming  sero-fibrinous. 

24 


370  TEXT-BOOK  OF  MEDICINE 

The  clinical  picture  just  sketched  is  that  of  tubercular  chyUform  pleurisy  ; 
indeed,  tuberculosis  is  the  cause  in  two-thirds  of  the  cases.  I  have  had  a 
remarkable  example. 

Patient  admitted  in  May,  1899,  to  the  Hotel-Dieu,  with  an  effusion  of  3  pints,  which 
had  Ijeen  practically  latent.  His  general  condition  appeared  excellent :  no  wasting,  no 
fever  ;  if  he  had  not  suffered  Avith  severe  dyspncea,  he  would  not  have  given  up  his 
work.  About  40  ounces  of  characteristic  chyhform  fluid  were  drawn  off.  He  felt 
better,  and  asked  to  go  out.  He  was,  however,  persuaded  to  remain  for  some  weeks. 
In  three  weeks  60  ounces  were  clra-«Ti  off  by  successive  pimctures.  The  effusion  at 
length  seemed  to  dry  up,  and  the  patient  went  out,  persuaded  that  he  -was  cured.  We 
saw  him  again  five  years  lat«r,  when  he  came  to  be  treated  for  sciatica.  He  was  work- 
ing without  feeling  any  malaise.  He  looked  well,  did  not  cough,  and  only  found  that 
he  readily  became  breathless,  and  at  times  felt  some  pain  in  the  chest.  The  physical 
signs  of  effusion,  however,  were  present,  and  thoracentesis  yielded  similar  fluid  to  that 
dra^vn  off  five  years  before.  His  condition  remained  good  for  about  a  month,  but 
then,  mthout  ajipreciable  cause,  his  temperature  ran  up,  and  severe  pain  in  the  side 
developed.  Exploratory  puncture  showed  the  chyhform  effusion  had  been  replaced  by 
pm'ulent  fluid,  containing  staphylococci.     He  died  four  months  later. 

In  other  more  rare  cases  the  disease  runs  a  rapid  course,  but  the  efiusion 
is  r.ather  lactescent  than  chyhform,  and  develops  in  the  course  of  confirmed 
phthisis.  I  have  recently  seen  such  a  case  in  which  the  fluid  was  in  turn  sero- 
fibrinous, serous,  lactescent,  and  purulent.     The  patient  died  in  ten  months. 

While  tuberculosis  is  present  in  two-thirds  of  these  cases  of  lactescent 
effusion,  cancer  is  only  present  in  one-third.  At  times  the  patient  has  had 
a  growth  for  a  long  wliile,  and  the  chyhform  effusion  is  only  a  secondary 
condition.  At  other  times  the  pleuro-pulmonary  cancer  is  primary.  The 
onset  of  the  malady  is  almost  silent.  Both  acute  dyspnoea  and  sharp  pains 
attract  the  patient's  notice,  and  we  find  a  very  large  effusion,  which,  on 
puncture,  shows  all  the  characters  of  chyhform  fluid.  In  some  cases  a  few 
red  corpuscles  may  be  present.  The  fluid  forms  again  with  extreme 
rapidity,  and  we  may  find,  after  evacuation,  that  the  resonajice  does  not 
return  to  normal.  In  a  short  while  puncture  gives  no  rehef  :  the  aspirating 
needle  has  to  travel  through  a  much  thickened  wall.  At  last  puncture 
yields  only  a  little  bloody  fluid,  and  the  signs  of  compression,  the  dyspnoea, 
and  the  pain  still  persist.  The  patient  wastes  and  grows  weak,  and  fever 
may  appear.  Such  a  picture  is  quite  opposed  to  that  of  tubercular  chyh- 
form pleurisy. 

It  is  always  easy  to  recognize  the  nature  of  chyhform  pleurisy  by  the 
appearance  of  the  fluid,  by  its  microscopical  analysis,  and  by  its  chemical 
composition.  It  is,  however,  more  difficult  to  ascertain  its  pathogenic 
cause.  If  the  patient  has  proved  phthisis  or  evident  local  tuberculosis, 
the  diagnosis  will  naturally  be  in  favour  of  tubercular  effusion.  On  the 
other  hand,  the  existence  of  visceral  cancer,  rapidly  progressive  course, 
signs  of  pressure  in  the  mediastinum,  with  oedema  and  collateral  circulation. 


DISEASES  OF  THE  PLEURA  371 

enlarged  glands  in  the  axilla,  and  the  appearance  of  phlebitis,  all  point  to 
cancerous  effusion.  The  final  appeal  must  always  be  made  to  laboratory 
methods.  Cyto-diagnosis,  as  a  rule,  shows  only  a  few  cells  in  a  case  of  can- 
cerous effusion.  Nattan-Larrier  found  neoplasm  cells,  while  endotheUal 
plaques  were  discovered  in  a  case  of  lactescent  effusion,  which  supervened 
in  the  course  of  leucocythsemia  (Sicard  and  Monod).  Inoculation  into  the 
peritoneum,  or  better,  into  the  mamma,  of  the  guinea-pig  will  often  prove 
that  the  chyhform  fluid  is  tubercular.  This  method  was  employed  in  two 
cases  under  my  care. 

The  causes  of  chyliform  effusion  in  the  pleura  have  been  as  much  dis- 
cussed as  the  causes  of  chyliform  effusion  in  the  peritoneum,  and  are  quite 
comparable  in  each  case.  The  older  writers  thought  that  the  effusion  of 
chyle  in  the  pleura  followed  rupture  of  the  thoracic  duct.  Tliis  opinion  no 
longer  holds  good.  In  one  of  Debove's  cases  the  thoracic  duct  was 
healthy,  and  a  similar  finding  occurred  in  two  of  my  cases.  Granulo- 
fatty  degeneration  of  the  chronically  thickened  layers  of  the  pleura  (Quincke) 
has  also  been  invoked.  In  Debove's  case  the  pleura  was  covered  with 
tissue  some  milhmetres  in  thickness,  made  up  of  several  superposed  layers, 
which  showed  numerous  fatty  granules  under  the  microscope.  In  one  of 
my  cases  Nattan-Larrier  found  very  dense  mature  fibrous  tissue,  which  had 
undergone  hyaline  degeneration  in  places.  Every  trace  of  fibrinous  exudate 
had  disappeared  ;  the  cellular  infiltration  was  but  little  marked  ;  the  vessels, 
though  scanty  in  the  superficial  layer  of  the  neo-membrane,  were  numerous 
in  the  deep  parts.  Some  giant  cells  were  also  present  near  the  lung,  which 
was  sclerosed. 

Recent  researches  seem  to  show  that  the  chyhform  aspect  of  the  fluid 
results  from  disintegration  of  its  cellular  elements  (leucocytes  or  cancer 
cells).  As  the  result  of  a  cause  which  has  so  far  escaped  us,  the  cellulai 
elements  in  suspension  in  the  fluid  are  said  to  degenerate,  and  give  rise 
to  fatty  and  albuminous  fluid  if  the  disintegration  is  incomplete,  and  to 
purely  fatty  fluid  if  the  transformation  is  perfect.  This  hypothesis  has  been 
confirmed  by  Nattan-Larrier,  who  has  seen  in  vitro  the  serous  fluid  from 
cancerous  pleurisy  change  aseptically  into  lactescent  fluid,  while  the  number 
of  cells  rapidly  diminished. 

Chylous  Effusion. — Apart  from  the  undoubted  cases  in  wliich  the  effusion 
is  not  chyle,  we  find  others  which  are  true  cases  of  chylothorax,  the  effusion 
being  chylous.  Shaw  has  collected  twenty-cases.  Traumatism  was  the 
cause  in  one-third  of  these  cases.  The  others  were  said  to  result  from  an 
obstacle  to  the  lymph-flow,  with  or  without  rupture  of  the  thoracic  duct, 
or  of  the  great  lymphatic  vessels  (cancerous  glands  or  lymphadenoma  in 
the  mediastinum,  obhteration  of  the  thoracic  duct,  thrombosis  of  the  sub- 
clavian vein).     The  diagnosis  is  easy  when  the  effusion  follows  trauma. 

24—2 


372  TEXT-BOOK  OF  MEDICINE 

A  man  had  his  chest  caught  between  the  driving-wheel  of  a  steam-engine  and  a 
wall.  He  was  taken  to  the  hospital,  where  the  left  clavicle  and  several  ribs  were 
found  to  be  fractured.  Two  days  later  effusion  was  discovered  in  the  left  pleura. 
Exploratory  puncture  yielded  milky  fluid  of  a  rosy  colour.  Chemical  and  microscopical 
examination  showed  the  presence  of  chyle,  mixed  ^vith  blood.  Ten  days  later  the  red 
corpuscles  had  disajipeared,  and  the  effusion  had  the  appearance  and  composition  of 
pure  chyle.  Absorption  took  place  mthout  complications,  and  the  patient  recovered 
fairly  rapidly  (Handmann). 

In  cases  of  this  nature  the  effusion  results  from  rupture  of  the  thoracic 
duct.  It  is  situated  on  the  left  side  (Wiesinger,  Kummel),  It  has  the  histo- 
logical composition  of  chyle,  but  its  chemical  composition  varies  with  the 
nature  of  the  fluid  and  the  time  of  digestion  ;  glucose  and  peptones  may  be 
found  in  it,  and  the  proportion  of  fat  will  increase  considerably  after  the 
ingestion  of  butter  (Strauss).  In  cases  of  this  nature,  when  the  rupture  is  due 
to  an  injury,  the  prognosis  is  not  bad. 

Let  us  now  note  a  third  group  of  cases,  in  which  the  lactescence  of  the 
effusion  is  not  the  result  of  a  local  infection,  but  the  consequence  of  a  general 
alteration  in  the  fluids  of  the  organism.  It  is  in  cases  of  this  kind  that  we 
see  the  coexistence  of  identical  effusions  in  the  various  serous  cavities ; 
chyliform  effusions  have  been  seen  at  the  same  time  in  the  peritoneum,  the 
pleura,  and  the  pericardium  (Bramwell).  The  blood-serum  (Achard),  the 
serous  fluid  from  blisters,  and  the  liquid  from  oedematous  areas  may  be 
opalescent.  This  opalescence  of  serous  effusions  is  comparable  to  the 
opalescence  of  the  blood-serum  described  by  Widal.  The  prognosis  depends 
upon  the  general  condition. 

Finally,  in  some  cases  chyliform  effusion  into  the  pleura  may  result  from 
the  presence  of  the  Filaria  sanguinis  (Lancereaux). 


XVII.  HYDROTHORAX. 

Hydrothorax  is  hydrops  of  the  pleura.  Both  pleurse  are  often  affected, 
and  the  fluid  is  analogous  to  blood-serum,  and  very  poor  in  corpuscles.  The 
condition  is  a  kind  of  serous  transudation  analogous  to  that  of  oedema. 

Hydrothorax  is  the  result  of  mechanical  causes,  of  which  the  most 
common  are  lesions  of  the  mitral  orifice,  and  of  dyscrasise,  of  which  the  most 
usual  are  cachexia  and  Bright's  disease. 

Hydrothorax  is  therefore  only  a  symptom  which  supervenes  as  a  com- 
plication in  the  various  morbid  states  I  have  just  enumerated.     It  estabhshes  j 
itself  in  an  insidious  fashion,  Avithout  fever  and  pain  ;   its  physical  signs] 
resemble  fairly  closely  those  of  pleuritic  effusion.     The  cyto-diagnosis  has 
been  given  under  Pleurisy. 


DISEASES  OF  THE  PLEURA  37^ 


XVIII.  PNEUMOTHORAX— HYDROPNEUMOTHORAX. 

Pneumothorax  (Itard)  implies  the  presence  of  air  or  of  gas  in  the  pleural 
cavity  ;  if  fluid  is  also  present,  the  lesion  takes  the  name  of  hydropneumo- 
thorax,  and  if  this  fluid  is  pus,  the  case  is  one  of  pyopneumothorax. 

Pathogenesis. — There  are  two  chief  varieties  of  pneumothorax  :  pneumo* 
thorax  by  perforation,  and  pneumothorax  by  putrefaction. 

The  former  is  the  more  frequent,  and  results  from  the  passage  of  air 
into  the  pleural  cavity.  Injury,  wounds  of  the  pleura  and  lung,  tuberculosis, 
emphysema,  strains,  infarcts,  superficial  haemorrhagic  nodules,  general  and 
interlobar  purulent  pleurisy,  foci  in  the  peribronchial  glands,  cysts,  or 
abscesses  of  the  hver  and  of  the  kidney,  are  the  usual  causes  of  these 
pleuropulmonary  perforations.  * 

1.  Strain  and  Emphysema. — Pneumothorax  may  appear  suddenly, 
following  a  strain,  whether  the  patient  have  emphysema  or  not.  An  emphy- 
sematous patient  may  also  be  suddenly  attacked  by  pneumothorax,  even 
though  he  has  made  no  effort.  In  these  various  cases  the  rupture  of  the 
air- vesicles  permits  the  air  to  reach  the  pleural  cavity,  the  vacuum  is 
destroyed,  the  lung  shrinks  and  collapses,  and  pneumothorax  is  produced. 
Galliard  has  collected  thirty-seven  cases  of  pneumothorax  from  strain. 

A  bugler  was  suddenly  taken  ill  with  pneumothorax  while  vigorously  blowing  his 
iastruraent.  A  clergyman  was  seized  with  pneumothorax  during  a  fit  of  hearty  laughter. 
A  man  was  taken  ill  with  pneumotliorax.  while  raising  a  chair  with  his  arm  extended. 
A  student  was  seized  ^vith  pneumothorax  while  dancing  vigorously. 

In  this  variety  of  pneumothorax  the  onset  is  sudden,  with  tearing  pain  in 
the  thorax,  and  very  acute  dyspnoea.  The  classical  signs  are  at  once  evident 
— tympanitic  resonance  and  amphoric  breathing.  Although  terrible  at  its 
onset,  this  form  is  not  grave,  for  there  were  only  tlu*ee  deaths  in  thirty-seven 
cases  (Galliard).  The  pneumothorax  remains  pure,  the  presence  of  fluid 
(hydrothorax)  is  very  rare,  and  suppuration  (pyothorax)  is  the  exception. 
The  perforation  usually  becomes  obhterated,  the  air  effused  into  the  pleural 
cavity  is  absorbed,  the  lung  resumes  its  function,  and  recovery  follows  in  a 
few  weeks. 

2.  Tuberculosis. — Tuberculosis  is  the  most  usual  cause  of  pneumo- 
thorax. Perforation  of  the  lung  may  supervene,  either  at  an  advanced  stage 
(cavity  and  softening)  or  at  the  onset  during  the  first  stage.  Cases  have, 
indeed,  been  quoted,  and  I  have  seen  them  myself,  in  which  pneumothorax 

*  Sauasicr,  who  has  collected  131  cases  of  pneumothorax,  classifies  them,  according 
to  their  causes,  as  follows:  Pulmonary  phthisis,  81;  pleurisy,  21;  gangrene  of  tlie 
lung,  7  ;  emphysema,  5  ;  pulmonary  apoplexy,  3  ;  cancer,  1  ;  abscess  of  the  hmg,  1  ; 
liydatid  of  the  lung,  1  ;  hepatic  abscess,  I  ("  Recherchos  sur  Ic  Pneumothorax,"  Paris, 
1S41). 


374  TEXT-BOOK  OF  MEDICINE 

occurred  in  an  apparently  healthy  person,  and  was  the  precursor  of  tubercu- 
losis that  had  so  far  shown  no  symptoms.  In  such  a  case  tubercular  pneumo- 
thorax resembles  that  due  to  emphysema  or  to  strain.  The  pathogenic 
diagnosis  is  extremely  difficult.  How  are  we  to  know  whether  pneumo- 
thorax, supervening  suddenly  in  an  apparently  healthy  subject,  is  or  is  not 
tubercular  ?  We  may  perhaps  use,  as  a  control  measure,  an  injection  ot 
2  milligrammes  of  tuberculin.  This  means  has  been  employed  by  Chauf!ard, 
and  the  absence  of  reaction  in  his  patient  proved  that  the  pneumothorax 
was  not  tubercular. 

It  was  formerly  held  that  purulent  change  in  an  effusion  following 
tubercular  pneumothorax  was  of  necessity  due  to  secondary  invasion  by 
other  micro-organisms :  Friedlander's  bacillus.  Staphylococcus  aureus, 
Bacillus  saprogenes,  etc.  (Netter). 

These  conclusions  are  no  longer  admitted.  Observations  have  shown 
that  tubercular  empyema  may  result  solely  from  the  infection  of  the  tubercle 
bacillus  without  the  presence  of  other  micro-organisms.  I  have  devoted  a 
clinical  lecture  to  "  purely  tubercular  pyopneumothorax  without  super- 
added infection,"  and  to  the  cases  already  observed  I  have  added  others 
which  leave  no  doubt  as  to  the  pathogenesis  of  the  pyopneumothorax. 

Speaking  generally,  pneumothorax  is  more  frequent  in  adults  than  in 
children ;  it  has,  however,  been  seen  in  children  of  all  ages,  even  in  those 
under  two  years  of  age ;  "  but  the  influence  of  age  varies,  according  to  the 
causes  of  the  pneumothorax.  Tubercles  produce  perforation  at  any  age  ; 
the  rupture  of  the  vacuoles  of  broncho-pneumonia  determines  it  exclu- 
sively between  the  ages  of  two  and  four  years." 

The  presence  of  air  in  the  pleural  cavity  is  generally  followed  by  hydro- 
thorax,  and  in  147  cases  collected  by  Moneret  the  pneumothorax  remained 
pure  in  sixteen  only  ;  fluid  formed  in  all  the  others.  Some  cases  have  been 
noted  in  wliich  the  fluid  remained  serous  for  a  very  long  time.  I  had  a 
patient'  under  my  care  in  whom  the  fluid  of  a  tubercular  hydropneumothorax 
remained  free  from  any  micro-organism  for  eight  months.  These  cases  are 
exceptional ;  most  frequently  the  fluid  becomes  purulent,  and  contains  the 
microbes  of  suppuration,  especially  when  the  perforation  is  consecutive  to 
a  tubercular  cavity  or  to  an  abscess  ;  in  some  cases  the  fluid  became 
purulent,  although  there  was  only  simple  rupture  of  the  pulmonary  alveoli 
(strain  or  emphysema). 

The  gases  in  the  pleura  vary  in  quantity  :  nitrogen  and  carbonic  acid 
predominate,  oxygen  being  in  the  smallest  proportion,  while  sulphuretted 
hydrogen  usually  accompanies  pyopneumothorax. 

Post  mortem  one  or  several  perforations  are  found  ;  their  size,  shape, 
and  situation  vary,  according  to  the  cause.  When  the  perforation  is  not 
readily  visible  on  the  surface  of  the  lung,  it  must  be  made  so.  For  this  purpose 


DISEASES  OF  THE  PLEURA  375 

the  pleural  cavity  is  filled  with  water,  and  insufflation  through  the  trachea 
is  performed.  The  bubbles  which  appear  at  the  mouth  of  the  fistula  indicate 
its  position  ;  the  pleuro-pulmonary  fistula,  however,  may  be  cicatrized  or 
obhterated,  and  the  corpus  delicti  passes  unnoticed. 

I  have  elsewhere  described  the  lesions  which  cause  pneumothorax. 

Symptoms. — The  invasion  of  pneumothorax  is  violent  or  quiet,  ac- 
cording to  the  cause  of  the  perforation.  When  the  irruption  of  air  affects 
a  healthy  pleura  free  from  adhesions,  the  lung  collapses,  and  the  symptoms 
are  sudden  ;  the  pain  in  the  side  is  severe,  and  the  dyspnoea  is  excessive. 
Under  other  circumstances,  when  the  lung  is  already  fixed  by  adhesions,  the 
onset  is  less  violent,  the  pain  and  dyspnoea  are  slower  to  appear,  and  are  less 
severe  ;  in  some  cases,  indeed,  the  disease  is  latent.  When  pneumothorax 
results  from  the  opening  of  a  purulent  collection  into  the  bronchi  (vomica), 
entrance  of  air  into  the  pleura  may  follow  the  voiding  of  the  pus  through  the 
bronchi. 

The  physical  signs  of  pneumothorax  are  as  follows  :  Mensuration  shows 
enlargement  of  the  thorax,  unless  chronic  pleurisy  has  already  caused 
retraction.  Percussion  yields  a  clear  and  tympanitic  sound,  metallic  in 
timbre  (Trousseau's  bruit  d'airain).*  The  vocal  fremitus  is  diminished  or 
abolished,  and  the  heart  may  be  displaced  by  gas  when  the  pneumothorax 
is  situated  on  the  left  side.  On  auscultation  the  breath-sounds,  the  cough, 
and  the  voice-sounds  become  amphoric,  and  the  rales  change  to  a  silvery 
sound,  known  as  metallic  tinkling.  There  is,  furthermore,  a  sign  which  I 
have  long  pointed  out :  If  the  patient  is  made  to  drink  small  mouthfuls  of 
fluid  during  auscultation,  the  swallowing  of  the  fluid  produces  a  gurgling 
sound  of  amphoric  timbre.  The  above  signs  result  from  the  presence  of  air 
in  the  pleura  ;  the  simultaneous  existence  of  fluid  and  of  gas  in  the  pleura 
shows  itself  by  a  splashing  noise,  audible  on  auscultation  even  at  a  distance, 
provided  the  patient  be  gently  shaken.  This  symptom  is  called  hippocratic 
succussion. 

The  tension  of  the  gaseous  effusion  is  variable,  according  as  the  perfora- 
tion of  the  lung  is  obhterated  or  not.  If  it  persists,  the  intrapleural  pressure 
is  practically  the  same  as  that  of  the  atmosphere  ;  if  it  is  obhterated,  the 
intrapleural  pres.sure  varies  from  -7  during  inspiration,  to  -f3  during 
expiration.     In  several  patients  I  have  found  that  these  figures  are  variable. 

Simple  pneumothorax  may  recover  in  three  or  four  weeks,  but  the 
nature  of  the  perforation  and  the  formation  of  pus  aggravates  tiie  prognosis. 
I  have,  however,  often  seen  the  cure  of  pneumothorax  and  of  hydropneurao- 
thorax  in  tubercular  patients. 

*  If  the  poslcrior  region  of  the  pfili(!nt's  chest  is  auBcnKated  wliilo  llio  fronl  is 
percussed,  the  percussion  yields  the  hriiit  d'airain.  Tlii.4  bruit  is  still  lid  (or  lieard  if 
the  percussion  is  made  by  moans  of  two  coins. 


376  TEXT-BOOK  OF  MEDICINE 

In  some  cases  pneumothorax  and  hydropneumotliorax  are  localized  to 
some  portion  of  the  thoracic  cavity  by  previous  adhesions  ;  tliis  condition 
is  partial  pneumothorax. 

Diagnosis. — Large  pleuritic  effusions  may  give  rise  to  amphoric  breath- 
ing,* but  the  other  signs  are  so  different  that  mistakes  are  not  possible 
between  gaseous  and  fluid  collections.  Large  cavities  in  phthisis  may 
simulate  pneumothorax,  but  are  nearly  always  localized  to  the  apex  of  the 
lung ;  the  rales  become  of  a  splashing  nature,  and  the  signs  of  amphorism 
are  less  marked. 

In  some  cases  partial  pneumothorax  and  hydropneumothorax  are  very 
difficult  to  diagnose,  and  it  is  essential  to  make  a  methodical  examination, 
dividing  the  thorax  into  three  regions — anterior,  axillary,  and  posterior 
(Jaccoud). 

I  have  described  a  partial  inferior  pneumothorax  with  pleuro-peritoneal 
symptoms.  It  must  not  be  confounded  either  with  subphrenic  abscess, 
which  is  an  abdominal  affection  with  pleural  symptoms,  or  with  certain 
cases  qf  subdiaphragmatic  peritonitis.  Pneumothorax,  or  hydropneumo- 
thorax, being  recognized,  it  is  still  necessary  to  diagnose  the  cause,  for  the 
aetiology  of  the  perforation  is  the  principal  basis  of  the  prognosis. 

The  treatment  varies  in  j^neumothorax,  hydropneumothorax,  or  pyo- 
pneumothorax. In  a  tubercular  patient  with  hydropneumothorax  it  is, 
perhaps,  preferable  not  to  withdraw  the  fluid,  for  the  spread  of  tuberculosis 
may  be  hindered  in  the  lung  thus  compressed.  In  a  case  of  pyopneumo- 
thorax Potain  obtained  striking  success  with  injections  of  steriUzed  air. 

I  have  treated  tubercular  pyopneumothorax  by  multiple  punctures  ;  at 
each  puncture  only  2  ounces  of  fluid  were  withdrawn,  and  an  intrapleural 
injection  of  solution  of  sublimate  was  given. 

Pneumothorax  by  Putrefaction. — I  have  so  far  dealt  with  pneumo- 
thorax by  perforation.  Essential  pneumothorax,  independent  of  perfora- 
tion and  consecutive  to  exhalation  of  gas  by  the  pleura,  was  formerly 
admitted.  This  view  is  no  longer  held,  but  some  authors  have  stated  that 
purulent  fluid  in  the  pleura  may  produce  gas  by  decomposition,  and  give 
rise  to  pneumothorax.  This  latter  form  no  doubt  does  exist,  and  is  due  to 
putrefaction,  caused  by  anaerobic  microbes.  I  have  dealt  with  pneumo- 
thorax by  putrefaction  under  Putrid  Pleurisy.  Pneumothorax  by  putre- 
faction is  the  opposite  of  pneumothorax  by  perforation ;  wliile  the  latter  is 
due  to  the  passage  of  air  into  the  pleural  cavity,  the  former  is  due  to  the 
production  of  gas  in  a  cavity  into  which  the  air  has  not  penetrated. 

*  These  amphoric  sounds  are  due  to  a  cavity,  filled  with  gas,  which  plays  the  j^art 
of  a  resonating  chamber.  Metallic  tinkUng  is  only  a  rale  which,  in  contact  with  this 
ca\-ity,  assumes  a  special  timbre,  and  it  is  not  essential  in  order  that  the  tinkling  may 
be  produced  to  have  a  communicatiou  between  the  cavitj'  and  the  bronchus  in  which 
the  rale  arises. 


CHAPTER  VI 
DISEASES  OF  THE  MEDIASTINUM 

I.  TUMOURS   OF   THE   MEDIASTINUM. 

Anatomy. — The  organs  of  the  mediastinum  are  so  numerous,  their  lesions  so  fre- 
quent, and  their  disposition  so  important,  by  reason  of  the  troubles  which  result  from 
these  lesions,  that  I  Avill  briefly  describe  the  anatomy  of  this  region. 

The  name  "  mediastinum  "  is  given  to  the  irregularly  shaped  cav-ity  which  is  filled 
by  numerous  organs,  and  occupies  the  space  between  the  sternum,  the  vertebral  column, 
and  the  inner  surface  of  the  lungs.  To  understand  the  construction  of  the  mechastinal 
cavity,  it  is  enough  to  know  the  relations  of  the  pleurae  in  this  situation.  The  pleur», 
after  being  in  contact  behind  the  sternum,  open  out,  and  in  the  interval  which  extends 
from  the  posterior  part  of  the  sternum  to  the  root  of  the  lung  they  circumscribe  a  space 
called  the  "  anterior  mediastinum."  They  continue  their  course  from  the  root  of  the 
lung  to  the  anterior  surface  of  the  vertebral  column,  and  circumscribe  a  second  space, 
known  as  the  "  posterior  mediastinum."  - 

The  height  of  tlie  anterior  mediastinum  equals  the  anterior  vertical  diameter  of  the 
thorax.  Its  shape  may  be  compared  to  a  triangular  pyramid,  two  sides  of  which  are 
lateral  and  one  posterior.  The  anterolateral  sides  are  formed  by  the  layers  of  the 
pleura  which  are  attached  to  the  sternum  ;  they  are  in  relation  (the  right  especially 
so)  with  the  lung.  The  posterior  side,  which  is  the  smallest,  is  in  relation  with  the 
oesophagus  below  and  with  the  oesophagus  and  the  thoracic  cavity  above.  In  this  tri- 
angular space  the  following  organs  are  contained  : 

The  pericardium,  extending  vertically  from  the  xiphoid  cartilage  to  the  middle  of 
the  first  piece  of  the  sternum,  and  horizontally  for  about  4  inches  to  the  left  of  the  middle 
line  of  the  sternum  and  1  inch  to  the  right. 

The  heart,  the  apex  of  which  corresponds  to  the  sixth  rib,  is  found  about  4  inches 
from  the  median  line  of  the  sternum.  The  arch  of  the  aorta,  which  corresponds  to  the 
middle  and  upper  part  of  the  sternum,  contains  the  cardiac  plexus  in  its  concavity. 

On  the  same  plane  as  these  vessels  we  find,  on  the  right  side,  the  innominate  artery 
and  the  superior  vena  cava  ;  on  the  left  the  common  carotid  and  subclavian  arteries, 
and  more  externally  the  recurrent  and  phrenic  nerves. 

Behind  these  organs  is  the  root  of  the  lung,  formed  by  (1)  the  bronchi  situated  on 
the  same  plane  as  the  inner  part  of  the  second  intercostal  spaces  ;  (2)  the  pulmonary 
arteries  ;  (3)  tlu!  pulmonary  veins. 

The  posterior  part  ol  the  mediastinum  is  vrry  didcrcnt  from  the  anterior  one.  Its 
li'ngth  is  nearly  equal  to  that  of  the  dorsal  column,  and  its  shape  that  of  a  four-sided 
jjyraraid,  with  its  apex  below.  The  lateral  sides  are  formed  by  the  pleuras  wliich  open 
out  above  to  receive  the  subclavian  arteries.  The  posterior  side  corresponds  to  the 
vertebral  column,  while  the  anterior  is  limited  by  the  bifurcation  of  the  trachea  in  its 
ui)pcr  fourth,  and  by  the  pericardium  in  its  lower  three-fourths.  In  this  irregular 
quadrangular  space  the  following  organs  are  met  with  : 

377 


378  TEXT-BOOK  OF  MEDICINE 

The  thoracic  aorta  and  cesophagus,  which  are  at  first  situated  on  the  same  trans- 
verse plane,  but  approach  one  another  during  their  descent,  so  that  the  oesophagus  is 
finally  placed  in  front  of  the  aorta,  and  helps  to  form  the  apex  of  the  pyramid. 

The  vena  azygos  major  occupies  the  right  side  of  the  vertebral  column,  behind  the 
cesophagus  ;  the  vena  azygos  minor  is  placed  on  the  left  side  of  the  dorsal  column, 
behind  the  aorta  ;  while  the  thoracic  duct  is  situated  between  the  two  azygos  veins. 

We  also  find  connective  tissue,  lymphatic  glands,  and  twigs  from  the  great  sym- 
pathetic plexus  and  the  pneumogastric  nerves  which  surromid  the  oesophagus. 

The  lymphatic  glands  have  a  special  importance,  from  the  numerous  diseases  that 
occur  in  them.  As  a  whole,  they  receive  the  lymphatic  vessels  from  the  pleura,  lungs, 
trachea,  bronchi,  heart,  pericardium,  and  chest-walls.  The  groups  of  glands  which 
deserve  special  attention  have  been  described  by  Barety  :  (1)  Right  and  left  peri- 
tracheo-bronohial  groups  ;  (2)  right  and  left  subbronchial  groups  ;  and  (3)  inter  bronchial 
groups. 

Pathological  Anatomy. — Among  the  numerous  tumours  Avhich  develop 
in  the  mediastinum,  we  shall  consider  :  (1)  Simple  adenopathy  ;  (2)  tubercu- 
lar adenopathy  ;  (3)  cancerous  adenopathy  ;  (4)  degeneration  of  the  thymus  ; 
(5)  aneurysm  of  the  aorta ;  (6)  abscesses  of  the  mediastinum ;  (7)  cancer  of 
the  oesophagus  ;  (8)  glandular  hypertrophy,  ^v'ith  or  without  leucocythaemia. 

1.  Simple  Adenopathy. — Acute  diseases  of  the  lungs  and  of  the  bronchi 
produce  engorgement  and  inflammation  of  the  tracheo-bronchial  glands, 
especially  in  children.  Pneumonia,  capillary  bronchitis,  and  the  catarrhs 
associated  with  measles,  whooping-cough,  or  influenza,  lead  to  adenopathy. 
The  glands  sometimes  become  much  enlarged  ;  inflammatory  congestion  and 
oedema  are  present,  and  sometimes  "  hyperaemia  and  effusion  of  blood  cause 
an  increase  in  size,  with  red  coloration  of  the  whole  gland  tissue,  which 
then  resembles  liver."     Acute  adenitis  sometimes  goes  on  to  suppuration. 

2.  Tubercular  Adenopathy. — The  tubercles  develop  along  the  vessels 
in  the  cavernous  or  in  the  folhcular  system  of  the  gland,  and  present  the  same 
characters  as  in  other  tissues.  The  tubercle  undergoes  fatty  change,  and 
when  the  granulations  are  confluent,  the  parts  situated  between  them  may 
undergo  caseous  degeneration. 

In  children  tubercuhzation  of  the  bronchial  glands  is  never  primary,  but 
always  consecutive  to  tuberculosis  of  the  lung ;  the  lesion  in  the  lung 
may  be  insignificant,  while  the  glandular  mischief  is  very  extensive 
(Parrot). 

3.  Malignant  Adenopathy. — Sarcoma  and  carcinoma  of  the  bronchial 
glands  are  often  consecutive  to  mahgnant  disease  of  the  lung ;  lymph- 
adenoma,  which  is  much  more  frequent  than  the  preceding  forms,  is 
generally  primary ;  it  develops  in  young  healthy  subjects,  and  at  times 
assumes  the  more  mahgnant  form  of  lymphosarcoma. 

These  malignant  tumours  grow  large,  invade  the  organs  of  the  mediasti- 
num, the  heart,  the  lungs,  and  envelop  the  vessels  and  nerves.  In  other 
cases  the  infection  is  carried  to  a  distance,  probably  by  way  of  the  lym- 


DISEASES  OF  THE  MEDIASTINUM  379 

phatics,  veins,  or  serous  membranes,  and  secondary  nodules  are  found  in  tlie 
kidney,  liver,  etc. 

4.  Degeneration  of  the  Thymus. — The  most  contradictory  opinions 
have  been  enunciated  on  the  subject  of  tumours  of  the  thymus  ;  their 
frequency  has  in  turn  been  exaggerated  and  denied.  It  is  certain  that  in 
children,  and  even  in  adults,  we  find  sarcomata  of  different  forms  and  slow 
evolution,  which  have  arisen  in  the  vestiges  of  the  thymus. 

5.  Glandular  hypertrophy,  with  or  without  leucocythsemia,  will  receive 
a  separate  description. 

6.  Syphilis  may  involve  the  mediastinal  glands  (see  Syphilis  of  the  Lung). 
Symptoms.— Besides  the  signs  and  symptoms  special  to  the  pathology 

of  each  of  the  organs  in  the  mediastinum  (cancer  of  the  oesophagus,  aneurysm 
of  the  aorta,  lymphadenoma,  glandular  tuberculosis,  etc.),  certain  signs  are 
common  to  all  tumours,  and  serve  to  give  a  complete  picture  of  the  pathology 
of  the  mediastinal  region.  This  is  what  I  have  named  the  mediastinal 
syndrome. 

For  example,  the  compression  of  a  bronchus,  of  a  venous  trunk,  or  of  a 
recurrent  nerve,  is  always  followed  by  the  same  effects,  whether  it  be  due  to 
aneurysm  of  the  aorta,  glandulai  hypertrophy,  lymjahadenoma,  or  cancer. 
These  common  signs  and  uniform  symptoms  are  nearly  all  tlie  result  of 
compression  exercised  by  tumours  upon  the  organs  in  the  mediastinal 
region.     They  are  as  follows  : 

1 .  Deformity. — This  deformity  affects  the  sternal  region.  The  first  piece 
of  the  sternum  may  be  raised,  or  the  bulging  may  predominate  at  the  sterno- 
clavicular joints  ;  sometimes  the  bones  are  worn  away,  as  in  aneurysm  of  the 
aorta,  and  the  expansile  tumour  takes  the  place  of  the  bone.  When  the 
swelling  is  due  to  masses  of  glands  (lymphadenoma,  cancer),  the  glands  in 
the  supraclavicular  hollow  are  often  enlarged. 

Other  signs  are  also  present :  normal  resonance  gives  place  to  dullness, 
which  varies  according  to  the  size  of  the  tumour,  and  may  often  be  found 
behind  in  the  interscapular  region  (Gueneau  de  Mussy).  Bronchophony 
and  bronchial  breathing  are  proper  to  changes  in  the  glands  near  the  trachea 
and  the  bronchi,  while  a  double  centre  of  pulsations  marks  the  existence  of 
aortic  aneurysm. 

When  the  disease  is  of  long  duration,  the  retraction  of  the  chest-wall, 
which  has  sometimes  been  observed,  is  probably  due  to  the  comj^ression  of 
a  large  bronchus,  with  impaired  activity  of  the  lung. 

2.  Compression  of  the  Bloodvessels. — This  result  is  very  common  in 
tumours  of  the  mediastinum.  "'  The  arteries  and  the  bronchial  veins  may 
be  compressed  by  the  suprabronchial  and  intertracheo-bronchial  glands,  the 
brachio-cephalic  venous  trunks,  and  the  branches  of  the  arch  of  the  aortA 
by  the  retrosterno-clavicular  glands  "  (Barety). 


380  TEXT-BOOK  OF  MEDICINE 

The  arterial  vessels,  being  more  resistant,  suffer  less  from  compression 
than  the  veins,  and  it  is  not  rare  to  see  an  aneurysm  of  the  aorta  or  a  large 
mass  of  glands  compressing  the  superior  vena  cava,  the  vena  azygos  major, 
and  the  innominate  vein.  When  the  superior  vena  cava  is  compressed,  the 
passage  of  blood  through  this  channel  into  the  right  auricle  is  difficult  or 
impossible,  and  the  result  is  blood-stasis  in  the  areas  which  pour  their  blood 
into  the  tributaries  of  the  superior  vena  cava — that  is  to  say,  in  the  head, 
the  upper  limbs,  and  the  upper  part  of  the  thorax. 

Following  the  blood-stasis,  we  observe  dilatation  of  the  subcutaneous 
venules  ;  bluish  networks  show  themselves  on  the  thorax,  shoulders,  and 
arms,  etc.,  while  the  jugular  veins  are  dilated.  This  venous  stasis  is  followed 
by  tlie  formation  of  a  collateral  circulation — that  is  to  say,  the  blood  which, 
as  a  rule,  flows  into  the  left  auricle  tlirough  the  superior  vena  cava,  now  takes 
another  course,  and  seeks  to  reach  the  same  goal  by  the  inferior  vena  cava. 
The  blood  passes  through  its  altered  channel  by  means  of  deep  and  super- 
ficial anastomoses,  which  join  the  superior  to  the  inferior  caval  system,  and 
which  from  actual  necessity  become  many  times  larger  than  the  normal. 

These  anastomoses  are  the  large  and  small  azygos,  intercostal,  internal 
mammary,  deep  epigastric,  superficial  epigastric,  and  circumflex  ihac  veins. 
By  these  altered  channels  the  blood  of  the  superior  caval  system  attempts  to 
pass  into  the  inferior  caval  one  in  order  to  reach  the  right  auricle.  Hence 
in  these  abnormal  cases  the  blood  flows  from  above  downwards  in  the 
cutaneous  veins  of  the  thorax  and  abdomen,  and  it  is  easy  to  prove  the 
direction  of  the  current  by  pressing  back  the  blood  in  a  dilated  venous 
segment,  and  alternately  removing  the  compression  in  the  upper  or  in  the 
lower  end  of  the  bloodless  segment. 

If  the  vena  azygos  major  participates  in  the  compression,  the  re-estabhsh- 
ment  of  the  circulation  takes  place  only  by  the  inferior  vena  cava.  In  the 
opposite  case  the  azygos  system  which  empties  itself  into  the  superior  vena 
cava  takes  part  in  the  re-establishment  of  the  circulation.  In  short,  the 
blood-stasis  in  the  veins,  the  situation  of  these  networks,  and  the  direction  of 
the  blood-current  give  valuable  information,  which  may  point  out  the 
obstacle  to  the  circulation  in  the  mediastinum. 

When  the  collateral  circulation  is  efficient,  the  symptoms  are  shght.  In 
the  opposite  case,  oedema  of  the  hands  and  face  is  seen,  the  lips  are  violet- 
coloured,  the  eyes  are  injected,  the  patient  suffers  from  giddiness,  nose- 
bleeding,  and  headache — in  short,  from  the  signs  of  cephaUc  congestion,  due 
to  venous  stasis. 

When  the  subclavian  artery  or  the  brachio-cephahc  trunk  is  compressed, 
the  radial  pulse  diminishes  in  size.  On  the  affected  side  compression  of 
the  pulmonary  artery  or  of  its  branches  has  several  times  been  noted ; 
ulceration  of  these  vessels  causes  fulminant  haemoptysis. 


DISEASES  OF  THE  MEDIASTINUM  381 

3.  Compression  of  the  Trachea  and  Bronchi. — The  left  bronchus  is 
more  often  compressed  than  the  right ;  the  vesicular  murmur  diminishes 
or  disappears  in  the  corresponding  lung,  but  the  thoracic  resonance  is  pre- 
served. The  union  of  these  two  symptoms — absence  of  breath-sounds  and 
preservation  of  resonance — eliminates  the  idea  of  an  effusion  into  the  pleura, 
and  can  only  be  explained  by  narrowing  or  by  compression  of  the  bronchus. 
When  the  calibre  is  much  diminished,  we  find  inspiratory  sucking-in,  which 
is  most  marked  in  the  supraclavicular  and  epigastric  hollows  (Gueneau  de 
Mussy). 

Compression  of  the  bronchi  and  of  the  trachea  often  produces  rough 
and  whisthng  inspiration,  which  has  received  the  name  of  stridor  (Cayol). 
This  sound  is  heard  whenever  stenosis  affects  the  larynx,  the  trachea,  or 
the  large  bronchi. 

4.  Changes  in  the  Pneumogastric,  Recurrent,  Phrenic,  and  Sym- 
pathetic Nerves. — The  symptoms,  consecutive  to  changes  in  these  nerves, 
difEer  according  as  the  nerve  is  irritated  (symptoms  of  excitation)  or 
destroyed  (symptoms  of  paralysis).  This  is  a  very  important  distinction. 
Hoarse  paroxysmal  cough,  resembling  that  of  whooping-cough,  has  been 
noted  in  a  great  number  of  cases  (Gueneau  de  Mussy)  of  bronchial  adeno- 
pathy. "  In  children  especially,  when  spasmodic  cough  shows  itself  at 
once  or  persists  long  after  genuine  whooping-cough,  there  is  reason  to  suspect 
compression  of  the  pneumogastric  nerve  by  degenerated  bronchial  glands  " 
(Verliac).  Dyspnoea,  with  or  without  paroxysms,  often  results  from 
compression  of  the  vagus  and  the  recurrent  nerves.  The  attack  may  simu- 
late asthma  (Herard),  or  may  resemble  angina  pectoris.  In  one  case  the 
symptoms  were  due  to  irritation  of  the  right  vagus,  which  was  congested 
and  adherent  to  the  swollen  and  degenerated  glands  (Barety).  I  have 
seen  an  analogous  case. 

Laryngeal  troubles  betray  themselves  by  the  raucous  nature  of  the  voice 
(dysphonia),  and  by  spasms  of  the  glottis.  The  changes  in  the  voice  are 
explained  by  the  paralysis  of  the  vocal  cord  supplied  by  the  affected  re- 
current nerve.  The  diagnosis  is  readily  verified  by  the  laryngoscope. 
Spasms  of  the  glottis  are  due  to  excitation  of  the  recurrent  nerve.  Ex- 
citation of  one  nerve  alone  is  sufficient  to  provoke  spasm  of  the  glottis 
(Krishaber).  The  change  in  the  phrenic  nerves  determines  diaphragmatic 
neuralgia  and  attacks  of  dyspnoea  (Bazin). 

InequaUty  of  the  pupils  is  often  seen,  and  arises,  doubtless,  from  changes 
in  the  great  sympathetic  nerve. 

5.  Dysphagia  is  due  to  the  compression  of  the  ccsophagus  by  media^ 
stinal  tumours,  tumours  of  the  aorta,  degeneration  of  glands,  etc.,  and  tu 
adherence  of  the  oesophagus  to  neighbouring  organs.  Its  perforation  lias 
been  noted  five  times  (Barety). 


382  TEXT-BOOK  OF  MEDICINE 

Diagnosis — Prognosis. — The  diagnosis  is  often  difficult.  Sometimes 
the  lesion  betrays  itself  only  by  an  isolated  phenomenon  —  viz.,  per- 
manent contraction  of  one  pupil,  paroxysmal  dyspnoea,  analogous  to  attacks 
of  asthma,  aphonia  simulating  a  malady  of  the  larynx,  spasmodic  and 
paroxysmal  cough  resembling  whooping-cough,  or  agonizing  retro-sternal 
pain,  which  is  nothing  less  than  angina  pectoris.  Even  when  attention  is 
directed  to  the  seat  of  the  disease,  the  difficulty  is  not  entirely  overcome,  for 
many  mediastinal  tumours  have  symptoms  in  common,  and  it  is  then  neces- 
sary to  diagnose  the  nature  of  the  tumour. 

If,  however,  they  have  characters  in  common,  they  also  have  some 
special  characters  which  aid  in  the  diagnosis.  Thus,  in  aneurysm  of  the 
aorta  we  often  find  a  movement  of  expansion,  a  double  centre  of  pulsations^ 
and  a  double  or  single  blowing  murmur.  Glandular  affections  of  the  media- 
stinum (lymphadenoma,  leukaemia)  are  generally  accompanied  by  glandular 
hypertrophy  in  other  regions,  as  the  neck,  the  axilla,  or  the  groin.  In 
tubercular  adenopathy  the  condition  of  the  lungs  must  be  carefully 
inquired  into.  Cancerous  degenerations  sometimes  involve  the  supra- 
clavicular glands. 

The  prognosis  is  generally  grave.  Tumours,  by  their  more  or  less  rapid 
progress,  compromise  the  respiration  and  the  circulation,  and  the  patient 
dies  either  slowly  from  asphyxia,  or  suddenly  from  syncope,  or  from  attacks 
of  suffocation.  Rapid  death  generally  depends  upon  changes  in  the  vagus 
and  recurrent  nerves. 

Certain  lesions  of  the  mediastinum  may  be  treated'  surgically  (Ziem- 
bicki).  Dr.  Potarca  (of  Bucharest),  in  a  work  entitled  "  Posterior  Intra- 
mediastinal  Surgery,"  has  reported  numerous  operations  performed  for 
purulent  collections  in  the  posterior  mediastinum,  phlegmon,  mediastinitis, 
suppuration  in  the  bones  or  the  glands,  and  abscesses  from  foreign  bodies. 

II.  CANCER  OF  THE  THORACIC  DUCT. 

The  thoracic  duct,  which  collects  the  lymph  from  the  lower  hmbs  and  the 
thoracic  and  abdominal  viscera,  extends  from  the  receptaculum  chyh  to 
the  left  subclavian  vein.  It  belongs,  therefore,  to  the  posterior  media- 
stinum, where  it  passes  up  between  the  two  azygos  veins  behind  the  oeso- 
phagus, until  it  crosses  the  posterior  surface  of  the  arch  of  the  aorta  and 
enters  the  cervical  region.  The  thoracic  duct  carries  matter  absorbed  by 
the  digestive  tract,  but  in  pathological  conditions  it  may  transport  microbes 
and  cellular  emboli  to  the  right  heart.  Secondary  cancer  of  the  duct  occurs 
when  cancer  cells  are  grafted  on  to  its  walls. 

Nattan-Larrier  has  described  two  cases  of  secondary  cancer  of  the  duct. 

The   organs  which  usually  give  rise  to  secondary  cancer   of  the   duct 


DISEASES  OF  THE  MEDIASTINUM  383 

are  the  stomach,  the  uterus,  and  the  testicle,  because  their  lymphatics 
pass  more  directly  to  the  duct ;  then  come  the  rectum,  the  pancreas,  the 
kidney,  and  the  ovary.  The  thoracic  duct  is  invaded  by  vascular  propaga- 
tion. The  degeneration,  affects  successively  the  lymphatics  from  the  can- 
cerous organ,  the  corresponding  glands,  their  efferent  lymphatics,  and 
finally  the  thoracic  duct.     Invasion  by  effraction  is  quite  exceptional. 

In  one-half  of  the  cases  the  entire  duct  is  involved,  in  one-quarter  the 
growth  stops  at  some  distance  from  the  termination  of  the  duct,  wliile  in 
more  rare  cases  the  lesion  is  hmited  to  the  origin  of  the  vessel.  When  the 
entire  duct  is  invaded,  it  resembles  a  vessel  injected  with  paraffin.  "  The 
receptaculum  is  as  large  as  the  thumb,  and  looks  hke  a  flabby,  nodular, 
whitish  cord,  wliile  a  granular  mass  exudes  on  puncture.  Below  the  recep- 
taculum we  find  a  network  of  cancerous  lymphatics  over  the  sides  of  the 
aorta.  Higher  up  we  find  the  duct,  properly  speaking ;  it  forms  a  trunk 
3  to  4  milhmetres  in  diameter,  wanding  over  the  posterior  surface  of  the 
aorta.  At  some  points  it  divides  into  three  or  four  branches,  which  remain 
separate  for  3  or  4  inches,  and  then  reunite  to  form  a  trunk  as  large  as  the 
primary  vessel.  After  passing  round  the  subclavian  artery  the  cancerous 
duct  reaches  the  vein,  which  it  perforates  at  the  junction  of  tliis  vessel  with 
the  internal  jugular  vein."  Sections  show  secondary  cancer  of  the  duct. 
The  epithehomatous  cells  are  fixed  in  the  connective  tissue,  and  form  buds, 
which  obhterate  the  lumen.  At  the  termination  of  the  duct  we  often  find 
a  cancerous  vegetation  which  floats  in  the  subclavian  vein. 

The  subjoined  case  is  very  typical : 

Woman  who  had  suffered  from  dyspepsia  for  many  years,  admitted  in  July,  1900. 
Repeated  melaena  and  hcematemesis,  complete  anorexia,  and  marked  wasting.  She 
complained  of  acute  epigastric  pain,  and  pali)ation  revealed  a  large  tumour  at  the  level 
of  the  greater  curvature  of  the  stomach. 

She  had  cancer  of  the  stomach,  confirmed  by  a  large  gland  in  the  left  supraclavicular 
fossa.  The  left  suVjcIavian  vein  soon  became  thrombosed.  Fever  appeared,  and  she 
died  from  streptococcal  septicaemia.  Post  mortem,  cancer  of  stomach  and  secondary 
growth  involving  the  entire  thoracic  duct,  which  was  completely  obliterated,  and  showed 
all  the  features  above  described. 

Cancer  of  the  thoracic  duct  shows  itself  by  symptoms  and  signs  which 
are  at  times  difficult  to  distinguish  from  those  due  to  the  primary  growth. 
Wasting  and  malnutrition  are  rapid.  Yet,  strange  to  say,  obhteration  of 
the  duct  is  not,  as  a  rule,  accompanied  by  lymphostasis.  In  three  cases  only 
did  milky  effusion  in  the  peritoneum  coincide  with  cancer  of  the  duct.  In 
two  cases  the  chyhform  ascites  was  due  to  cancer  of  the  ijcritoneum,  and 
in  the  third  case  the  chylous  effusion  was  due  to  the  spread  of  the  growth 
to  the  subperitoneal  lacteals.  We  must  therefore  admit  that  the  lymph- 
flow  is  usually  re-cstabUshed  by  the  collateral  channels.  Phlebitis  of  the 
left  arm  is  fairly  common,  and  is  due  to  thrombosis,  which  starts  from  the 


384  TEXT-BOOK  OF  MEDICINE 

anastomosis  of  the  duct  with  the  vein.  The  phlebitis  is  seen  in  25  per 
cent,  of  cases.  The  existence  of  glands  in  the  left  supraclavicular  fossa 
has  been  noted  in  half  of  the  cases. 

The  discovery  of  a  prelumbar  tumom-,  accompanied  by  double  vari- 
cocele, would  point  to  invasion  of  the  thoracic  duct,  since  the  prelumbar 
glands  are  affected  in  all  cases  of  epithelioma  of  this  tube.  Nevertheless, 
the  prelumbar  glands  may  be  cancerous,  while  the  duct  is  not  invaded. 
No  one  of  these  signs  has  absolute  value,  but  their  appearance  in  cancer 
of  the  stomach  or  of  the  uterus  would  lead  us  to  think  of  secondary  growth 
in  the  thoracic  duct. 


PART    II 

DISEASES  OF  THE  CIRCULATORY  SYSTEM 

CHAPTER  I 
DISEASES  OF  THE  PERICARDIUM 

I.  ACUTE  PERICARDITIS. 

Pericarditis  is  inflammation  of  the  pericardium. 

Senac  (1783)  was  the  first  to  separate  pericarditis  from  other  diseases 
of  the  heart.  In  1806  Corvisart  applied  to  it  the  signs  given  by  percussion  ; 
in  1824  ColUn,  assistant  to  Laennec,  discovered  the  pericardial  rub  (bruit 
de  cuir  neuf),  and  some  years  later  Bouillaud  created  cardiac  pathology. 

i^tiology. — The  so-called  primary  (a  frigore)  pericarditis  does  not 
exist.  The  secondary  form  is  sometimes  associated  with  a  neighbouring 
lesion  (pleurisy,  aneurysm  of  the  aorta).  It  may  follow  injury,  but  usually 
occurs  in  infectious  diseases  and  constitutional  maladies. 

Pericarditis  associated  with  pneumonia  may  be  parapneumonic  or 
metapneumonic.  It  may  be  dry,  sero-fibrinous,  hgemorrhagic,  or  purulent. 
The  fluid  does  not  contain  much  fibrin,  and  the  pus  is  homogeneous. 
Pneumococcal  pericarditis  may  be  independent  of  any  pulmonary  lesion. 

The  eruptive  fevers,  and  especially  scarlatina,  may  be  accompanied 
by  pericarditis.  The  fluid  may  be  sero-fibrinous,  htemorrhagic,  or  purulent, 
and  almost  always  contains  the  streptococcus. 

Pericarditis  in  erysipelas  is  also  associated  with  the  streptococcus 
(Denuce). 

Pericarditis  consecutive  to  influenzal  broncho- pulmonary  lesions  is 
associated  with  several  microbes,  among  which  the  streptococcus  is  the  chief. 

Pericarditis  in  Bright's  disease  is  said  in  some  cases  to  be  of  toxic 
origin. 

Tubercular  pericarditis  is  sero-fibrinous,  ha3morrhagic,  or  purulent, 
and  due  to  Koch\s  bacillus,  with  which  other  organisms  may  be  associated. 

Purulent  pericarditis  consecutive  to  pyaemia  is  duo  to  staphylococci  or 
streptococci,  but  it  is  sometimes  impossible  to  find  the  point  of  entry. 

385  25 


386  TEXT-BOOK  OF  MEDICINE 

The  most  frequent  cause  is  acute  rheumatism,  which  is  probably  a 
microbic  disease.  The  pericarditis  appears  during  the  first  and  second 
weeks  of  articular  rheumatism,  but  may  appear  at  the  same  time  as  the 
articular  lesions,  or  even  apart  from  them.  In  some  cases  it  is  associated 
with  endocarditis  or  with  pleurisy.  It  attacks  patients  at  any  age,  but  by 
preference  young  children  and  infants. 

Pathological  Anatomy. — Acute  pericarditis  has  been  divided,  Hke 
pleurisy,  into  two  varieties,  according  as  it  is  dry  or  accompanied  by 
effusion.  In  acute  pleurisy,  however,  effusion  is  the  rule,  while  in  peri- 
carditis it  is  the  exception.  In  ten  patients  suffering  from  rheumatic 
pericarditis,  effusion  is  perchance  found  but  twice.  From  an  anatomical 
point  of  view,  acute  dry  pericarditis  does  not  exist,  for  a  certain  quantity 
of  exudate  is  always  found  post  mortem.  CUnically,  however,  the  effusion 
is  not  considered,  unless  it  is  sufficient  to  cause  special  signs,  and  from  this 
point  of  view  pericarditis  with  effusion  is  somewhat  rare. 

Pericarditis  may  be  partial  or  general.  It  is  usually  situated  near  the 
aorta  and  at  the  base  of  the  heart.  The  visceral  layer,  or  epicardium,  is 
always  the  more  affected.  At  first  the  congested  vessels  form  a  fine  net- 
work on  the  surface  of  the  serosa,  which  loses  its  polish  and  becomes  covered 
with  a  fibrinous  exudate,  the  papillary  aspect  of  which  (cor  hirsutum)  has 
caused  it  to  be  compared  to  a  cat's  tongue,  or  to  sUces  of  bread  and  butter 
which  have  been  pressed  together  and  then  quickly  separated.  The  papillae 
are  formed  of  fibrin,  epithehal  cells,  and  pus  corpuscles.  Their  special  form 
is  due  to  the  incessant  movements  wliich  are  given  to  the  fibrin  by  the  heart. 
The  outer  layer  of  the  serosa  takes  no  part.  The  connective  tissue  of  the 
serosa  shows  embryonic  infiltration,  and  the  lymphatic  vessels  are  crammed 
with  fibrin  and  white  corpuscles.  The  quantity  of  fluid  varies  from  a  few 
drachms  to  a  pint  or  more ;  it  may  be  sero-fibrinous  (rheumatism, 
pneumonia),  haemorrhagic  (tuberculosis,  Bright's  disease,  scurvy,  cancer, 
and  cachexia),  or  purulent  (scarlatina,  pneumonia,  typhoid  fever,  and 
puerperal  conditions).  The  heart  muscle  often  shows  superficial  myo- 
carditis. Tubercular  pericarditis  deserves  special  mention.  It  super- 
venes in  the  course  of  acute  or  of  chronic  tuberculosis,  or  occurs  as  a  primary 
local  tuberculosis.  Effusion  may  or  may  not  be  present,  and  in  the  former 
case  the  fluid  is  often  hsemorrhagic.  In  recent  cases  the  tubercular  tissue 
contains  bacilli  but  they  may  be  absent  in  old  cases  (Cornil  and  Babes). 
The  mediastinal  glands  are  indurated  and  enlarged,  while  the  cellular 
tissue  around  them  is  adherent  to  the  pleura  and  the  lungs.  Tubercular 
pericarditis  sometimes  ends  in  adherent  pericardium. 

Description. — The  invasion  is  very  variable,  and  although  this  diversity 
of  onset  may  not  be  solely  imputable  to  its  causes,  pericarditis  is  usually 
insidious  and  latent  (Stokes),  and  far  more  rarely  acute  and  painful. 


DISEASES  OF  THE  PERICARDIUM  387 

The  patient  sometimes  complains  of  more  or  less  severe  oppression,  with 
palpitation  and  pain  in  the  precordial  or  in  the  epigastric  region,  or  between  the 
shoulders.  As  a  rule,  especially  in  rheumatic  pericarditis,  these  symptoms, 
and  especially  the  pain,  are  absent  or  shght.  In  some  exceptional  cases, 
however,  the  symptoms  of  acute  pericarditis  are  very  marked  :  the  face  is 
pale  ;  the  patient  is  anxious  ;  the  pain  may  be  terrible,  accompanied  by 
chill  and  Upothymia,  and  analogous  to  the  pain  of  angina  pectoris — a  fact 
vrhich  would  prove  that  the  cardiac  plexus  and  the  phrenic  nerve  are  affected 
by  the  inflammation. 

Auscultation  during  the  onset  of  the  malady  reveals  a  rub.  This  rub, 
which  is  at  first  systoUc,  soon  becomes  systolic  and  diastolic.  It  is  a  sound 
that  comes  and  goes — i.e.,  a  "bruit  de  frou-frou.'*  As  the  friction  sounds 
are  not  absolutely  synchronous  with  the  heart  sounds,  it  is  preferable  to 
say  that  the  one  is  mesosystolic  and  the  other  mesodiastolic.  The  want 
of  synchronism  depends  on  the  fact  that  for  both  layers  of  the  pericardium 
to  produce  a  friction  sound  it  is  necessary  that  "  the  displacement  of  the 
surface  of  the  heart  should  have  reached  a  certain  degree,  that  the  muscular 
contraction  should  have  just  commenced,  and  that,  in  consequence  of  the 
form  and  volume  of  the  heart,  the  surfaces  in  contact  be,  so  to  say,  relaxed, 
after  having  been  dragged  apart  more  or  less  suddenly  "  (Potain). 

The  pericardial  rub  has  special  characters.  It  is  more  rasping  than  the 
cardiac  murmur,  and  is  not  propagated  in  the  direction  of  the  blood-stream. 
It  has  its  maximum  intensity  about  the  third  intercostal  space,  where  the 
anterior  surface  of  the  heart  is  more  directly  in  relation  with  tlie  chest, 
and  increases  in  intensity  when  the  jJatient  bends  forward  or  when  the 
stethoscope  is  firmly  appUed  to  the  chest-wall.  Lastly,  it  is  not  absolutely 
isochronous  with  the  normal  sounds  of  the  heart.  In  some  cases  the  rub 
is  intense  and  general. 

It  often  happens  that  the  systolic  rub  commences  a  little  before  the 
systole  ;  it  is  presystohc,  and  causes  a  triple  sound,  called  the  "  bruit  de 
galop  "  (Bouillaud).  This  bruit  de  galop  has  a  special  rhythm,  and  its 
three  periods  are  divisible  in  the  following  manner  :  The  first  two  sounds, 
which  are  short  and  hurried,  are  formed,  one  by  presystohc  friction,  and  the 
other  by  the  normal  sound  of  the  heart,  with  or  without  friction  ;  while  the 
tliird  sound  corresponds  to  the  normal  second  sound  of  the  heart,  or  to  this 
sound  covered  by  a  friction  sound.  This  bruit  de  galop,  composed  of  two 
short  sounds  and  one  long  one,  must  not  be  confounded  with  the  sounds, 
called  "  l)ruit  de  caille  "  and  "  bruit  de  rappel,"  the  rhythm  of  which  is 
a  sign  of  mitral  stenosis,  and  is  inverse  to  the  bruit  de  galop,  being  made 
up  of  a  long  and  two  short  sounds. 

The  single  or  double  rulj,  witli  or  witliout  bruit  de  gah»[),  is  therefore  a 
sign  of  dry  pericarditis  ;  but  when  oifusion  is  present,  the  fluid  separates 

25—2 


388  TEXT-BOOK  OF  MEDICINE 

the  layers  of  the  pericardium,  and  the  rub  disappears.  In  some  cases, 
however,  the  rub  may  still  be  perceptible  towards  the  base  of  the 
heart,  in  spite  of  a  large  effusion.  In  proportion  as  the  effusion  forms, 
the  fluid  collects  in  the  dependent  regions  of  the  pericardium.  A  small 
effusion  passes  unnoticed,  but  large  ones  cause  the  following  signs  and 
symptoms  : 

On  inspection  and  palpation,  we  find  that  the  cardiac  waves  and  the 
impulse  of  the  heart  against  the  chest-wall  become  gradually  effaced.  On 
auscultation,  the  heart  sounds  become  faint  and  tend  to  disappear.  Bulging 
of  the  precordial  region,  so  characteristic  in  a  child  suffering  from  peri- 
cardial effusion,  is  less  marked  in  the  adult,  because  the  ribs  are  more 
resistant,  and  the  pericardium,  distended  by  the  effusion,  finds  room  at  the 
expense  of  the  diapliragm,  which  it  pushes  down,  and  at  the  expense  of  the 
posterior  mediastinum,  which  it  pushes  back. 

The  most  valuable  sign  of  pericardial  effusion  is  dullness.  This  dullness 
varies  according  to  the  quantity  of  fluid  effused.  Its  shape  and  limits 
furnish  valuable  information.  Pericardial  dullness  is  triangular  or  conical 
in  shape,  with  its  apex  reaching  as  high  as  the  third  rib,  where  the  peri- 
cardium is  reflected  on  to  the  great  vessels ;  its  base  blends  with  the  dia- 
phragm. In  large  effusions,  which  amount  to  about  a  pint,  the  vertical 
line  of  dullness,  which  extends  from  the  apex  of  the  cone  to  its  base,  measures 
6  or  7  inches,  and  the  fine  of  horizontal  dullness,  which  is  close  to  the  base 
of  the  cone,  has  nearly  the  same  length.  Percussion,  therefore,  rather  than 
the  other  signs,  shows  the  daily  progress  of  the  effusion. 

When  the  effusion  is  abundant,  it  gives  rise  to  more  or  less  marked 
symptoms,  which  include  dysphagia,  pallor  and  puffiness  of  the  face, 
dyspnoea,  which  is  sometimes  acute  and  accompanied  by  fainting  and 
angina,  cyanosis  and  oedema  of  the  peripheral  parts,  small  intermittent 
pulse,  and  pulsus  paradoxus.  Some  of  these  symptoms — namely,  the 
smallness  and  irregularity  of  the  pulse — may  be  due  to  compression  of  the 
auricles,  which  offer  less  resistance  to  the  effusion  than  the  ventricles.  The 
pulsus  paradoxus  is  found  in  cases  of  effusion  and  of  pericardial  adhesions, 
and  consists  of  three  or  four  pulsations,  followed  by  suppression  of  the 
radial  pulse  for  a  like  period,  with  no  interruption  of  the  heart-beats.  The 
disappearance  of  the  pulsations  coincides  with  the  end  of  inspiration. 
Dyspnoea,  angina,  attacks  of  suffocation,  and  threatening  asphyxia,  may 
be  due  to  the  pericardial  effusion  when  it  is  associated  with  endocarditis, 
pulmonary  congestion,  and  pleuritic  effusion  that  often  accompany  peri- 
carditis, especially  in  the  case  of  acute  rheumatism.  Several  of  these 
symptoms  may  also  be  present  in  the  paralytic  form  of  pericarditis,  which  is 
due  to  degeneration  of  the  heart  muscle.  In  such  cases  the  patient  may 
succumb  from  asystole. 


DISEASES  OF  THE  PERICARDIUM  389 

The  course  of  pericarditis  is  irregular  ;  its  duration  is  uncertain,  and  the 
fever  cycle  indefinite.  The  absorption  of  the  fluid  is  followed  by  the 
gradual  disappearance  of  symptoms,  and  the  rub  (frottement  de  retour) 
again  appears.  When  the  pericarditis  has  been  slight,  without  effusion, 
as  in  rheumatic  cases,  the  serous  membrane  returns  to  its  normal  condition, 
and  recovery  takes  place  in  one  or  two  weeks. 

Diagnosis — Prognosis. — Apart  from  the  exceptional  cases  in  which  the 
symptoms  are  acute,  pericarditis  is  a  disease  which  must  be  carefully 
looked  for,  because  it  develops  without  warning.  Repeated  auscultation 
is  necessary  in  patients  who  have  one  of  the  diseases  enumerated  under 
the  setiology  of  pericarditis,  especially  in  those  who  are  suffering  from 
articular  rheumatism,  and  it  will  then  be  possible  to  recognize  the  rub  at 
its  onset. 

The  diagnosis  must  be  made  in  each  form.  The  rub  can  be  distinguished 
from  cardiac  murmurs  by  the  signs  indicated  above.  The  diagnosis  from 
the  pleuritic  rub  is  very  simple,  because  the  patient  can  at  will  stop  breathing, 
and  at  the  same  time  suppress  the  rub  of  pleurisy. 

I  will  briefly  recapitulate  the  signs  by  which  pericardial  effusion  may  be 
diagnosed.  The  shape  and  situation  of  the  dullness  are  the  most  valuable 
points  ;  then  come  the  disappearance  of  the  cardiac  impulse,  the  faintness 
and  disappearance  of  the  heart  sounds,  and  the  pulsus  paradoxus.  Let 
us  not  forget  that  the  pericardial  rub  may  persist,  in  spite  of  a  large  effusion. 
Pericardial  effusion  and  encysted  effusion  in  the  left  pleura  present  some 
analogy,  but  the  situation  and  the  conical  shape  of  the  dullness  in  the 
precordial  region,  the  weakening  of  the  cardiac  impulse,  and  the  remote- 
ness of  the  heart  sounds,  are  in  favour  of  pericarditis.  Hypertrophy  of 
the  heart  and  pericardial  effusion  have  two  signs  in  common — i.e.,  the 
extent  of  the  dullness  and  the  weakening  of  the  heart  sounds.  In  hyper- 
trophy the  dullness  coincides  with  the  apex  of  the  heart,  while  it  descends 
lower  than  the  apex  in  pericardial  effusion  (Gubler). 

In  its  common  forms  acute  rlioumatic  pericarditis  is  not  a  serious  malady. 
The  gravity  of  the  prognosis  depends  on  the  abundance  of  the  effusion, 
and  on  certain  complications,  such  as  endocarditis,  pleurisy,  congestion  of 
the  lungs,  inflammation  of  the  myocardium,  and  ventricular  thrombosis, 
which  causes  sudden  death.  The  prognosis  also  depends  on  the  causes 
which  have  given  rise  to  pericarditis.  The  rheumatic  form,  for  example,  is 
not  nearly  so  grave  as  the  tubercular  one. 

Treatment. — If  the  inflammation  is  inteiLse,  and  especially  if  the  pain 
is  severe,  blood-letting  should  be  performed.  We  may  prescribe  leeches 
or  f'U])j)ing  to  the  precordial  region,  and  employ  blisters,  or  apply  ice-bags, 
which  are  left  in  situ.  When  the  heart  muscle  is  weak,  digitalis  or  caffeine 
is  administered,  and  the   pain  is  relieved  by  subcutaneous  injections  of 


390  TEXT-BOOK  OF  MEDICINE 

morphia.  If  the  efEusion  threatens  to  bring  on  asphyxia  or  syncope,  the  fluid 
should  be  withdrawn  without  delay. 

The  history  of  paracentesis  of  the  pericardium  and  the  operative 
technique  have  been  minutely  described  by  Trousseau  ;  but  this  opera- 
tion has  been  modified,  and  I  may  say  much  simpUfied,  since  I  have 
employed  the  aspirator.  I  omit,  therefore,  the  old  procedure,  and  mention 
the  conclusions  given  in  my  memoir  on  paracentesis  of  the  pericardium 
("  Traite  de  1' Aspiration  "). 

Experiments  performed  on  the  cadaver  give  the  following  conclusions  : 

1.  In  an  adult  the  pericardium  may  contain  an  amount  of  fluid,  which 
in  exceptional  cases  may  exceed  2  pints. 

2.  Whatever  be  the  degree  of  fullness,  the  pericardium  reaches  its  greatest 
transverse  diameter  at  the  level  of  the  fourth,  or  sometimes  of  the  fifth, 
intercostal  space. 

3.  At  tliis  level  the  pericardium  is  not  covered  by  the  left  lung.  The 
lung,  on  the  contrary,  forms  a  notch,  simulating  a  crescent,  which  extends 
from  the  fourth  to  the  sixth  rib,  and  persists  even  when  the  lung  is  in- 
sufflated. This  notch  coincides  with  the  maximum  point  of  the  transverse 
diameter  of  the  distended  pericardium,  and  consequently  leaves  a  space 
free  for  the  aspirating  needle. 

4.  The  pericardium,  distended  by  fluid,  extends  beyond  the  left  border 
of  the  sternum  for  as  much  as  4  or  5  inches. 

5.  I  therefore  recommend  paracentesis  in  the  fifth  left  intercostal  space, 
about  2  inches  from  the  left  border  of  the  sternum. 

For  this  purpose  a  No.  2  needle  is  employed.  The  aspirator  is  emptied 
of  air,  and  the  puncture  is  made  at  the  proper  spot.  When  the  needle  has 
gone  J  inch  into  the  tissue — i.e.,  as  soon  as  the  needle  is  no  longer  in  relation 
with  the  external  air — the  corresponding  tap  of  the  aspirator  is  opened, 
and  a  vacuum  results  in  the  needle,  which  becomes  an  aspirating  one. 
With  the  vacuum,  so  to  say,  in  hand,  we  then  proceed  to  search  for  the 
effusion.  The  needle  is  pushed  in  slowly  until  the  effusion  flows  through 
the  glass  index. 

For  the  dangerous  operation  proposed  by  Aran,  Jobert,  and  Trousseau, 
I  have  substituted  a  simple  needle-prick,  which  is  absolutely  harmless,  and 
demands  neither  special  skill  nor  exceptional  surgical  knowledge. 

Paracentesis  does  not  give  the  good  results  of  thoracentesis,  because  it 
has  been  chiefly  employed  in  secondary  pericarditis,  which  is  often  asso- 
ciated with  tuberculosis,  and  is  therefore  incurable.  In  some  cases, 
especially  when  the  fluid  is  purulent,  pericardotomy  is  indicated. 


DISEASES  OF  THE  PERICARDimi  391 

II.  CHRONIC  PERICARDITIS— ADHERENT  PERICARDIUM. 

Pathological  Anatomy. — Chronic  pericarditis  may  be  primary  or  conse- 
cutive to  acute  pericarditis.  The  aetiology  is  the  same  in  both  cases.  The 
false  membranes  and  the  adhesions  which  are  the  chief  lesions  in  clironic 
pericarditis  present  different  aspects.  The  false  membranes  arise  in  the 
serosa,  as  vascular  buds,  which  unite  to  form  adhesions  between  the  two 
layers  of  the  serous  membrane.  The  adhesions  may  be  partial  or  general. 
When  partial,  they  fix  the  apex  of  the  heart,  surround  its  base  like  a  ring, 
or  form  septa  and  cavities,  filled  with  fluid  and  degenerated  cells.  When 
general,  they  obliterate  the  cavity  and  lead  to  pericarditis  obliterans 
(Stokes)  or  ankylosis  of  the  heart  (Bouillaud).  If  the  inflammatory 
process  also  affects  the  external  layer  of  the  pericardium,  this  in  turn  forms 
adhesions  with  the  neighbouring  organs — viz.,  pleura,  lung,  diaphragm, 
and  chest-wall.  The  false  membranes  may  be  an  inch  in  thickness  ;  they 
are  haemorrhagic,  infiltrated  with  tubercles,  or  encrusted  with  calcareous 
salts.  The  ossiform  patches  in  the  pericardium  are  no  more  osseous  tissue 
than  the  cartilaginiform  patches  are  composed  of  cartilaginous  tissue,  for 
the  latter  do  not  possess  chondroblasts,  and  are  composed  of  lamellar  con- 
nective tissue  and  elastic  fibres  (Cornil  and  Ranvier). 

When  chronic  pericarditis  is  accompanied  by  effusion,  the  fluid,  which  is 
variable  in  quantity,  may  be  purulent  or  haemorrhagic,  and  contains  shreds 
of  membranes.  The  muscular  fibre  of  the  heart,  which  has  become  flabby 
and  yellowish,  is  more  or  less  affected  by  fatty  degeneration,  and  we  find, 
as  the  case  may  be,  enlargement  of  the  cavities,  hypertrophy  or  atrophy 
of  the  heart,  and  insufficiency  of  the  tricuspid  and  mitral  valves. 

Description. — When  chronic  pericarditis  ends  in  adhesions,  it  readily 
passes  unnoticed.  It  is  only  evident  if  friction  sounds  exist,  if  the  effused 
fluid  is  abundant,  or,  lastly,  if  the  adhesions  are  very  extensive. 

At  the  points  where  the  false  membranes  are  not  adherent  a  rasping  rub 
is  audible.  If  the  effusion  is  sufficiently  abundant,  it  shows  itself  by  the 
signs  described  under  acute  pericarditis. 

Adherent  pericardium,  if  uncomplicated,  may  give  no  symptoms ;  but 
if  it  is  accompanied  by  degeneration  of  the  myocardium  and  dilatation  of 
tiie  heart,  it  shows  itself  by  the  subjoined  signs  and  .symptoms. 

In  the  first  place  the  adhesions  cause  trouble  in  the  cardiac  circulation. 
In  the  normal  condition  the  intrapericardial  vacuum  favours  the  filling  of 
the  cavities  of  the  heart  during  dia.stole  ;  if,  however,  adliesions  form,  the 
expulsion  of  blood  is  hindered  during  the  systole,  and  the  cavities  do  not  fill 
during  diastole,  because  the  vacuum  is  suppressed.  Adherent  pericardium 
causes  the  following  symptoms  :  The  patient  is  a  prey  to  more  or  less  acute 
and  constant  dyspnoea,  which  increases  with  the  least  effort.     He  experi- 


392  TEXT-BOOK  OF  MEDICINE 

ences  precordial  pain,  which  may  disappear  during  rest,  but  at  times  returns 
with  the  least  exertion  or  fatigue.  On  pressure  we  find  tenderness  of  the 
phrenic  nerve  in  the  neck  and  in  the  region  of  the  diaphragm. 

On  examination  of  the  thorax,  bulging  of  the  precordial  region  is  often 
seen.  Percussion  may  show  considerable  increase  in  the  size  of  the  heart. 
On  palpation  the  systohc  shock  is  much  less  marked  than  in  the  normal 
condition. 

General  adhesions  produce  signs  which  are  most  marked  when  the 
adhesions  involve  the  chest-wall :  these  signs  are — retraction  of  the  inter- 
costal spaces  during  systole  (Wilhams),  systohc  retraction  of  the  epigastric 
angle,  and  reduphcation  of  the  heart  sounds. 

The  muscle  often  degenerates,  becoming  less  resistant,  and,  with  the 
assistance  of  the  false  membranes,  dilatation  of  the  ventricles  and  con- 
secutive insufficiency  of  the  valves  result.*  Congestion  and  oedema,  asphyxia, 
asystole,  and  sudden  death  may  follow. 


Ill .  H YDROPERIC ARDIUM— H YDROPNEUMOPERICARDIUM. 

Hydropericardium  is  dropsy  of  the  pericardium.  It  is  not  the  result 
of  an  inflammatory  process  like  pericarditis,  but  occurs  in  the  course  of  other 
diseases.  Hydropericardium  is  due  either  to  mechanical  causes  which 
embarrass  the  circulation  in  the  cardiac  vessels,  or  to  dyscrasiae  and  cachectic 
states  which  modify  the  composition  of  the  blood.  The  signs  of  hydro- 
pericardium and  most  of  its  symptoms,  except  fever,  are  those  of  peri- 
carditis with  effusion.  Hydropneumopericardium  denotes  the  simul- 
taneous presence  of  gas  and  fluid  in  the  pericardium.  Here,  as  in  pleurisy, 
it  has  been  asked  if  purulent  fluid  may,  by  decomposition  of  its  elements^ 
produce  gas.  This  view  is  no  longer  admitted.  The  common  causes  of  hydro- 
pneumopericardium are  injury,  communication  between  the  pericardium 
and  an  abscess  of  the  Hver  (Graves),  the  oesophagus  (Chambers),  or  a  cavity 
in  the  lung  (Dowel).  The  presence  of  gas  in  the  pericardium  shows  itself 
by  a  tympanitic  sound  in  the  precordial  region.  On  auscultation  the  heart 
sounds  assume  a  metallic  tone,  and  if  the  fluid  is  in  sufficiently  large 
amount,  the  heart,  striking  the  fluid  and  gas,  produces  a  kind  of  gurghng, 
analogous  to  the  noise  of  a  windmill  wheel  (Laennec). 

*  These  secondary  lesions  affect  not  only  the  right  ventricle  and  tricuspid  valve, 
but  also  the  left  ventricle  and  mitral  valve  ( Jaccoud). 


CHAPTER  II 
DISEASES  OF  THE  ENDOCARDIUM 

I.  ACUTE  ENDOCARDITIS. 

Endocarditis  is  inflammation  of  the  endocardium. 

Discussion. — It  is  customary  to  divide  acute  endocarditis  into  two 
groups  :  on  the  one  hand  simple,  more  or  less  benign  endocarditis,  and  on 
the  other  infective  endocarditis,  which  corresponds  to  the  old  name  malig- 
nant. This  division,  though  convenient  for  a  theoretical  description,  is 
one  which  I  consider  artificial,  as  it  is  known  to-day  that  every  case  of  acute 
endocarditis  is  more  or  less  of  an  infective  nature,  and  dependent  upon 
the  presence  of  micro-organisms.  Further,  upon  what  are  we  to  base 
our  division  of  acute  endocarditis  ?  Not  on  the  nature  of  the  lesions,  for 
infective  endocarditis,  which  so  often  causes  vegetations  and  ulcerations, 
has  not  alone  the  privilege  of  causing  these  lesions.  We  find  cases  of  simple 
endocarditis,  which  are  so  benign  that  they  do  not  enter  into  the  category 
of  "  infective,"  but  yet  they  may  be  accompanied  by  vegetations  which  lead 
to  embolism  and  to  ulcerations  of  the  valves  or  the  chordae  tendinese. 

Can  the  aetiology  of  endocarditis  and  the  bacteriological  knowledge 
acquired  during  the  past  few  years  serve  as  a  basis  of  classification  ?  For 
example,  can  rheumatic  endocarditis  be  considered  as  being  characterized 
by  its  relatively  benign  course,  by  lesions  that  are  limited  to  the  heart,  and 
by  the  absence  of  embolic  complications  ?  And  can  endocarditis  in  the  puer- 
peral state,  in  certain  cases  of  pneumonia,  of  scarlet  fever,  etc.,  be  infective 
and  accompanied  by  cardiac  and  extracardiac  lesions,  by  mechanical  and 
septic  emboli,  and  characterised  by  general  characters  and  symptoms  that  are 
too  often  exceedingly  grave  ?  Not  so  ;  aetiology,  althougli  having  a  relative 
part  in  the  anatomical  and  clinical  evolution  of  endocarditis,  cannot  be  the 
starting-poiiit  of  a  division,  for  exceptions  would  be  met  with  every  moment. 
Endocarditis  in  the  course  of  scarlatina,  of  smallpox,  or  of  erysipelas,  which 
are  eminently  infectious  diseases,  is  often  benign  and  almost  latent,  while 
endocarditis  in  the  course  of  trut^  rhoumatisni  may  exceptionally  assume 
a  typhoid  and  iiuiiigiiant  form. 

The  nature  of  endocarditis,  the  variety  of  its  lesions,  the  diversify  of  its 

393 


394  TEXT-BOOK  OF  MEDICINE 

micro-organisms,  the  benign  or  grave  nature  of  its  course,  depend,  as  always, 
on  the  co-operation  of  certain  causes  which  mutually  support  or  oppose  one 
another.  We  must  especially  remember  the  specific  origin  of  the  disease, 
the  quantity  and  quality  of  the  pathogenic  agent,  the  previous  condition  of 
the  endocardium,  and  the  state  of  receptivity  and  of  resistance  of  the 
individual.  I  shall,  in  order  to  faciUtate  description,  adopt  the  artificial 
division  of  endocarditis  into  two  groups,  first  stating  the  fact  that  they 
are  related  cHnically  by  numerous  intermediary  forms.  In  the  first  group 
I  shall  describe  simple  acute  endocarditis,  and  shall  choose  for  my  type 
the  most  common  of  all— rheumatic  endocarditis  ;  in  the  second  group  I 
shall  have  to  discuss  the  chief  forms  of  infective  endocarditis — viz.,  pneu- 
monic, pyaemic,  puerperal,  etc. 

In  the  course  of  this  description  we  shall  find  that  certain  cases  of  endo- 
carditis do  not  merit  the  name  "  infective,"  for  they  show  no  symptoms  of 
infection.  On  the  other  hand,  they  do  not  merit  the  name  of  "  simple," 
for,  in  spite  of  the  benign  nature  of  their  symptoms,  they  are  sometimes 
accompanied  by  the  formation  of  large  emboli,  which  block  the  arteries 
of  the  limbs  or  of  the  brain.  I  call  these  cases  emboligenous,  this  term  being 
applied  to  emboU  of  a  certain  size,  and  not  including,  of  course,  capillary 
emboK  and  the  formation  of  haemoptoic  or  of  septic  infarcts,  lesions 
described  under  infective  endocarditis.  We  may,  therefore,  see  simple 
emboligenous,  and  infective  or  mahgnant,  endocarditis. 

Simple  Acute  Endocarditis. 

/Etiology. — Many  infectious  diseases — blennorrhagia,  scarlatina,  diph- 
theria, variola,  the  setiologic  importance  of  which  has  been  too  much  ex- 
aggerated (Quinquaud),  erythema  nodosum  (Trousseau),  chorea  (See),  facial 
erysipelas  (Jaccoud),  pneumonia,  and  malaria — may  cause  endocarditis, 
which  is  often  microbic,  and  from  its  characters  and  symptoms  would  in 
many  cases  deserve  the  name  of  simple  endocarditis  ;  often,  indeed,  so 
simple  that  it  would  pass  unnoticed  without  minute  examination  of  the 
heart,  and,  in  fact,  several  of  these  cases  recover  without  leaving  any 
sequelae. 

Such  cases  will  not  serve  as  the  type  in  the  present  description.  I 
would  rather  choose  rheumatic  endocarditis,  which  is  the  most  common  of 
all,  but  conforms  to  the  type  of  simple  acute  or  subacute  non-infective 
endocarditis. 

Acute,  subacute,  or  chronic  articular  rheumatism  may  provoke  endo- 
carditis (Bouillaud),  but  it  is  chiefly  in  the  course  of  acute  articular  rheu- 
matism that  endocarditis  develops.  I  refer  the  reader  to  the  article  on 
rheumatism,  where  this  question  is  treated  in  detail.  Endocarditis  usually 
appears  in  the  second  week  of  the  rheumatic  attack,  but  in  some  exceptional 


DISEASES  OF  THE  ENDOCARDIUM  395 

cases  it  precedes  the  articular  manifestations.  Rheumatic  endocarditis 
especially  affects  adults  and  children. 

Pathological  Anatomy. — The  inflammation  nearly  always  chooses  the 
endocardium  of  the  left  heart,  affects  the  mitral  more  often  than  the  aortic 
valves,  the  central  face  of  these  valves  more  often  than  the  parietal  one, 
and  their  free  edge  rather  than  other  parts.  This  locahzation  depends  on 
several  causes  :  (1)  the  mechanical  effects  of  pressure  and  friction  exercised 
at  these  points  by  the  blood-current ;  (2)  the  lessened  resistance  of  the  affected 
parts  of  the  valves,  which  are,  at  the  same  time,  more  worn  out  and  not  so 
well  organized  (Peter). 

In  order  to  understand  the  changes  in  endocarditis  (acute  or  chronic), 
we  must  remember  the  structure  of  the  endocardium,  which  much  resembles 
that  of  the  endarterium.  The  endocardium  is  composed  of  an  endothelium 
made  up  of  a  single  layer  of  flat  cells  ;  a  second  layer,  formed  by  flattened 
cells  that  are  superposed  and  separated  by  lamellar  substance  ;  and  a  tliird 
layer  of  elastic  tissue  and  of  bundles  of  connective  tissue  (Cornil). 

The  first  layer  is  not  found  post  mortem ;  the  second  layer  is  very 
thin  at  the  level  of  the  valves  ;  the  third  layer  (fibro-elastic  tissue),  at  the 
free  edge  of  the  auriculo-ventricular  valves,  gives  origin  to  the  tendons  of 
the  papillary  muscles.  The  auriculo-ventricular  valves  may  be  consi- 
dered as  a  fold  of  endocardium,  the  two  lips  of  which  are  united  by  fibrous 
connective  tissue,  insuring  resistance  (Ranvier).  The  arterial  valves 
result  from  the  folding  back  of  the  internal  membrane  of  the  arteries  on 
the  ventricular  endocardium. 

When  endocarditis  is  slight  and  transient,  it  is  rather  exudative  than 
proliferative.  The  type  of  prohferative  endocarditis  is  the  rheumatic  form, 
which  we  are  now  considering.  The  inflammation  chiefly  attacks  the  mitral 
valve,  the  edges  of  which  are  swollen,  thickened,  and  much  vascularized, 
while  in  the  normal  state  the  capillary  vessels  are  few  in  number.  These 
vessels  are  affected  by  endarteritis,  and  their  lumen  is  almost  obli- 
terated. 

The  changes  develop  in  the  layer  of  flattened  cells.  Micro-organisms 
often  cause  the  embryonic  elements  to  proliferate  and  form  granulations, 
which  are  so  small  and  so  numerous  that  they  give  to  the  endocardium  a 
rough  appearance.  These  granulations,  which  were  at  first  taken  for 
collections  of  fibrin,  are  really  composed  of  embryonic  tissue,  covered  by  a 
thin  layer  of  fibrin.  They  are  friable,  soft,  and  transparent  in  the  acute 
stage,  and  some  show  at  their  centre  vessels  in  process  of  formation.  The 
granulations  may  invade  fairly  large  surfaces  of  the  parietal,  ventricular, 
or  auricular  endocardium,  but  are  usually  found  at  a  small  distance  from 
the  free  edge  of  the  valves,  where  they  form  a  wavy,  maiuTnillatod  line. 

The  granulations,  which  sometimes  reach  the  size  of  a  pin's  lioad  or  of 


396  TEXT-BOOK  OF  MEDICINE 

a  pea,  may  be  villous,  filamentous,  nummular,  warty,  or  raspberry-like, 
and  surround  the  valves  like  a  garland.  They  may  give  rise  to  emboli, 
which  are  carried  in  every  direction.  These  complications,  however,  will 
be  discussed  later  under  Embohgenous  and  Ulcerative  Endocarditis. 

Description. — The  phenomena  of  invasion  in  acute  endocarditis  are, 
so  to  say,  non-existent.  Rigors,  dyspnoea,  and  palpitation  are  not  seen, 
or  at  least  are  so  slight  that  endocarditis  passes  unnoticed  in  a  case  of 
articular  rheumatism,  unless  the  heart  is  examined  daily. 

In  valvular  endocarditis  we  find  blowing  murmurs,  which  are  related 
to  the  seat  of  the  lesions  and  will  be  described  under  Valvular  Lesions.  All 
the  orifices  of  the  heart  may  be  affected,  but  for  the  moment  it  is  enough  to 
say  that  the  mitral  orifice  is  most  generally  attacked,  and  the  aortic  orifice 
is  next  in  frequency.  The  murmur  that  characterizes  mitral  endocarditis 
is  heard  at  the  apex  of  the  heart — that  is  to  say,  below  and  outside  the  nipple  ; 
this  soft  murmur  is  nearly  always  systohc,  mitral  insufficiency  being  the  rule 
and  stenosis  the  exception,  during  the  acute  stage  of  endocarditis  (Bouillaud). 
The  duration  is  rarely  more  than  two  or  three  weeks.  After  this  time  the 
trouble  resolves  and  the  murmur  disappears,  but  the  mischief  may  become 
chronic,  when  the  murmur  also  persists. 

Endocarditis  which  is  consecutive  to  such  infectious  diseases  as  ery- 
sipelas, mumps,  erythema  nodosum,  etc.,  may  recover  without  leaving  any 
trace.  Recovery,  however,  is  not  to  be  reUed  on.  A  patient  who  has 
suffered  from  rheumatism  or  scarlatina,  and  been  considered  as  cured  because 
the  murmur  has  disappeared,  may  yet  suffer  from  chronic  endocarditis, 
which  is  latent  in  its  evolution.  The  morbid  process  is  not  extinct,  but 
proceeds  slowly  and  insidiously  to  alter  the  tissues  wliich  it  has  attacked, 
and  often  creates  irremediable  lesions,  that  may  only  appear  after  years. 
Simple  acute  endocarditis,  however,  presents  no  immediate  danger,  and  its 
gravity  results  from  the  chronic  valvular  lesions  wliich  so  often  follow. 

Local  blood-letting,  leeches,  cupping,  blisters  to  the  precordial  region, 
and  the  preparations  of  digitahs  form  the  basis  of  treatment.  We  must 
never  lose  sight  of  the  frequent  change  from  the  acute  to  the  chronic  state. 
Bhsters  and  applications  of  the  cautery  must  therefore  be  continued  for  a 
lengthy  period  when  the  disease  has  left  some  traces. 


Ulcerative,  Infective,  or  Malignant  Endocarditis — Emboligenous 

Endocarditis. 

Pathogenesis. — The  acute  endocarditis  just  described  presents  no  imme- 
diate gravity  ;  it  is  only  formidable  in  the  future,  because  of  the  chronic 
valvular  lesions  which  too  often  follow.  We  find,  however,  another  form 
of  acute  endocarditis,  called  typhoid,  ulcerative,  infective,  or  malignant, 


DISEASES  OF  THE  ENDOCARDIUM  397 

wliicli  at  its  onset  or  in  its  course  may  show  a  typhoid  or  septic  character, 
and  ends  fairly  frequently  in  death. 

We  know  to-day  that  there  is,  not  one,  but  several  varieties  of  infective 
endocarditis. 

Discussion  of  their  pathogenesis  is  singularly  simpUfied  since  the  dis- 
covery of  bacteria  ;  their  aetiology  is  no  longer  given  up  to  simple  hypothesis, 
as  was  formerly  the  case,  and  we  can  Avith  some  method  group  the  lesions 
and  the  symptoms  that  are  peculiar  to  each  variety.  The  nature  and 
the  degree  of  virulence  of  the  micro-organisms,  the  previous  condition  of 
the  endocardium,  the  conditions  of  resistance  or  receptivity  of  the 
individual,  are  all  factors  which  have  to  be  taken  into  account. 

This  question  may,  I  tliink,  be  stated  as  follows  :  The  endocardium, 
whether  healthy  or  previously  injured  so  that  it  is  in  a  State  of  receptivity, 
offers  a  favourable  site  for  the  arrest  and  development  of  certain  pathogenic 
agents. 

These  agents  may  have  the  most  varied  origins.  Some  enter  the  economy 
by  the  skin  (abrasions,  excoriated  corns,  boils,  burns,  wounds,  erysipelas, 
injuries) ;  others  are  introduced  through  the  mucosa  of  the  uterus  (abortion 
and  accouchement),  through  the  genito- urinary  mucosa  (lesions  of  the  urethra 
and  bladder),  and  through  the  digestive  mucous  membranes  (stomatitis,  ton- 
silUtis,  ulcerations  of  the  stomach,  the  intestines  and  the  bile-ducts) ;  others, 
again,  penetrate  through  the  serous  membranes  (lesions  of  the  peritoneum, 
pleura,  and  synovial  membranes)  ;  some  are  introduced  through  the 
respiratory  channels  (broncho-pneumonia,  ulcerative  lesions  of  the  lung, 
gangrene,  and  bronchiectasis)  ;  others  may  enter  through  bone  lesions 
(osteomyelitis)  ;  finally,  in  some  cases  the  entrance  gateway  cannot  be 
found,  in  which  event  we  invoke  auto-infection,  calling  the  endocarditis 
primary. 

Many  microbes  may  cause  infective  endocarditis.  I  shall  first  cite  the 
pyogenic  microbes,  streptococci  and  staphylococci ;  then  the  pneumococcus, 
the  bacillus  of  typhoid  fever  and  of  tuberculosis,  the  gonococcus,  and  other 
microbes  not  classified,  or  not  yet  found  in  other  diseases  (Weichselbaum, 
Gilbert  and  Lion). 

These  microbes  are  chiefly  aerobic,  a  fact  which  doubtless  explains 
their  preference  for  the  left  heart  and  for  oxygenated  blood.  Endocarditis 
of  the  right  heart  is  more  rare.  Cases  have,  however,  been  published. 
These  microbes,  after  entering  the  economy  by  one  of  the  gateways  above 
enumerated,  arc  carried  by  the  blood  to  the  heart,  and  invade  the  endo- 
cardium, either  superficially,  through  the  crevices  in  the  connective  tissue, 
or  deeply,  by  way  of  tiic  small  vessels.  This  invasion  may  be  helped  by 
previous  changes  in  the  serous  membrane.  After  implantation  on  their 
culture  medium,  the  pathogenic  agents,  either  alone  or  in  combination. 


398  TEXT-BOOK  OF  MEDICINE 

crown  their  work  of  destruction,  and  the  pathological  process  may  assume 
several  forms.  In  the  first  variety  the  lesion  leads  to  the  formation  of 
vegetations  which  are  more  or  less  bulky  and  friable.  These  vegetations 
become  detached  from  the  endocardium,  and  are  launched  into  the  vessels 
in  the  form  of  emboh.  If  the  embolus  is  of  large  size,  it  obliterates  a  fairly 
large  artery,  and  causes  secondary  complications,  which  depend  on  the 
obhterated  vessel  (hemiplegia,  aphasia,  and  gangrene).  If  the  embolus  is 
of  smaller  size,  it  causes  infarcts  in  the  kidney,  spleen,  intestine,  or  lung, 
and  the  symptoms  depend  on  the  organ  invaded.  In  this  first  category  of 
complications  the  embolus  causes  simple  obstruction  of  the  vessels.  The 
embolism  is  called  mechanical  and  may  be  formidable,  but  is  not  septic. 
In  short,  the  cases  of  endocarditis  which  form  this  first  variety  are  embo- 
ligenous,  but  do  not  deserve  the  name  of  infective,  because  they  do  not  give 
rise  to  septic  or  infective  emboli. 

In  the  second  variety  the  morbid  process  goes  on  to  necrosis  and 
ulceration,  and  in  most  cases  vegetations  and  ulcerations  are  present  to- 
gether. These  ulcerations  may  perforate  the  valves,  tear  away  the  pillars, 
and  detach  shreds  of  the  chordae,  giving  rise  to  mechanical  embolism. 
Here  also  the  endocarditis  may  not  be  infective,  but  rather  ulcerative,  with 
vegetations.  It  is  emboligenous  and  most  grave,  but  the  process  may  not 
be  infective. 

Lastly,  in  the  third  variety  I  place  the  true  cases  of  infective  endo- 
carditis. Ulcerations  and  vegetations  are  as  a  rule  present,  but  the  impor- 
tant feature  is  that  their  products  are  septic  and  infective  :  they  pour 
septic  capillary  emboh  into  the  blood-stream,  and  their  symptoms  recall  the 
picture  of  typhoid  or  purulent  infection. 

From  this  rapid  enumeration  we  see  that  we  should  be  wrong  in  including 
all  cases  of  severe  or  of  fatal  endocarditis  under  the  term  "  infective." 
There  is  a  place  for  intermediate  cases,  according  as  the  morbid  process  is 
accompanied  by  infecting  pathogenic  agents  or  not. 

Pathological  Anatomy. — At  the  onset  of  malignant  endocarditis  (I  in- 
tentionally preservet  his  epithet  "  malignant,"  as  it  applies  to  every  endo- 
carditis which  is  not  of  the  simple  type)  under  the  influence  of  micro-organisms, 
we  find  in  the  valvular  tissue  infiltration  of  wandering  cells,  hypertrophy 
and  multiplication  of  cells,  and  desquamation  of  the  endothehal  layer, 
which  is  replaced  by  fibrin.  In  the  meshes  of  the  fibrinous  reticulum  colonies 
of  bacteria  are  found,  which  "  penetrate  by  more  or  less  large  chinks 
into  the  interior  of  the  valves." 

In  cases  of  malignant  endocarditis,  the  inflammation  nearly  always  gives 
rise  to  large  vegetations  and  deep  ulcerations.  In  such  a  case  we  find 
on  the  sigmoid  or  on  the  mitral  valves,  on  the  chordae  tendinese,  on  the 
papillary  muscles,  and  on  the  median  septum,  a  vegetation  of  the  size  of  a 


DISEASES  OF  THE  ENDOCARDIUM  399 

pea  or  of  a  strawberry,  or  a  collection  of  smaller  vegetations,  of  which  some 
are  flattened,  papilUform,  or  raspberry-hke,  while  others  are  pedunculated 
and  ready  to  break  of?. 

These  vegetations,  wliich  are  formed  largely  of  embryonic  tissue  and  are 
covered  by  a,  mass  of  fibrin,  are  very  rich  in  microbes,  which  are  found 
either  on  the  surface  in  the  fibrinous  layers  or  in  the  deep  parts  of  the 
vegetations.  It  is  probable,  therefore,  that  the  bacteria  deposited  on  the 
valves  by  the  blood-stream  develop  in  the  superficial  fibrinous  layers,  and 
then  penetrate  tlirough  the  crevices  of  the  connective  tissues  as  far  as  the 
surface  and  the  central  parts  of  the  valves.  It  is  also  possible  that  bacteria 
are  primarily  introduced  by  the  vessels  in  the  valves. 

In  some  cases  the  vegetations  soften  into  a  kind  of  atheromatous  pulp, 
composed  of  granulations,  cellular  debris,  fatty  elements,  and  various  septic 
micro-organisms.  These  different  elements,  when  launched  into  the  blood- 
stream, cause  a  source  of  emboh,  which  are  sometimes  mechanical,  at 
other  times  septic,  and  affect  the  brain,  hmbs,  spleen,  hver,  intestines,  kidneys, 
etc.  The  organs  affected  show  hsemoptoic  and  suppurative  infarcts,  with 
miliary  abscesses,  abscesses  of  the  sldn  and  the  joints,  suppuration  of  the 
cranial  and  spinal  meninges ;  diarrhoea,  albuminuria,  and  enlargemeut  of 
the  spleei*  are  found,  and  the  patient  often  succumbs  to  gangrenous, 
typhoid,  toxic,  or  infectious  comphcations,  etc. 

The  spleen  is  usually  bulky,  as  happens,  moreover,  in  many  infectious 
diseases. 

During  hfe  the  blood  contains  micro-organisms  which  can  be  cultivated. 

Let  us  now  pass  on  to  the  ulcerations  of  mahgnant  endocarditis.  They 
commence  as  small  superficial  yellowish  patches  ;  Httle  by  httle  they  become 
deeper  and  more  extensive,  and  may  perforate  the  valves,  causing  valvular 
aneurysms  (Foerster,  Pelvet).  The  aneurysms  of  the  sigmoid  valves  are 
formed  at  the  expense  of  the  superior  face  of  the  valves,  those  of  the  mitral 
valves  at  the  expense  of  the  inferior  face.  This  localization  is  regulated  by 
the  direction  of  the  blood-current,  the  enlargement  taking  place  on  the  side 
of  the  greater  blood-pressure. 

These  ulcerations  also  cause  perforation  of  the  intraventricular  septum 
and  rupture  of  a  pillar,  or  of  the  chordjE  tendineaB.  This  condition  forms  a 
new  source  of  emboli.  In  many  cases,  let  me  repeat,  mahgnant  endocarditis 
is  at  first  vegetative  and  ulcerative.  If  we  analyze  the  cases  and  consult 
the  results  of  autopsies,  we  shall  find  a  double  process  of  exuberant  prohfera- 
tion  and  deep  ulceration.  These  different  processes  explain  the  method  of 
formation  of  (Mnboli  and  their  multiple  varieties. 

Experimental  pathology  has  succeeded  in  producing  infective  endo- 
carditis. Ribbert,  in  1885,  by  injecting  |  gramme  of  culture  of  Stdpluj- 
lococcus  aureus  into  the  ear  of  a  rabbit  caused  embolic  foci  of  carditis  and  of 


400  TEXT-BOOK  OF  MEDICINE 

valvular  endocarditis,  with  consecutive  lesions  of  acute  endocarditis.  Wys- 
sokowitsch  varied  the  experiments.  By  means  of  a  silver  sound  passed 
into  the  right  carotid  he  first  injured  the  cardiac  valves,  and  then  introduced 
micro-organisms  of  different  kinds  {Staphylococcus  pyogenes.  Streptococcus 
septicus,  etc.),  producing  not  only  parasitic  foci  of  endocarditis,  but  he  also 
found  in  the  different  organs  emboU  with  infarcts  and  abscesses  which 
contained  the  same  microbes  as  in  the  endocardium. 

Description. — In  infective  endocarditis  the  general  symptoms  are,  as  a 
rule,  much  more  important  than  the  local  signs.  On  auscultation,  one  or 
several  murmurs  may  be  recognized,  depending  on  the  severity  of  the  lesion 
and  on  the  orifice  affected.  In  some  cases  the  murmur  is  soft  or  masked  by 
pericarditis,  in  other  cases  it  acquires  a  musical  tone  called  whining  (Bouil- 
laud).  This  whining  murmur,  which  is  also  met  with  in  chronic  valvular 
lesions,  has  a  peculiar  interest  in  ulcerative  endocarditis.  It  may  be  due 
to  the  vibration  of  a  body  (pillar,  cord,  or  vegetation)  floating  in  front  of  an 
orifice,  and  has  often  given  warning  of  the  onset  of  embolism  (Gubler, 
Potain). 

Embohsm,  whatever  its  origin,  may  act  in  a  mechanical  way,  obliterate 
a  cerebral  artery,  such  as  the  Sylvian  artery,  or  its  branches,  and  give  rise 
to  apoplexy,  hemiplegia,  aphasia,  or  softening  of  the  cerebral  tissues.  The 
embolism  may  obliterate  the  artery  of  a  limb  and  produce  consecutive 
gangrene.  These  compUcations  are  very  serious,  but,  I  repeat,  they  are 
not  infective,  and  the  endocarditis  which  has  given  rise  to  them  is  purely 
emboligenous,  causing  compUcations  of  a  mechanical  and  not  of  an  in- 
fective nature. 

In  other  cases,  on  the  contrary,  the  endocarditis  is  essentially  infective, 
the  general  symptoms  dominate  the  scene,  and  we  see  from  the  first  that 
the  patient  is  sufEering  from  an  infective  disease  of  a  typhoid  or  pysemie 
type. 

When  ulcerative  endocarditis  assumes  the  typhoid  form,  dryness  of  the 
tongue,  prostration,  rapid  elevation  of  temperature,  shivering  fits,  which 
appear  during  the  first  days  of  the  attack,  are  symptoms  that  give  the 
patient  a  "typhoid  look";  add  to  this,  broncho-pulmonary  congestion,  stupor, 
ballooning  of  the  belly,  enlargement  of  the  spleen,  albumin  aria,  and  diar- 
rhoea, and  we  see  the  difficulty  of  diagnosis  between  this  typhoid  state  and 
typhoid  fever.  However,  the  diagnosis  of  endocarditis  is  aided  by  the 
murmurs  audible  at  the  orifices  of  the  heart,  by  the  absence  of  lenticular 
rose  spots,  by  the  course  of  the  symptoms,  by  examination  and  culture  of 
microbes  in  the  blood,  and  by  negative  sero -diagnosis.  This  endocarditis 
appears  to  depend  on  the  presence  of  encapsuled  lanceolated  microbes 
(Jaccoud). 

The  pyaemic  form  of  ulcerative  endocarditis  closely  resembles  purulent 


DISEASES  OF  THE  ENDOCARDIUM  401 

infection.  We  find  repeated  chills  and  liigh  temperature,  and,  indeed,  the 
case  is  really  one  of  infection,  because  the  endocarditis  throws  septic  emboK 
and  specijBc  bacteria  into  the  blood-stream.  These  capillary  emboli  form 
ecchymotic  spots  on  the  surface  of  the  skin  and  the  serous  membranes, 
suppurative  infarcts,  mihary  abscesses,  and  superficial  or  deep  foci  of  gan- 
grene, and  provoke  suppurative  subarachnoid  meningitis.  The  patient 
has  a  subicteric  tint ;  abscesses  develop  under  the  skin,  and  death  follows 
in  dehrium.  This  pysemic  form  is  chiefly  met  with  when  the  micrococci  of 
suppuration  are  present  in  the  blood  (Jaccoud). 

When  the  valves  of  the  right  heart  are  affected,  the  lungs  present  ecchy- 
motic spots,  haemoptoic,  gangrenous,  or  suppurating  infarcts  and  abscesses, 
varying  in  size  from  a  pea  to  a  nut.  The  diagnosis  is  based  on  auscultation 
of  the  heart,  and  on  the  finding  of  foci  of  suppuration  or  of  phlebitis. 

For  description  I  have  chosen  different  types  of  infective  endocarditis, 
but  I  would  hasten  to  say  that  these  types  are  not  always  so  clearly  marked 
clinically,  and  the  different  varieties  just  described  are  often  combined. 

The  course  and  duration  of  the  disease  vary  in  each  case.  Marked 
elevation  of  temperature  is  not  always  seen.  The  disease,  instead  of  being 
continuous,  may  show  successive  attacks,  with  complete  remissions  of 
fairly  long  duration.  The  prognosis  is  not  absolutely  bad,  and  recovery  has 
occurred  in  a  fairly  large  number  of  cases  (Jaccoud).  The  typhoid  form 
may  last  several  weeks,  but  the  pysemic  form  is  more  serious  and  rapid. 

Varieties. — I  shall  now  enumerate  the  chief  varieties  : 

1.  Rheumatic  Endocarditis.  —  Rheumatism  causes  simple,  euiboii- 
genous,  or  infective  endocarditis.  The  simple  form  is  much  the  most 
common,  and  has  served  as  our  descriptive  type  of  acute  endocarditis. 
Rheumatism,  however,  may  give  rise  to  embohgenous  endocarditis,  with 
large  emboU  in  the  cerebral  arteries  and  in  the  vessels  of  the  hmbs  (Jaccoud). 
It  may  also  caase  infective  endocarditis  of  the  typhoid  form.  Infective 
endocarditis  rarely  arises  during  a  first  attack  of  rheumatism ;  it  usually 
shows  itself  in  the  individual  whose  endocardium  is  already  the  seat  of 
chronic  endocarditis.  This,  says  Jaccoud,  is  the  most  usual  cause  of 
infective  rheumatic  endocarditis.  The  pathogenic  agent  of  rheumatism  is 
still  unknown,  but  in  some  cases  the  lesions  in  malignant  rheumatic  endo- 
carditis are  due  to  the  association  of  microbes. 

2.  Pneumonic  Endocarditis. — Pneumococcal  endocarditis  may  be  para- 
pneuuKjiiic  or  metapueumonic  ;  it  may  precede  pneumonia  (prepncumonic) 
or  be  quite  independent.  Tliis  variety  has  a  tendency  to  form  vegetations 
rather  than  ulcers,  and  sometimes  causes  small  abscesses  in  the  endocardium. 
It  affects  the  aortic  more  often  than  the  mitral  orifice,  but  has  also  been 
found  in  the  light  heart,  affecting  the  tricuspid  and  pulmonary  valves, 
rneumonic  endocarditis  is  rarely  emboligenous,   because  the  vegetations 

26 


402  TEXT-BOOK  OF  MEDICINE 

are  implanted  upon  a  large  base.  It  rarely  gives  rise  to  capillary  emboli, 
but  is  sometimes  infective  and  suppurative ;  meningitis  is  fairly  often  asso- 
ciated with  it. 

Pneumonic  endocarditis  may  develop  in  patients  who  have  had  no 
previous  cardiac  defect.  Old  lesions  of  the  valves  are,  however,  singularly 
favourable  to  its  development.  The  pneumococcus  is  not  always  the  sole 
cause  ;  other  microbes — streptococci  and  certain  unclassified  bacilh — are 
sometimes  associated  with  it. 

This  endocarditis  usually  passes  unnoticed  if  we  do  not  examine  the  heart 
in  patients  suffering  from  pneumonia.  It  fairly  often  assumes  the  simple 
form,  and  may  recover  without  leaving  any  traces.  Pneumonic  endo- 
carditis has  been  produced  experimentally  in  the  rabbit  (Netter),  after  the 
valves  have  previously  been  injured. 

3.  Endocarditis  in  Pregnancy  and  the  Puerperal  State.— In  infective 
endocarditis  associated  with  pregnancy  it  is  necessary  to  distinguish 
endocarditis  gravidarum,  which  supervenes  during  pregnancy,  from  endo- 
carditis which  follows  post-puerperal  trauma  of  the  uterus.  The  latter  is 
only  a  variety  of  septicgemia,  and  is  much  more  serious  than  the  former. 
Non-puerperal  trauma  of  the  uterus  may  j)roduce  the  same  result. 

Endocarditis  gravidarum  is  less  frequent  than  the  puerperal  form.  Its 
origin  is  more  difficult  to  study,  for  it  does  not  appear  to  depend  on  an  infec- 
tion of  uterine  origin.  This  variety  cannot,  however,  be  looked  upon  as  a 
simple  one  supervening  in  the  coujse  of  pregnancy.  The  gravid  state 
makes  the  prognosis  of  the  disease  worse,  and  the  foetus  itself  suffers  from 
the  maternal  infection.  The  researches  of  Nattan-Larri-er  have  shown  that 
maternal  endocarditis  causes  important  histological  changes  in  the  organs 
of  the  foetus.  The  toxines  in  the  blood  of  the  mother  pass  through  the 
placenta,  and  determine  reaction  of  the  blood-forming  organs  ;  while  the 
liver  and  kidneys  show  lesions  of  degeneration  which  vary  directly  with 
the  severity  of  the  infection.  The  evolution  of  gravid  endocarditis  is, 
moreover,  variable,  and  bacteriological  examinations  have  shown  that  it 
may  be  produced  by  the  pneumococcus,  the  streptococcus  (Netter,  Weichsel- 
baum),  or  by  unclassified  bacilh  (Girode). 

Puerperal  endocarditis  shows  vegetations  and  ulcers,  and  the  resulting 
capillary  emboli  are  septic  in  nature,  and  may  lead  to  hsemoptoic  or  sup- 
purating infarcts.  It  is  generally  due  to  a  streptococcus  of  extreme  virulence. 
The  chnical  picture  is  habitually  that  of  the  pysemic  form,  and  though 
the  prognosis  is  very  grave,  recovery  may  take  place.  Some  years  ago,  with 
Champetier  de  Eibes,  I  saw  a  case  of  post-puerperal  endocarditis,  with 
septicsemic  symptoms,  multiple  abscesses,  and  mitral  lesions.  The  patient 
recovered  from  the  infection  and  the  cardiac  lesion — at  least,  the  murmurs 
disappeared. 


DISEASES  OF  THE  ENDOCARDIUM  403 

These  attenuated  forms  depend,  doubtless,  on  a  streptococcus  of  slight 
virulence.  The  streptococcus  is  not  the  only  pathogenic  agent  which  may- 
be met  with  in  puerperal  endocarditis.  Other  microbes  may  infect  the 
uterine  wound,  and  give  rise  to  septicsemia  with  endocardial  lesions.  The 
staphylococcus  (Ch.  Leer),  the  pneumococcus  (Schahl  and  Hergott),  the 
coh  bacillus  (H.  Rendu),  have  been  found  either  in  isolated  cases  or  in 
epidemics  of  puerperal  infection  in  which  the  streptococcus  was  not  present. 

4.  Endocarditis  of  Septicsemic  and  Pyaemic  Origin.— This  form  is 
very  common,  and  is  consecutive  to  a  suppurating  wound  on  the  surface  of 
the  body  or  in  the  deep  tissues  of  the  organs  (urethra,  kidney,  bladder). 
It  is  chiefly  due  to  the  entrance  of  the  Streptococcus  pyogenes  and  the  Staphylo- 
coccus pyogenes  into  the  blood,  either  alone,  together,  or  associated  with 
other  microbes. 

When  the  mischief  is  due  to  the  streptococcus,  the  ulcerations  may  be 
extensive,  but  the  vegetations  are  usually  small,  soft,  and  greyish.  Infarcts 
are  very  frequent,  and  suppurate  rarely,  unlike  those  caused  by  the  staphylo- 
coccus, which  suppurate  frequently. 

When  endocarditis  is  due  to  the  Staphylococcus  aureus,  as  in  the  case 
of  boils,  or  of  osteomyelitis,  as  well  as  of  many  central  or  peripheral  sup- 
purative lesions,  the  disease  more  usually  affects  the  left  than  the  right 
heart.  Vegetations  are  more  common  than  ulcerations  ;  the  vegetations 
are  small  and  soft,  while  the  infarcts  are  suppurative.  Miliary  abscesses 
are  found  in  the  spleen,  kidneys,  lungs,  and  brain.  The  cUnical  picture 
recalls  the  description  of  purulent  infection,  with  typhoid  state,  eruptions, 
and  cutaneous  suppurations.  In  the  Necker  Hospital  I  had  a  patient  suffer- 
ing from  mahgnant  endocarditis  of  the  typhoid  form,  caused  by  the  Staphylo- 
coccus albus,  which  was  found' in  a  pure  state  during  life,  and  after  death 
in  the  pus  from  the  miliary  abscess  in  the  endocardium. 

Streptococcal  endocarditis  consecutive  to  erysipelas  is  extremely  rare. 
Curable  endocarditis,  however,  is  found  fairly  frequently  during  the  course 
of  erysipelas. 

5.  Typhoid  Endocarditis.  —  Primary  typhoid  endocarditis,  due  to 
Eberth's  bacillus,  is  very  rarely  seen.  Cases  of  secondary  typhoid  endo- 
carditis, due  to  tlie  coli  bacillus  and  other  microbes,  are  more  frequent. 

6.  Biliary  lithiasis  may  provoke  infective  endocarditis,  by  reason  of 
germs  derived  from  the  bile-ducts.  The  infection  appears  to  be  due  to 
micro-organisms  derived  from  the  intestine. 

7.  Tubercular  Endocarditis.— This  form  has  only  been  seen  in  acute 
miliary  tuberculosis.  It  appears  either  in  the  form  of  isolated  granula- 
tions— i.e.,  miliary  tubercles,  which  exist  most  often  on  the  free  edge  or 
auricular  face  of  the  mitral  valve-  or  in  the  form  of  vegetations. 

In  certain  cases  Koch's  bacilU  have  been  fouuil  in  these  lesions,  which 

26—2 


404  TEXT-BOOK  OF  MEDICINE 

may  therefore  be  considered  specific.  Further,  tubercular  endocarditis 
has  been  produced  experimentally  in  the  rabbit  by  intravenous  injection 
with  cultures  of  Koch's  bacillus,  preceded  by  injury  of  the  aortic  valves. 
The  vegetations  on  the  valves,  produced  at  the  same  time  as  the  general 
miUary  tuberculosis,  contained  the  tubercle  bacillus.  More  rarely  these 
lesions  are  caseous.     Koch's  bacilh  are  also  present  in  them. 

These  various  lesions  are  latent,  and  do  not  produce  special  symptoms. 

Lesions  of  the  endocardium  in  tubercular  patients  are  not  absolutely 
rare,  but  they  are  not  always  due  to  Koch's  bacillus.  The  latter  are  cases 
of  old  endocarditis,  independent  of  tuberculosis  or  of  recent  more  or  less 
vegetating  lesions,  which  have  nothing  specific  as  regards  histological 
structure,  and  in  which  bacteriological  examination  sometimes  reveals  other 
micro-organisms  than  Koch's  bacillus.  These  recent  lesions  fomid  post 
mortem  in  tubercular  patients,  most  frequently  upon  the  mitral  valve,  may 
therefore  be  considered  as  due  to  secondary  infections  (P.  Tessier). 

8.  Blennorrhagie  Endocarditis. — If  the  reader  will  turn  to  the  chapter 
on  Blennorrhagia,  he  will  find  cases  of  endocarditis  due  to  the  gonococcus. 

II.  CHRONIC  ENDOCARDITIS. 

>Etiology. — Chronic  endocarditis  arises  from  the  same  causes  as  acute 
endocarditis,  rheumatism  claiming  the  largest  share.  In  alcohohc,  sypliiUtic, 
gouty,  or  elderly  persons  it  is  sometimes  secondary  to  fatty,  fibrous,  or 
atheromatous  changes  which  invade  the  arterial  system.  The  coexistence 
of  tuberculosis  and  mitral  endocarditis  has  been  nqted  by  Potain  and 
Tessier.  Chronic  endocarditis  often  follows  the  acute  form,  but  at  other 
times  it  is  primary,  and  becomes  estabhshed  in  an  insidious  manner.  Its 
course  is  slow.  The  valvular  lesions  develop  unknown  to  the  patient,  and 
in  rheumatic  cases  many  people,  whose  health  is  apparently  excellent,  only 
show  the  first  symptoms  of  valvular  mischief  after  a  forgotten  attack  of 
acute  articular  rheumatism. 

Pathological  Anatomy. — The  vegetations,  which  are  soft  and  friable 
in  acute  endocarditis,  are  here  hard  and  fibrous,  and  the  vessels  that  are  so 
numerous  in  the  acute  stage  over  the  swollen  mitral  valve  disappear  in 
proportion  as  the  lesion  becomes  chronic.  The  inflammatory  process,  which 
commences  in  the  layer  of  flattened  cells,  reaches  the  subjacent  layer, 
which  is  rich  in  connective  tissue,  and  gives  rise  to  fibrous  tissue.  In  this 
fibrous  tissue  we  find  islets  undergoing  fatty  change,  atheromatous  centres 
and  calcareous  incrustations,  lesions  wliich  present  great  analogy  with 
endarteritis  deformans.  Tliis  change  in  the  endocardium,  and  the  retractile 
property  of  the  fibrous  tissue  explain  the  alterations  in  the  valves  and  orifices 
of  the  heart. 


DISEASES  OF  THE  ENDOCARDIUM  405 

Every  part  of  these  orifices  is  invaded.  The  chordae  tendineae  and  the 
auriculo-ventricular  valves  are  shortened  and  indurated  ;  tlie  fibrous  zone 
which  surrounds  the  orifices  is  hypertrophied.  The  musculi  papillares  are 
also  affected.  They  are  sometimes  thickened  and  shortened — the  valves 
may  be  three  or  four  times  larger  than  normal — or,  on  the  other  hand, 
atrophied  or  adherent.  Their  edges  are  fused,  jagged,  thickened,  and 
covered  mth  granulations.  The  vegetations  are  chiefly  situated  on  the 
auricular  surface  of  the  auriculo-ventricular  valves  and  on  the  ventricular 
surface  of  the  sigmoid  valves.  These  lesions,  in  which  adhesions,  fibrosis, 
atheroma,  and  calcification  are  combined,  finally  cause  deformity  of  the 
orifices,  and  impede  the  action  of  the  valves  ;  insufl&ciency  of  the  valves  and 
narrowing  of  the  orifices  then  follow.  The  muscular  fibre  of  the  ventricles 
and  auricles  hypertrophies  because  of  the  increased  work,  and  compensation 
is  established  ;  but  later  when  the  muscular  fibre  is  also  invaded  by 
the  morbid  process,  the  columnse  carnese  and  the  ventricles  show  fibrous 
changes,  and  their  vessels  are  affected  by  endarteritis,  which  causes  mal- 
nutrition. The  degenerated  cardiac  muscle  no  longer  fights  with  the  same 
efficiency. 

In  some  cases  (old  age,  alcoholism)  the  lesions  do  not  begin  in  an  inflam- 
matory, but  in  a  retrogressive  process,  which  in  its  turn  induces  inflamma- 
tion. Atheroma  plays  the  principal  part.  The  atheromatous  degeneration 
appears  here,  as  in  some  cases  of  endarteritis,  to  be  the  primary  lesion 
(Cornil  and  Ranvier). 

The  symptoms  of  chronic  endocarditis  closely  resemble  those  of  valvular 
lesions  of  the  heart,  wliich  will  be  studied  in  the  following  sections. 

III.  VALVULAR  LESIONS  OF  THE  HEART. 

General  Survey. — Whether  endocarditis  is  of  microbic  origin,  as  in 
most  acute  and  also  in  many  chronic  cases,  or  is  consecutive  to  the  athero- 
matous lesions  of  gout  and  old  age,  the  lesion  may  cause  transient  or  per- 
manent insufficiency  and  stenosis.  An  orifice  is  said  to  be  stenosed,  when 
instead  of  allowing  ten  parts  of  blood  to  pass  at  each  beat  of  the  heart,  it 
only  allows  seven,  five,  or  even  less,  to  do  so.  Insufficiency  is  present  when 
the  valves  which  normally  prevent  all  regurgitation  of  blood  no  longer 
plug  the  orifice,  and  hence  allow  the  blood-wave  to  regurgitate.  The  four 
orifices  of  the  heart  (arterial  or  auriculo-ventricular)  may  be  affected,  but 
those  of  the  left  heart  are  much  more  often  involved  than  those  of  the  rigiit. 
Stenosis  and  insufficiency  are  often  combined  at  the  same  orifice  ;  each  of 
them  may,  however,  show  itself  alone.  This  dissociation  is  chiefly  seen 
iu  insufficiency  due  to  mechanical  causes.  Thus  enlargement  of  the  right 
ventricle  brings  with  it  dilatation  of  the  tricuspid  orifice  and  insufficiency 


406  TEXT-BOOK  OF  MEDICINE 

of  the  valves,  just  as  enlargement  of  the  aorta,  may  bring  with  it  dilatation 
of  the  aortic  orifice  and  insufficiency  of  the  sigmoid  valves. 

Further,  whatever  be  the  mechanism  of  the  lesion,  whichever  be  the 
orifice  affected,  as  soon  as  the  distribution  of  the  blood- waves  is  not  regular, 
and  one  of  the  parts  of  the  cardiac  machinery  is  affected,  the  whole  circula- 
tion feels  the  shock.  It  is  true  that  the  shock  is  felt  more  or  less  slowly 
according  to  the  orifice  damaged  and  to  the  efficacy  of  compensation, 
but  the  final  result  is  the  same,  and,  as  Jaccoud  has  forcibly  said,  valvular 
lesions  raise  the  pressure  in  the  veins  and  lower  it  in  the  arteries,  which  is 
equivalent  to  saying  that  they  finally  cause  passive  congestion,  oedema, 
dropsy,  thrombosis,  and  haemorrhage,  with  all  their  train  of  functional 
troubles. 

Valvular  lesions  may,  nevertheless,  be  neutralized,  even  for  a  long  time, 
provided  they  are  compensated.  Compensation  is  a  kind  of  substitution, 
due  to  dilatation  of  the  cavities  of  the  heart  and  to  hypertrophy  of  its  walls. 
Let  us  take,  for  example,  aortic  insufficiency  :  The  left  ventricle  is  subjected 
to  an  excess  of  pressure  by  the  surplus  of  regurgitated  blood,  and  its  muscular 
fibre  undergoes  marked  hypertrophy.  This  mechanism  of  compensation, 
which  exists  in  different  degrees,  according  to  the  orifices  affected, 
renders  the  valvular  lesions  harmless  for  a  period  varying  in  duration  with 
the  nature  and  the  seat  of  the  lesion. 

A  time  comes,  however,  when  the  compensation  is  no  longer  sufficient. 
The  cardiac  muscle,  which  is  badly  nourished  and  invaded  by  fibrous  tissue, 
wliile  its  vessels  are  damaged  by  endarteritis,  has  no  longer  the  necessary 
energy  to  face  the  danger.  The  functional  troubles  bedome  more  marked ; 
congestion,  blood-stasis,  and  dropsy  progress  ;  malnutrition  becomes  general ; 
irremediable  lesions  develop  in  the  organs  ;  cyanosis,  dyspnoea,  and  coma 
gradually  reach  their  maximum  ;  and  the  condition  is  summed  up  in  a  single 
word — asystole  (Beau). 

While  the  heart  is  being  worn  out,  the  small  vessels  which  form  the 
peripheral  and  local  circulation  become  affected  and  lose  their  resistance. 
Each  organ  becomes  diseased  in  its  turn,  and  the  disease  of  the  heart  is 
changed  into  a  disease  of  the  whole  organism. 

Asystole,  however,  may,  under  the  influence  of  proper  treatment,  or 
even  spontaneously,  improve  for  a  time ;  but  after  some  remissions, 
of  an  uncertam  duration,  the  patient  reaches  the  stage  of  cardiac 
cachexia  (Andral).  The  disease  is  no  longer  confined  to  the  heart,  but 
affects  the  whole  body.  "  Thus,  when  he  has  ceased  to  live,  the  patient 
has  in  reality  only  ceased  to  die  "  (Peter). 

In  patients  dying  from  cardiac  cachexia  we  find  general  changes.  The 
lungs  are  the  seat  of  congestion,  oedema,  infarcts,  and  haemorrhage.  The 
brain  is  congested;  the  cerebral   sinuses  are  engorged  with  dark  blood. 


DISEASES  OF  THE  ENDOCARDIUM  407 

The  liver,  which  is  large  and  indurated,  presents  the  so-called  "  nutmeg 
change."  The  kidney,  which  is  enlarged,  shows  multiple  arborizations  on 
its  surface.  The  spleen  is  engorged  with  blood.  The  heart  is  generally- 
enlarged  ;  its  muscular  fibre  is  pale,  degenerated,  and  studded  with  fatty 
and  fibrous  islets.  It  contains  clots — some  yellowish,  fibrinous,  firm  and 
adherent,  and  consequently  of  old  formation ;  others  soft,  cruoric,  and  of 
recent  formation. 

Diseases  of  the  heart  have  not  always  this  slowly  progressive  course. 
Some  patients  die  suddenly  (aortic  insufficiency)  ;  others  are  stricken  down 
by  comphcations  (pulmonary  haemorrhage,  cerebral  embolism).  In  some 
the  disease  is  rapid,  and  cachexia  is  established  in  a  few  months,  while 
in  others  infective  endocarditis  is  grafted  upon  an  old  valvular  lesion,  and  is 
sometimes  fatal. 

Signs  and  Symptoms. — The  chnical  account  of  diseases  of  the  heart 
cannot  be  dealt  with  in  a  general  survey,  because  the  symptoms  of  mitral 
disease  are  very  different  from  those  of  aortic  disease.  I  refer  the  reader, 
then,  to  the  separate  study  of  each  orifice.  This  statement  does  not  hold 
good  with  regard  to  the  signs  of  cardiac  lesions,  and  notably  to  the  abnormal 
sounds,  the  mechanism  of  which  will  be  better  grasped  in  a  general  survey. 

Mechanism  of  Abnormal  Sounds. — Locally,  the  valvular  lesions  of 
the  heart  are  shown  by  morbid  sounds  called  murmurs  and  reduplications, 
the  interpretation  of  which  rests  upon  the  previous  knowledge  of  the  physio- 
logical sounds. 

In  the  normal  state  two  sounds  are  heard  at  the  apex  :  the  first  is  long 
and  well  marked,  the  second  is  duller  and  shorter.  At  the  junction  of  the 
sternum  and  the  second  right  intercostal  space  two  sounds  are  also  heard, 
but  the  rhythm  is  the  inverse  of  that  at  the  apex.  The  first  or  systolic 
sound  is  dull ;  the  second  or  diastolic  sound  is  longer  and  more  marked. 
As  two  sounds  are  produced  at  each  orifice  of  the  heart,  and  as  there  are 
four  orifices,  it  follows  that  eight  sounds  are  produced  in  each  cardiac  cycle  ; 
but  only  four  are  perceptible  (two  at  the  apex  and  two  at  the  base),  because 
in  the  normal  condition  they  blend  and  give  rise  to  two  sounds  at  the  apex 
and  two  sounds  at  the  base.  To  what  are  these  sounds  due  ?  Each  of 
them  is  composed  of  a  chief  element,  caused  in  situ,  and  an  accessory  or 
propagated  element. 

First  Sound. — At  the  apex  of  the  heart  the  first  sound  has  for  its  chief 
element  the  Knap})iiig  of  the  valves  (mitral  and  tricuspid),  and  for  its  accessory 
element  the  re-echoing  of  the  first  sound  of  the  base,  which  is  due  to  a  sudden 
distension  of  the  arterial  walls  (aorta  and  pulmonary  artery)  by  the  blood- 
wave.  At  the  base  of  the  heart  the  first  sound  is  formed  of  the  same 
elements,  with  tliis  difference — tiiat  the  element  which  was  accessory  at  the 
apex  becomes  here  the  cliicf  one,  and  vice  versa. 


408  TEXT-BOOK  OF  MEDICINE 

Second  Sound. — At  the  apex  of  the  heart  the  second  sound  has  for 
its  chief  element  the  passage  of  blood  into  the  ventricles  (Skoda's  interpreta- 
tion), and  for  its  accessory  element  the  snapping  of  the  sigmoid  valves. 
At  the  base  of  the  heart  the  second  sound  is  made  up  of  the  same  elements, 
with  this  difference — that  the  element  which  was  accessory  at  the  apex 
becomes  here  the  chief  one,  and  vice  versa. 

In  short,  whether  it  be  a  case  of  valvular  snapping  or  of  sudden  distension 
of  the  walls,  all  normal  sounds  of  the  heart  are  solid  sounds  (Monneret)  ; 
that  is  to  say,  produced  by  the  vibration  of  solid  parts.  In  pathological 
conditions,  however,  the  solid  sounds  undergo  the  following  modifications  : 
First,  they  are  replaced  by  murmurs — that  is  to  say,  by  fluid  sounds,  due 
to  vibrations  of  a  blood- wave  traversing  a  diseased  orifice ;  secondly,  they 
are  reduplicated,  the  roduphcation  occurring  in  the  first  or  in  the  second 
period  ;  thirdly,  they  may  disappear  without  other  modifications,  and  without 
being  replaced  by  any  abnormal  sound. 

The  blowing  murmurs  are  variable  in  tone  and  intensity.  They  may 
be  softened  and  prolonged  (aortic  insufficiency),  hissing  like  a  jet  of  steam 
(mitral  insufficiency),  strident  (aortic  stenosis),  or  so  little  marked  that  they 
resemble  rather  a  dull  rumbhng  than  a  blowing  sound  (mitral  stenosis). 
In  some  cases  the  murmur  is  changed  into  a  musical  sound,  called  whining 
(Bouillaud).  The  whining  is  due  either  to  the  nature  of  the  lesion  of  the 
orifice,  or  to  some  floating  shred  thrown  into  vibration  in  front  of  an 
orifice  by  the  blood- wave. 

I  cannot,  however,  too  strongly  insist  on  this  point  that  the  presence 
of  a  murmur  or  of  a  reduplication  is  not  sufficient  t6  prove  an  organic 
lesion.  We  find  reduphcations  and  murmurs  which  have  nothing  to  do 
with  the  lesion  of  an  orifice.  Such  are  the  important  extra-cardiac  murmurs, 
so  carefully  described  by  Potain  ;  such  are  the  normal  reduplications, 
"  resulting  from  transitory  changes  which  the  movements  of  respiration 
cause  in  the  pressure  of  the  blood  contained  in  the  heart  and  the  great 
vessels  "  (Potain). 

Such,  also,  are  the  aortic  and  mitral  murmurs  due  to  chloro-ansemia. 

Let  us,  however,  return  to  the  organic  murmurs  of  the  heart  and  apply 
the  preceding  data  to  each  of  the  valvular  lesions. 

1.  Mitral  insufficiency  is  characterized  by  a  systolic  murmur  at  the 
apex.  During  the  ventricular  systole  in  the  normal  condition  the  blood- 
wave  from  the  left  ventricle  passes  completely  into  the  aorta,  because  the 
mitral  valve  plugs  the  auriculo -valvular  orifice  ;  but  in  the  pathological  state, 
as  the  valve  is  not  able  to  plug  this  orifice,  part  of  the  ventricular  blood- 
wave  flows  back  into  the  auricle,  and  a  systolic  murmur  is  produced. 
This  murmur  has  its  maximum  near  the  apex  of  the  heart,  at  the  level  of 
fche  mitral  orifice  below  or  outside  the  nipple. 


DISEASES  OF  THE  ENDOCARDIUM  409 

2.  Mitral  stenosis  is  characterized  by  a  diastolic  murmur,  by  a  pre- 
systolic murmur,  or  by  reduplication  of  the  second  sound.  In  order  to 
understand  the  mechanism  and  the  value  of  these  pathological  sounds  which 
are  heard  at  the  apex  of  the  heart,  we  must  briefly  discuss  the  ventricular 
diastole.  During  diastole  the  ventricle  is  dilated,  the  auriculo-ventricular 
orifice  opens  widely,  and  the  blood  passes  through  the  auricle  into  the 
ventricle.  The  passage  of  the  blood  is,  however,  somewhat  slow.  It  begins 
gradually  during  the  ventricular  diastole,  and  terminates  more  suddenly 
during  the  pause,  when  the  auricle  is  contracted.  If,  then,  the  murmur 
of  stenosis  is  produced  during  the  first  part  of  the  passage  (which  is  very 
rare),  it  is  diastohc  (Herard)  ;  if  it  is  produced  during  the  second  part  of  the 
passage,  it  corresponds  to  the  pause,  and  is  therefore  presystolic  (Gendrin). 
The  murmur  of  mitral  stenosis  is  not  loud,  because  the  blood-wave  is  feebly 
pushed  through  the  constricted  orifice,  even  when  the  auricle  is  hyper- 
trophied.  Accordingly,  this  murmur  is  rather  a  presystolic  booming  or 
rumbling  (Duroziez). 

Mitral  stenosis  is  also  characterized  by  reduplication  of  the  second 
sound,  and  as  the  second  part  of  this  reduphcation  may  be  blowing,  we 
find  a  rhythm  of  three  beats,  composed  of  one  long  and  two  short  periods. 
Several  theories  exist  as  to  this  reduplication  of  the  second  sound  :  the 
one  supposes  that  there  is  a  want  of  sjmchronism  between  the  second  sounds 
in  the  two  ventricles ;  the  other  holds  that  the  want  of  synchronism  exists 
between  the  second  sound  at  the  ventricular  orifice  and  the  second  one  at 
the  arterial  orifice  (Jaccoud).  While  in  the  normal  condition  these  two 
elements  are  blended,  in  mitral  stenosis  they  are  dissociated,  the  ventricular 
being  behind  the  arterial  sound.  According  to  Potain,  the  dissociation 
depends  on  the  closure  of  the  aortic  and  pulmonary  valves,  the  closure  of 
the  aortic  valves  being  premature. 

However  this  may  be,  reduplication  of  the  second  sound,  with  or  without 
a  presystolic  murmur,  is  a  sign  of  mitral  stenosis. 

3.  Aortic  insufficiency  is  characterized  by  a  diastolic  murmur  at  the 
base.  The  reasons  are  :  at  the  moment  wlien  the  blood- wave  has  just  been 
launched  from  the  ventricle  into  the  aorta,  the  backward  movement  finds, 
normally,  an  impassa])]e  barrier  in  the  sigmoid  valves.  When,  however, 
these  valves  are  unable  to  plug  the  orifice,  some  of  the  blood  flows  back  into 
the  ventricle,  and  a  diastolic  murmur  is  produced. 

4.  Aortic  stenosis  is  characterized  by  a  systolic  murmur  at  the  base. 
If  the  blood-wave  tlirown  by  the  ventricle  meets  with  a  coiistrictcd  instead 
of  an  open  orifice,  a  systolic  murmur  is  produced. 


410  TEXT-BOOK  OF  MEDICINE 

IV.  MITRAL  ORIFICE— INSUFFICIENCY  AND  STENOSIS. 

Mitral  insufficiency  is  present  when  the  mitral  valve,  which  normally 
closes  the  Left  aujiculo-ventricular  orifice  in  order  to  prevent  regurgitation 
of  blood,  does  not  plug  this  orifice,  but  allows  the  blood  to  flow  back  into  the 
left  auricle.  Mitral  stenosis  is  present  when  the  lumen  of  the  orifice  has 
lost  its  normal  dimensions. 

Stenosis  and  insufficiency  are  most  often  combined,  and  we  then  speak 
of  mitral  disease.  If  one  only  is  present,  we  speak  of  pure  stenosis  or  of  pure 
insufficiency.  In  many  cases  the  process  begins  with  insufficiency,  and 
stenosis  occurs  later.  Lastly,  in  some  patients  stenosis  appears  to  develop 
from  special  causes,  and  remains  indefinitely  in  a  pure  condition. 

Pathological  Anatomy. — Mitral  stenosis  may  be  due  to  concentric 
thickening  and  retraction  of  the  fibrous  ring.  In  most  cases,  however,  the 
condition  is  due  to  lesions  of  the  valves  and  their  chordse.  A  welding 
of  the  free  edge  of  the  valves  occurs  at  the  level  of  the  commissures.  This 
welding  might  be  compared  to  the  narrowing  of  the  aperture  between  the 
eyelids  from  adhesions  of  their  commissures  (Bouillaud).  The  tendinous 
pillars  inserted  on  the  edge  of  the  valves  participate  in  the  cicatricial  process. 
They  become  rigid,  thickened,  and  retracted,  and  pull  down  the  bicuspid 
valve,  which  takes  the  shape  of  a  rigid  and  flattened  funnel. 

In  this  manner  stenosis  is  brought  about,  but  as  a  rule  neither  the  fibrous 
ring  nor  the  vegetations  of  the  auricular  surface  of  the  valve  take  any  part. 
The  mitral  orifice,  which  normally  is  large  enough  to  admit  the  thumb, 
becomes  so  narrow  that  it  will  scarcely  admit  a  goose-quill. 

Dilatation  and  hypertrophy  of  the  left  auricle,  followed  by  that  of  the 
right  auricle  and  ventricle,  are  the  consequence ;  the  left  ventricle  remains 
practically  normal.  The  slowing  of  the  blood-stream  and  the  blood-stasis 
in  the  left  auricle  favour  the  formation  of  stratified  clots,  which  are  often 
adherent  to  its  posterior  wall.  These  clots,  which  pass  into  the  left  ventricle, 
and  are  launched  into  the  blood- stream  during  systole,  may  become  the 
source  of  more  or  less  bulky  emboli.  On  the  other  hand,  the  slowing  of 
the  blood-stream  and  the  blood-stasis  in  the  right  auricle  favour  the  forma- 
tion of  clots,  which  are  also  fibrinous  and  adherent.  These  clots,  which  are 
launched  from  the  right  ventricle  into  the  lungs,  are  the  most  common 
cause  of  pulmonary  infarcts. 

Mitral  insufflciency  is  the  result  of  lesions  which  affect  the  valves  or 
the  fibrous  ring.  The  lesions  of  the  valves  are  thickening,  induration  and 
incrustations  of  the  edges.  There  is  no  welding  of  the  valvular  com- 
missures. Under  the  influence  of  the  retractile  tissue  the  shortening 
and  retraction  of  the  valves  oppose  the  complete  adjustment  of  their 
auricular  surface  during  systole,  and  insufficiency  residts.     The  shortening 


DISEASES  OF  THE  ENDOCARDIUM  411 

of  the  chordae  tendinese,  which  are  also  thickened  and  indurated,  opposes 
the  complete  straightening  of  the  valve  during  systole,  and  this  helps  to 
cause  insuflEiciency.  The  papillary  muscles,  by  their  fibrous  retraction,  may 
act  in  the  same  manner.  Rapture  of  the  chordae  tendineae  may  be  a  cause 
of  insufficiency,  and  I  would  also  mention  valvular  aneurysms  and  vegeta- 
tions. Mitral  insufficiency,  due  not  to  a  lesion  of  the  valves  and  pillars, 
but  to  dilatation  of  the  fibrous  ring,  does  exist,  but  is  relatively  rare.  In  this 
case  the  left  ventricle,  during  its  dilatation,  drags  upon  the  papillary  muscles 
and  the  tendinous  pillars,  and  consequently  produces  abnormal  tension  of 
the  valves  and  insufficiency.  Dilatation  of  the  left  ventricle,  which  has 
previously  lost  some  part  of  its  contractility,  is  said,  according  to  some 
authorities,  to  be  a  cause  of  pure  mitral  insufficiency,  either  transient  or 
permanent. 

Mitral  insufficiency  induces  dilatation  and  hypertrophy  of  the  left  auricle, 
the  right  auricle,  and  the  right  ventricle.  The  left  ventricle,  however, 
which  is  almost  unaffected  in  stenosis,  shows  slight  hypertrophy  in  in- 
sufficiency. 

Description. — We  see  persons  among  the  leisured  classes  (rather  than 
in  hospital  patients),  who  for  many  years  have  suffered  from  some  mitral 
lesion,  without  having  shown  any  symptoms,  because  the  heart  muscle  is 
not  overworked,  and  the  lesion  is  well  compensated.  The  functional  hyper- 
activity of  the  muscle  and  the  compensatory  hypertrophy  of  the  right  ven- 
tricle struggle  successfully  against  the  evil  distribution  of  the  blood-waves, 
and  undertake  the  maintenance  of  equilibrium.  Dilatation  and  hyper- 
trophy of  tlie  right  ventricle  compensate  as  far  as  possible  for  the  increase 
in  the  pulmonary  arterio-venous  tension,  so  that  mitral  insufficiency  and 
stenosis  may  be  latent  for  a  long  while.  When,  however,  the  cardiac  muscle 
becomes  feeble,  or  is  attacked  by  some  morbid  change,  such  as  fibrosis,  end- 
arteritis of  the  small  vessels,  or  granulo-fatty  degeneration,  which  endangers 
its  nutrition  and  its  tone,  we  find  visceral  congestions,  peripheral  and 
splanchnic  oedema,  which  result  from  the  cardiac  disease. 

Breathlessness  and  dyspnoea,  with  or  without  palpitation,  are  generally 
the  first  functional  troubles  in  mitral  lesions,  because  the  pulmonary  circula- 
tion, which  is  so  close  to  the  mitral  lesion,  is  naturally  the  first  to  be  affected; 
bronchial  catarrh,  congestion,  oedema,  and  ha3morrhage  of  the  lungs  are 
among  more  or  less  remote  results.  These  lesions  produce  increasing  dis- 
tress, witli  attacks  of  dyspnoea  and  haemoptysis. 

Breathlessness  may  for  a  long  time  be  the  only  symptom  of  the  mitral 
lesion.  The  patient  is  "  short  of  breath  "  ;  he  does  not  notice  it  while  at 
rest,  but  when  he  walks  upstairs  or  makes  an  effort,  distress  appears.  At 
this  period  the  embarrassment  of  the  pulmonary  circulation  docs  not  betray 
itself  by  any  physical  signs  on  auscultation.     The  slowing  of  the  blood- 


412  TEXT-BOOK  OF  MEDICINE 

stream  and  the  marked  pressure  to  which  the  flow  in  the  pulmonary  artery  is 
subjected  are  two  of  the  causes  of  this  dyspnoea.  On  account  of  the  mitral 
lesion  the  blood  tarries  or  flows  back  into  the  left  auricle,  the  blood-pressure 
increases  in  the  auricle,  the  pulmonary  veins  and  arteries,  and  the  distension 
of  the  capillaries  of  the  pulmonary  alveoli  provokes  rigidity  and  swelling  of 
the  lung.  Indeed,  according  to  some  authors,  this  rigidity  and  swelling  is 
said  to  be  the  chief  cause  of  cardiac  dyspnoea. 

Later,  as  the  result  of  pulmonary  oedema,  the  dyspnoea  becomes  more 
persistent  or  intense,  and  auscultation  reveals  subcrepitant  rales,  which  are 
usually  present  at  both  bases  of  the  lungs.  During  this  progressive  dyspnoea, 
or  even  apart  from  it,  the  patient  sometimes  experiences  attacks  that  are 
more  frequent  by  night  than  by  day,  and  similar  to  those  of  asthma,  so 
that  this  paroxysmal  dyspnoea  has  been  called  "  cardiac  asthma."  This 
name  is  bad.  Mitral  disease  does  not  produce  true  asthma  ;  the  attack  has 
not  the  characters  of  the  dyspnoea  seen  in  asthma.  Let  us  analyze  such  an 
attack  in  a  cardiac  case.  The  breathing  is  rapid  and  panting,  inspiration 
and  expiration  are  short  and  jerky,  palpitation  is  frequent,  the  pulse  is 
small,  the  face  is  pale,  and  the  lips  are  cyanosed.  In  asthma  the  picture  is 
quite  different :  the  breathing  is  not  accelerated,  inspiration  is  slow  and 
painful,  while  expiration  is  whistling,  spasmodic,  and  three  or  four  times  as 
long  as  inspiration  ;  palpitation  is  absent,  and  the  pulse  preserves  its  normal 
rate.  In  some  cardiac  cases  the  attacks  of  dyspnoea  form  the  chief  symptom, 
and  the  only  sign  of  mitral  disease  may  at  first  be  attacks  of  cardiac  dyspnoea, 
just  as  in  ceitain  cases  of  Bright's  disease  the  renal  lesion  is  heralded  by 
attacks  of  ursemic  dyspnoea. 

The  mitral  lesion  also  shows  itself  by  such  symptoms  as  palpitations 
and  feeling  of  weight  or  of  constriction  in  the  precordial  region.  These 
symptoms  are  especially  increased  by  strain  or  by  active  movements. 

Haemorrhage  from  the  lung  (known  under  the  faulty  term  of  pulmonary 
apoplexy)  and  haemoptysis,  wliich  accompanies  it,  are  more  common  in 
mitral  than  in  other  lesions  of  the  heart.  These  haemorrhages  may  be  due 
to  the  mechanical  obstruction  of  the  pulmonary  circulation,  but  are  in  most 
cases  the  result  of  small  emboH,  which  arise  from  clots  in  the  right  auricle, 
are  arrested  in  the  pulmonary  arterioles,  and,  like  all  capillary  emboli, 
produce  a  haemorrhagic  infarct.  These  infarcts,  described  under  Pulmonary 
Embolism,  are  frequently  followed  by  haemoptysis.  Haemoptysis  may  be  seen 
at  different  periods  of  mitral  disease,  more  usually  at  a  somewhat  advanced 
one.  According  to  the  classical  description,  it  appears  in  the  form  of  blood- 
stained sputum  of  a  blackish  colour  and  alliaceous  odour  (Gueneau  de 
Mussy),  and  lasts  for  days  and  weeks  (Grisolle).  Cardiac  haemoptysis  may, 
however,  appear  before  any  other  symptom,  and  through  a  determinant 
cause  (fatigue,  excess,  or  pregnancy). 


DISEASES  OF  THE  ENDOCARDIUM  413 

Pulmonary  infarcts,  especially  when  they  are  cortical,  cause  sero-fibrinous 
or  puriforni  pleurisy,  that  is  usually  insidious  and  more  frequent  on  the 
right  side. 

Peripheral  oedema,  starting  over  the  malleoh,  is  fairly  often  seen  in 
mitral  disease.  At  first  the  oedematous  infiltration  is  absent  in  the  morning 
after  the  night's  rest,  but  later  it  becomes  permanent,  and  may  affect  the 
thighs,  the  scrotum,  and  the  trunk  (anasarca).  The  skin  of  the  legs  and  of 
the  thighs  is  tliickened,  red,  and  prone  to  erythema,  erysipelas,  and  gangrene, 
especially  after  acupuncture.  At  an  advanced  period  of  heart  disease  the 
pleura,  peritoneum,  and  pericardium  often  contain  fluid.  Deep-seated 
oedema  affecting  the  cellular  tissue  of  the  splanchnic  cavities  is  of  great 
importance,  as  we  shall  see  later  under  Treatment. 

Visceral  congestions  appear  at  different  periods.  I  have  already  said 
that  congestion  of  the  lung,  with  or  mthout  pulmonary  oedema,  is  generally 
the  first  to  supervene.  The  obstacle  to  the  pulmonary  circulation  has  a 
double  result :  first,  haematosis  being  incomplete,  the  general  nutrition 
suffers ;  second,  the  embarrassment  in  the  lesser  circulation  gradually 
reachas  the  greater  circulation,  the  right  heart  grows  weak,  and  general 
circulatory  distress  follows. 

The  liver  often  shows  congestion  (nutmeg  or  cardiac  hver,  with  or 
without  cirrhosis).  The  lesion  shows  itself  by  increase  in  the  size  of  the 
organ,  with  acute  pains  in  the  hypochondrium,  jaundice,  and  epistaxis. 
The  cardiac  liver  is  often  accompanied  by  ascites.  These  lesions  are  most 
marked  in  cardiac  patients  who  are  also  alcohohcs. 

Gastro-intestinal  congestion  provokes  dyspeptic  troubles,  with  indiges- 
tion, feehng  of  weight  in  the  stomach,  and  somnolence. 

Congestion  of  the  kidneys  is  shown  by  scanty  urine,  with  sediment  and 
albumin,  lesions  which  rarely  end  in  Bright's  disease. 

Congestion  of  the  encephalon  and  faulty  oxygenation  in  the  bulb 
produce  insomnia  (Peter),  nocturnal  delirium,  maniacal  excitement 
(Raynaud),  and  convulsions. 

Such  are  the  lesions  and  symptoms  of  mitral  disease.  They  usually 
run  a  slow  course,  and  may  last  many  years  before  they  endanger  life.  The 
predominance  of  pulmonary,  hepatic,  or  gastric  troubles  masks  for  a  time 
the  true  cause  of  the  disease.  At  length  the  affected  muscle  can  no  longer 
struggle  against  the  obstacles  at  the  periphery.  The  disease  is  no  longer 
limited  to  the  heart ;  every  organ  is  affected  on  its  own  account,  and  the 
entire  organism  is  invaded.  This  progressive  course  is  interrupted  by 
periods  of  asystole.  The  patient,  who  very  rarely  dies  suddenly  (con- 
trary to  aortic  insufficiency),  at  length  reaches  the  final  stage  of  cardiac 
cachexia. 

Cerebral  embolism  may  supervene  at  any  period  of  mitral  disease.     It 


414  TEXT-BOOK  OF  MEDICINE 

is  more  common  in  stenosis  than  in  insufficiency,  and  produces  troubles, 
such  as  cerebral  softening,  right  hemiplegia,  aphasia,  etc.,  which  will  be 
discussed  under  Cerebral  Embolism.  In  some  cases  the  embolus  follows 
another  course — obUterates  the  peripheral  arteries  of  the  limbs  and  may 
produce  gangrene. 

The  preceding  description  refers  to  mitral  disease  as  a  whole — that  is  to 
say,  the  double  lesion  of  insufficiency  and  stenosis.  The  functional  troubles 
of  mitral  insufficiency  in  some  respects  resemble  those  of  stenosis.  Ausculta- 
cion,  therefore,  must  differentiate  between  these  two  lesions. 

We  find,  however,  a  variety  of  pure  mitral  stenosis,  which  merits  a 
separate  description.  It  is  much  more  frequent  in  women  than  men,  and 
is  seen  in  young  girls  and  young  women.  It  is  independent  of  rheumatism 
and  of  the  other  causes  which  usually  produce  endocarditis.  This  stenosis 
is  sometimes  associated  with  chlorosis,  and  has  also  been  looked  upon  as  a 
lesion  of  evolution — i.e.,  an  aplasia — analogous  to  the  stenosis  of  the  aorta 
and  the  arteries  which,  according  to  some  authors,  is  said  to  be  the  anatomical 
characteristic  of  chlorosis.  Potain,  in  fifty-five  cases  of  pure  mitral 
stenosis,  with  autopsies,  has  found  pulmonary  tuberculosis  in  nine  of 
them. 

Fibrous  endocarditis,  which  in  tubercular  patients  goes  on  to  mitral 
stenosis,  is  said  by  Teissier  to  be  due,  not  to  a  bacillary  infection,  but  to 
a  tubercular  intoxication.  "  This  fibromatous  process,  resulting  from  the 
phthisiogenic  intoxication,  may  be  present  in  hereditary  cases  of  tubercu- 
losis, and  show  itself  by  a  like  evolutionary  tendency.  Mild  local  tuberculosis 
(pulmonary,  glandular,  or  osseous),  as  well  as  the  attenuated  hereditary 
forms  (chlorosis,  lymphatism,  congenital  debility),  may  be  the  actual 
factor  or  the  hereditary  caus^  of  a  pure  mitral  stenosis." 

Whatever  may  be  its  origin  and  its  pathogenesis,  this  constriction  causes 
such  slight  functional  troubles  that  it  may  be  latent  for  years  ;  but  it  is  none 
the  less  serious,  for  it  is  frequently  accompanied  by  cerebral  embohsm,  with 
hemiplegia  and  aphasia. 

Examination  of  the  Heart  and  Pulse. — In  mitral  disease  the  apex  is 
displaced,  because  of  the  cardiac  hypertrophy,  and  the  beat  is  in  the  sixth 
or  seventh  space,  external  to  the  nipple.  The  precordial  dullness  and 
bulging  are  less  extensive  in  mitral  than  in  aortic  lesions,  because  the 
hypertrophy  of  the  right  heart  is  less  considerable  than  that  of  the  left  heart. 
If  the  hand  is  applied  over  the  heart,  we  often  feel  a  systohc  thrill.  The 
pulse  is  small,  because  the  mitral  lesion  diminishes  the  column  of  the 
blood-wave  driven  into  the  aorta.  It  is  unequal  and  irregular,  because 
the  contractions  of  the  left  ventricle  are  not  of  equal  strength  and  do  not 
follow  at  equal  intervals  consecutively  to  the  muscular  change  in  the 
heart  (Stokes),  and  perhaps  also  consecutively  to  the  disturbance  of  the 


DISEASES  OF  THE  ENDOCARDIUIH  415 

cardiac  innervation  (Peter).  These  pathological  characters  of  the  pulse  are 
revealed  by  the  sphygmograph. 

The  cardiac  arrhythmia,  perceptible  on  palpation  and  auscultation 
(G.  See),  is  therefore  characterized  by  irregular  beats.  This  arrhythmia  only 
shows  itself  at  an  advanced  period  of  the  disease  ;  it  is  sometimes  excessive 
and  is  a  kind  of  ataxia  of  the  heart.  Intermittences  have  been  divided  into 
true  and  false.  True  intermittence  affects  the  pulse  and  the  heart  at  the 
same  time,  the  arterial  pulsation  being  absent,  because  the  ventricular 
systole  is  lacking.  The  so-called  false  intermittence  would  be  better  named 
"  incomplete."  The  cardiac  systole  persists,  but  is  too  feeble  to  launch' 
a  sufficient  blood-wave,  and  the  arterial  pulsation  is  w^anting.  Bouillaud 
has  called  this  a  stumble  on  the  part  of  the  heart.  These  intermittences 
are  more  marked  in  insufficiency  than  in  stenosis,  because  part  of  the  blood- 
wave  passes  back  into  the  auricle  instead  of  the  whole  wave  entering  the 
aorta. 

Mitral  insufRciency  shows  itself  by  a  somewhat  rasping  systolic  murmur, 
which  may  be  of  a  musical  character  and  has  its  maximum  below  and 
external  to  the  nipple.  It  is  called  the  "  apical  murmur,"  in  opposition  to 
the  basal  murmurs,  which  are  situated  at  the  aortic  orifice.  Further,  the 
maximum  is  not  exactly  at  the  apex  of  the  heart,  but  rather  at  the  middle 
part  of  the  ventricle  and  at  the  level  of  the  valvular  vein  (Peter).  This 
murmur  is  sometimes  soft  and  analogous  to  a  bellows  murmur ;  at  other 
times  harsh  and  vibrating,  like  a  jet  of  steam.  It  is  propagated  towards 
the  axilla,  and  is  very  clear  behind,  between  the  scapulae. 

Mitral  stenosis  shows  itself  by  various  signs,  which  may  be  isolated  or 
associated  in  the  same  patient.  When  the  signs  are  complete,  and  the 
patient  has  not  arrhythmia,  we  find  a  special  rhythm  of  morbid  sounds. 
Analysis  shows  that  mitral  stenosis  may  be  characterized  by  a  diastolic 
murmur  (rare),  by  a  rumbhng  or  presystolic  murmur,  or  by  a  reduplica- 
tion of  the  second  sound,  while  the  second  portion  of  this  reduplication 
may  be  blowing. 

Mitral  lesions  are  often  accompanied  by  accentuation  of  tlie  second 
pulmonary  sound,  from  the  exaggerated  distension  which  the  pulmonary 
vessels  undergo.  The  coexistence  of  insufficiency  and  stenosis  is  shown  by 
the  simultaneous  presence  of  the  signs  indicated  under  each  of  these  lesions. 

Sometimes,  on  auscultation  of  a  patient  with  symptoms  of  mitral  disease, 
no  morbid  sound  is  heard,  and  the  physical  signs  of  the  lesion  only  reveal 
themselves  by  a  disturbance  of  tlie  cardiac  rhythm.  It  must  be  admitted 
in  such  a  case  that  myocarditis  is  the  chief  lesion,  and  that  the  valvular 
miscliicf  is  of  but  s1i<,fht  moment. 

Diagnosis — Prognosis.  I  n^jx^at  here  that  the  presence  of  a  munuiir  or 
of  a  reduplication  is  not  enough  to  prove  the  existence  of  a  mitral  lesion. 


416  TEXT-BOOK  OF  MEDICINE 

Some  reduplications  have  nothing  to  do  with  the  lesion  of  an  orifice.  Such 
are  the  normal  redupUcations  "  resulting  from  transitory  changes  which 
the  movements  of  respiration  cause  in  the  pressure  of  the  blood  contained 
in  the  heart  and  great  vessels  "  (Potain).  Certain  murmurs  do  not  depend 
upon  any  valvular  lesion.  Such  are  the  murmurs  of  chloro- anaemic  origin, 
the  febrile  murmurs,  and  the  blowing  sounds  of  extracardiac  origin, 
described  by  Potain.  It  has  been  said  that  the  murmur  of  mitral  in- 
sufficiency is  distinguished  from  other  non-organic  murmurs  in  that  it  alone 
is  heard  behind  between  the  inner  border  of  the  scapula  and  the  dorsal 
•spine.  This  is  true  with  regard  to  the  mitral  murmur  of  a  certain  intensity, 
but  this  distinction  loses  its  value  when  the  murmur  is  shght. 

The  form  of  mitral  disease  indicates  fairly  the  gravity  of  the  prognosis. 
Pure  insufficiency  or  constriction  is  less  serious  than  if  the  two  lesions  be 
associated. 

Intercurrent  diseases,  such  as  typhoid  fever,  eruptive  fevers,  influenza, 
and  pneumonia,  may  have  an  evil  influence  on  the  mitral  lesion,  since  they 
may  sometimes  graft  terrible  secondary  infections  upon  it.  I  would 
repeat  here  that  infective  endocarditis  usually  supervenes  in  patients  whose 
previously  affected  valves  present  a  locus  minoris  resistentiae.  Excess, 
fatigue,  worry,  and  pregnancy  have  a  deplorable  effect  upon  diseases  of  the 
heart.  It  is  opportune  to  recall  Peter's  aphorism  relative  to  women  suffering 
from  cardiac  lesions  :  "  Daughters,  no  marriage  ;  wives,  no  pregnancies ; 
mothers,  no  nursing." 

Treatment. — The  treatment  of  valvular  lesions  in  general  and  of  mitral 
lesions  in  particular  is  not  confined  to  the  lesion  of  the  orifice  or  of  the 
valves,  but  concerns  the  resulting  compfications  and  also  the  concomitant 
changes  hi  the  myocardium.  In  this'  section  I  am  deafing  only  with  the 
treatment  of  "  diseases  of  the  heart "  properly  so  called  ;  the  treatment  of 
cardio-aortic  lesions  will  be  given  later. 

We  have  just  seen  that  the  symptoms  consecutive  to  the  nutral  lesion 
only  appear  when  the  cardiac  muscle  is  worn  out.  As  long  as  the  muscle  is 
capable  of  facing  the  danger  and  the  compensation  is  sufficient,  all  is  well, 
or  nearly  so  ;  but  when  compensation  becomes  feeble,  compUcations  which 
in  nearly  all  cases  have  a  peripheral  origin — i.e.,  visceral  congestion  and 
oedema — then  appear. 

Imperfectly  compensated  valvular  lesions  lower  the  pressure  in  the 
cardio-arterial  system,  and  raise  it  in  the  venous  system  of  the  lesser  and 
greater  circulations.  Venous  stases  and  oedema  then  appear.  The  stases 
affect  the  lungs,  kidneys,  brain,  Uver,  etc.  ;  the  oedema  affects  the  cellular 
tissue  of  the  periphery  and  of  the  splanchnic  cavities,  the  organs  susceptible 
of  becoming  infiltrated  (lung,  brain),  and  the  serous  cavities  (pleura,  peri- 
cardium, and  meninges).     The  tendency  of  diseases  of  the  heart  is  therefore 


DISEASES  OF  THE  ENDOCARDIUM  417 

to  change  the  patient  into  a  kind  of  sponge  ;  liis  organs  are  saturated  with 
badly  circulating  blood,  while  his  connective  tissue  is  saturated  with  serous 
fluid.  In  such  a  medium  the  anatomical  elements  and  the  organs  partially 
lose  their  function. 

Whether  the  disease  shows  itself  by  shght  symptoms,  such  as  trifling 
dyspnoea,  malleolar  oedema,  and  palpitations  ;  whether  it  betrays  itself  by 
more  serious  compHcations,  such  as  orthopnoea,  hepatic  troubles,  ohguria, 
anasarca,  and  arrhythmia  ;  or  whether  it  finally  produces  the  symptom- 
complex  of  asystole,  the  therapeutic  indications  are  the  same.  It  remains 
to  be  seen  what  drugs  are  most  apt  to  answer  to  these  therapeutic  indications. 

Most  authorities  who  have  discussed  this  question  say  :  Since  the  troubles 
in  diseases  of  the  heart  arise  from  weakening  of  the  heart  muscle  and  from 
lowering  of  the  arterial  tension,  restore  the  tone  and  the  contractile  power 
of  the  heart  muscle,  and  at  the  same  time  you  will  raise  the  arterial  pressure. 
For  this  purpose  employ  cardiac  tonics.  Further,  as  the  lowering  of  the 
arterial  pressure  brings  about  the  elevation  of  the  venous  tension,  with 
oedema  and  congestion,  lower  this  venous  tension,  and  for  this  purpose 
employ  blood-letting,  purgatives,  and  diuretics. 

A  table  of  these  tonics  and  diuretic  medicines  has  been  drawn  up.  See 
has  published  several  excellent  papers  on  the  question  of  cardiac  drugs  and  of 
the  therapeutic  physiology  of  the  heart,  and  I  borrow  the  following  classifica- 
tion from  liis  ^\Titings  : 

Cardiac  tonics  :  Strophanthus,  strophanthin,  spartein. 

Diuretic  cardiac  tonics :  Digitalis,  digitalin,  Convallaria  majalis, 
convallaraarin. 

Diuretic  drugs  :   CafEein,  theobromin,  potash  salts,  lactose. 

Respiratory  drugs  :  Iodide  of  potash,  morphia. 

Our  patient  may  be  a  prey  to  arrhythmia,  dyspnoea,  and  oedema  ;  he 
may  be  in  a  condition  bordering  on  asystole  or  be  suffering  from  marked 
asystole.  What  medicine  is  to  be  given,  and  what  indications  are  to  be 
followed  ?  Is  strophanthin  superior  to  spartein  ?  is  spartein  superior  to 
digitahs  ?  and  is  not  the  latter  inferior  to  digitalin  ?  Is  theobromin 
superior  to  caflfein,  and  cafEein  superior  to  convallamarin  ?  I  think  that 
many  physiciaas  will  hesitate,  and  I  have  experienced  myself  the 
doubts  they  will  experience  in  making  a  choice.  Such  cardiac  tonics  as 
strophanthin  and  spartein  had  at  one  time  some  vogue,  in  Germany 
especially,  so  that  it  might  truly  be  said  that,  prior  to  the  discovery  of  these 
drugs,  the  therapeutics  of  diseases  of  the  heart  were  in  their  infancy. 
CafEein  and  theobromin  are  so  vaunted  by  some  clinicians  that  it  might 
be  said  that  before  the  discovery  of  those  drugs  we  could  not  cause  diuresis 
in  a  cardiac  patient,  I  have  closely  followed  the  action  of  tiicsc  drugs,  and 
I  have  succeeded  in  forming  a  clear  opinion  as  to  their  worth.     As  far  as 

27 


418  TEXT-BOOK  OF  MEDICINE 

I  am  concerned,  I  consider  that  the  famous  cardiac  tonics  are  often  medicines 
which  weaken  the  contractile  power  of  the  muscle  under  the  pretext  of  im- 
proving its  tone.  I  have  also  found  that  theobromin,  which  is  a  valuable 
diuretic  when  properly  handled,  sometimes  weakens  the  renal  function 
under  the  pretext  of  exciting  it.  I  am  very  far  from  contesting  the  worth 
of  these  drugs,  but  I  think  that  most  of  them  are  far  from  possessing  in 
asystole  the  value  of  digitahs,  when  it  is  well  prepared  and  properly  ad- 
ministered. Further,  as  I  have  neither  the  intention  nor  the  pretension  of 
undertaking  here  a  comparative  study  of  all  the  cardiac  drugs,  I  shall 
simply  give  the  results  of  my  experience,  and  point  out  the  treatment 
which  I  have  employed  for  several  years. 

Let  us  take  first  the  most  serious  case — namely,  a  patient  suffering  from 
symptoms  bordering  on  asystole  or  from  complete  asystole.  The  face  is 
pale  and  covered  with  sweat ;  the  conjunctivae  are  yellowish  ;  the  lips  and 
ears  are  bluish  ;  the  hands  are  swollen  and  cold,  and  the  fingers  cyanosed ; 
the  pulse  is  small  and  irregular  ;  oedema  has  invaded  the  feet,  legs,  thighs, 
genital  organs,  and  abdomen,  and  tends  to  spread  higher  ;  the  Uver  is  en- 
larged and  very  painful ;  respiration  is  panting,  interrupted  by  terrible 
attacks  of  suffocation,  and  asphyxia  appears  imminent.  The  patient 
seated  in  his  chair  or  resting  on  his  pillows,  dare  not  move  for  fear  of  suffoca- 
tion. For  a  month  he  has  not  gone  to  bed,  and  sleep  is  impossible,  save  for 
snatches.  The  urine  is  scanty  and  contains  much  sediment.  Auscultation 
of  the  heart  is  impossible  ;  auscultation  of  the  lungs,  thougli  difficult,  yet 
permits  recognition  of  rales,  due  to  oedema  and  pulmonary  congestion. 
Such  is  the  disease  :  what  is  the  remedy  ? 

I  think  we  must  consider  both  the  heart  and  the  periphery.  It  is  uni- 
versally said  that  the  condition  is  due  to  degeneration  of  the  muscular  fibre, 
which  must  be  given  fresh  energy  by  means  of  the  cardiac  tonics.  Letulle 
has  shown  that  the  muscular  degeneration  is  not  so  great.  If  the  heart 
is  weakened,  this  degeneration  plays  only  a  small  part.  I  am  convinced 
that  the  most  important  part  comes  from  the  peripheral  obstacles,  from  the 
blood  which  engorges  the  organs,  from  the  serous  fluid  wliich  impregnates 
the  superficial  and  the  splanchnic  cellular  tissue. 

In  the  presence  of  these  obstacles  the  heart  becomes  weakened  in  pumping 
on  the  blood-wave,  which  advances  with  difiiculty.  The  arterioles  fail  to 
help  it,  the  local  circulations  are  at  a  standstill,  and  all  the  functions  of  the 
economy  are  in  distress.  I  have  often  made  the  following  comparison  : 
When  a  cart  is  too  heavily  loaded  and  can  advance  no  farther,  the  team  will 
not  move  by  whipping  the  tired  horses,  but  it  will  do  so  if  we  Hghten  the 
load.  Similarly :  in  the  case  of  the  heart  the  desired  effect  will  not  be  ob- 
tained by  excessive  stimulation  of  its  already  weakened  muscle  ;  we  shall 
obtain  the  result  by  hghtening  its  work,  by  diminishing  the  excess  of  venous 


DISEASES  OF  THE  ENDOCARDIUM  419 

tension,  and  by  removing,  as  far  as  possible,  the  dam  produced  by  congestion 
and  oedema,  and,  above  all,  by  improving  the  tone  of  the  cardiac  muscle, 
which  is  often  rather  exhausted  than  degenerated. 

To  obtain  these  results  I  employ  in  a  fairly  systematic  fashion  the  follow 
ing  treatment : 

Six  leeches  are  apphed  to  the  precordial  and  hepatic  regions,  and  some 
5  or  6  ounces  of  blood  are  withdrawn.  I  cannot  too  strongly  recommend 
the  use  of  leeches,  which  is  far  too  much  neglected.  I  sometimes  prescribe 
two  or  three  leeches  over  the  heart  and  over  the  liver,  and  I  repeat  this 
treatment  several  days  in  succession,  with  great  benefit  to  the  patient. 

At  the  same  time  I  prescribe  digitahs  in  the  form  of  infusion  or  of 
Trousseau's  diuretic  wine.  The  drug  has  a  direct  cardio-vascular  action 
and  an  indirect  diuretic  action.  It  stimulates  the  tone  of  the  heart  and 
the  vasoconstriction  of  the  peripheral  arterioles. 

This  combined  action  restores  to  the  normal  the  inverted  current  of 
the  interstitial  exchanges.  The  arterioles  and  the  heart  muscle  combine 
their  energies  to  bring  about  a  squeezing  action  on  the  parenchymata  and 
the  connective  spaces.  Digitahs,  by  its  action  on  the  heart  and  the  vessels, 
restores  to  the  cardio-vascular  mechanism  the  functional  energy  wliich  was 
lacking,  and  as  Potain  says ;  "  It  is  also  an  indirect  diuretic,  which  causes 
the  fluid  of  dropsy  and  of  oedema  to  re-enter  the  circulation  and  be  eliminated 
by  the  kidneys." 

The  immediate  result,  as  Loeper  has  shown,  is  a  serous  plethora  of  the 
blood,  characterized  by  diminution  in  the  total  of  albumin  and  in  the  red 
corpuscles,  which  are  widely  scattered  through  an  increased  quantity  of 
fluid,  and  by  increase  of  the  chlorides  and  other  principles  wliich  have  accu- 
mulated in  the  tissues.  The  above  is  the  first  effect  of  digitalis,  and  iscalled  the 
blood  stage  (Loeper) ;  the  urinary  stage  at  once  follows,  and  polyuria  results. 
The  polyuria  varies  directly  with  the  amount  of  oedema  due  to  asystole ; 
it  often  assumes  the  guise  of  a  crisis  which  carries  off  in  the  urine  the  excess 
of  chlorides,  phosphates,  and  sulphates  in  the  tissues.  Improvement  then 
follows.  Digitahs  alone,  without  other  drugs,  may  yield  the  good  results  just 
mentioned.  I  feel,  however,  that  it  is  preferable  to  add  a  true  diuretic  which 
acts  on  the  kidney,  wliile  the  digitahs  acts  upon  the  heart  and  the  vessels. 

Trousseau's  diuretic  wine  is  a  diuretic  which  does  not  exhaust  the  kidney 
and  a  cardiac  tonic  which  does  not  exhaust  the  heart.     The  formula  is ; 


White  wine 
Alcohol  (90  per  cent.) 
Juniper  berries 
Acetate  of  potash 
Digitalis  leaves 
Sc^uill 


7  pints 
17  ounces 
12       „ 

7       „ 

-I       j> 

1       „ 


'>7 o 


420  TEXT-BOOK  OF  MEDICINE 

I  give  1  ur  2  tablespoonfuls  daily  for  five  or  six  days.     One  table 
spoonful  contains  3  grains  of  digitalis,  10  grains  of  acetate  of   potash,  15 
grains  of  jumper  berries,  and  IJ  grains  of  squill. 

We  must  note  that  Trousseau's  formula  has  been  altered,  and  that  the 
wine  in  the  Codex  and  hospital  formulae  contains  10  instead  of  3  grains  of 
digitaUs  in  a  tablespoonful.  A  physician  ignorant  of  this  incomprehensible 
change  would  thus  give  his  patient  a  far  larger  dose  than  he  intended. 
I,  therefore,  ask  for  a  return  to  the  classical  formula,  wliich  should  never 
have  been  tampered  with. 

For  the  diuretic  wine  we  may  substitute  infusion  of  digitalis  and  theo- 
bromin  given  together. 

Make  an  infusion  of  digitahs leaves,  15 grains  in  3f  ounces  of  boiling  water, 
filter,  and  add  8  drachms  of  syrup  of  currants.  Give  1  ounce  daily  for  a 
week  ;  stop  the  drug,  and  repeat  if  need  be.  At  the  same  time  theobromin 
is  given  in  daily  doses  of  7  grains. 

It  is  absolutely  necessary  for  the  patient  to  take  milk  as  a  food  and  as 
a  diuretic.  He  m.ay  take  it  to  his  hking  :  boiled  or  fresh,  hot,  cold,  or  iced. 
The  milk  should  be  given  every  two  hours  in  doses  of  3  or  more  ounces, 
according  to  the  tolerance  of  the  patient.  To  alter  its  taste  we  may  add 
orange-flower  water  or  a  spoonful  of  tea  or  of  coffee,  and  we"  may  aerate 
it  by  aid  of  the  sparklet.  If  the  milk  is  badly  digested,  lime-water  is 
added.  In  case  of  intolerance,  cow's  milk  is  stopped,  and  recourse  made 
to  goat's  or  to  ass's  milk,  kephir.  or  koumiss.  All  other  food  is  forbidden. 
Ices  made  with  coffee,  vanilla,  citron,  or  with  fruits  are  permitted. 

To  produce  active  diuresis,  I  give  lactose  dissolved  in  Evian  or  in  Vittel 
water.  When  lactose  is  simply  tlirown  into  the  water,  the  patient  com- 
plains of  the  mixture,  because  the  sugar  does  not  dissolve  well  in  cold  water. 
The  following  solution  must  therefore  be  made  :  The  lactose  is  first  dissolved 
in  a  small  quantity  of  hot  water,  and  the  solution  poured  into  a  bottle  of 
Evian  water,  from  which  an  equivalent  quantity  of  fluid  has  previously 
been  withdrawn.  We  have  then  a  drink  which,  although  not  disagreeable 
to  taste,  may  be  rendered  more  agreeable  by  the  addition  of  orange-juice, 
lemon- juice,  or  champagne.  A  cup  of  milk  and  a  cup  of  lactose  solution 
are  taken  alternately  every  one  or  two  hours. 

In  short,  leeches,  digitahs,  diuretics,  and  especially  Trousseau's  wine, 
are  used  almost  systematically  for  patients  who  come  into  hospital  with 
asystole,  or  in  a  condition  bordering  on  it.  My  cases  are  described  in  the 
hospital  records,  where  they  may  be  consulted,  and  I  may  say  that,  under 
this  treatment,  which  is  simple  and  easy,  success  is  the  rule  and  failure 
the  exception.  The  urine,  which  has  been  as  low  as  6  ounces  before  treat- 
ment, amounts  to  2  or  3  pints  after  a  few  days. 

A  patient,  for  example,  who  drinks  daily  4  pints  of  milk  and  2  pints  of 


DISEASES  OF  THE  ENDOCARDIIJIM 


421 


lactose  solution — that  is  to  say,  about  6  pints  of  fluid — sometimes  passes 
about  8  to  10  pints  of  urine.  The  urine  exceeds,  therefore,  the  fluid  ingested 
by  2  to  4  pints.  This  excess  comes  from  the  fluid  which  was  enmeshed  in 
the  form  of  oedema  in  the  superficial  and  in  the  splanchnic  cellular  tissue. 
When  care  is  taken  to  weigh  the  patient  daily,  and  to  measure  exactly  the 
quantity  of  the  fluid  ingested  and  of  the  urine  voided,  we  find  that  the  weight 
of  the  patient  diminishes  by  about  1  pound  per  pmt  of  urine  excreted  in 
excess.  In  a  case  of  anasarca  I  have  verified  the  fact  that  a  patient  may 
hold  20  to  30  pints  of  fluid  in  liis  cellular  tissue.  The  attention  is  as  a  rule 
only  evoked  by  superficial  oedema,  but  there  is  also  hidden  in  the  splanchnic 
cavities  oedema  which  escapes  notice  and  is  most  serious,  because  of  the 
embarrassment  it  causes  in  the  different  functions. 

The  subjoined  chart  shows  the  result  in  a  woman  who  was  moribund 
and  cyanosed.     The  amount  of  urine  was  about  3  to  4  ounces.     Under 


Weight  of 
the  Invalid 
in  Kilos 

60 
Z5 

^0 
65 
60 
55 

50 

Quantify  of 

Urine 
in  Litres. 

7 
6 
5 

2 

1 

Resuff  oStainee/  in\  16  eliPiys 

V 

s, 

^ 

v.. 

■^, 

T'  IK 

y 

> 

\ 

^ 

y^ 

x^ 

^.N 

y 

r 

V. 

>k, 

"^ 

^ 

\ 

y 

Y 

> 

^:. 

IN 

< 

fe^ 

^ 

,/ 

r 

\ii> 

^^< 

^S/'^-J 

es 

•* 

-^ 

^L 

'  ^//os 

Da''"'^'' 

21 

22 

23 

2a 

26 

26 

27 

26 

/ 

2 

3 

a 

5 

6 

7    6 

9 

rebruary                              March 

Fio.  19. — Weight  and  Ukine  Chart. 


treatment  the  improvement  was  so  rapid  as  to  be  a  brilliant  therapeutic 
success.  In  a  fortnight  she  passed  100  pints  of  urine,  and  as  the  anasarca 
disappeared,  she  lost  nearly  60  pounds  in  weight.  The  chlorides  at  the 
commencement  of  the  urinary  crisis  amounted  to  1  ounce. 

By  the  means  just  quoted  the  oedema  disappears,  the  visceral  congestion 
diminishes,  the  dyspnoea  improves,  and  the  heart-beats  become  regular. 
In  place  of  distress,  a  delightful  feehng  of  quiet  obtains,  movement  is  possible 
without  attacks  of  suffocation,  the  broncho-pulmonary  rales  tend  to  dis- 
appear, and  the  patient  can  he  down  in  bed  and  sleep. 

In  some  cases,  however,  disappointments  occur.  Some  patients  are 
refractory  to  treatment,  others  vomit  the  milk  and  solution  of  lactose,  no 
matter  what  we  do.  The  difficulty  is  surmounted  by  giving  iced  water  in 
small  amounts  and  by  enemata  composed  of  6  ounces  of  the  lactose  solution. 


422  TEXT-BOOK  OF  MEDICINE 

If,  after  some  days  of  the  above  treatment,  no  improvement  has  accrued, 
and  if  the  asystole  becomes  worse,  we  must  lessen  the  work  of  the  heart  and 
reheve  the  patient's  suffering  by  withdrawing  the  fluid  from  the  pleura  and 
the  peritoneum.  We  must  treat  the  oedema  of  the  limbs  and  genital  organs 
in  the  same  way,  and  provide  points  of  exit.  We,  therefore,  make  punctures, 
which  are  sometimes  followed  by  lymphangitis,  erysipelas,  or  patches  of 
gangrene,  in  spite  of  antiseptic  precautions,  or  else  we  apply  the  cautery 
once  or  twice  to  each  hmb  ;  Vienna  paste  makes  an  issue  which,  once  opened, 
acts  like  a  fountain.     In  urgent  cases,  however,  punctures  are  preferable. 

I  have  not  yet  spoken  of  morphia  or  of  heroin  ;  not  that  I  reject  their 
use — on  the  contrary,  I  think  that  they  are  excellent  adjuvants  in  severe 
dyspnoea,  but  they  should  be  prescribed  in  very  small  doses. 

I  must  now  mention  certain  accidents  which  may  occur  unless  the  case 
be  carefully  watched.  The  use  of  digitalis  or  digitalin,  even  in  small  doses, 
must  not  be  too  long  continued,  because  the  drug  may  be  cumulative,  and 
lead  to  sudden  asystole.  An  inexperienced  or  careless  physician  mistakes 
the  condition  for  obstinate  asystole,  and  goes  on  with  digitalis,  being  lucky 
if  he  does  not  increase  the  dose.  "  Characteristic  pallor  of  the  face  and 
general  coldness,  with  cyanosis,  are  signs  of  advanced  poisoning,  because 
they  indicate  vasoconstriction  due  to  the  predominant  action  of  the  sympa- 
thetic nerve.  Tachycardia,  arrhythmia,  and  pulsus  bigeminus  are  symptoms 
of  vasoparesis  ;  such  a  condition  is  asystole  due  to  digitalis  "  (Huchard). 

Another  matter  deserves  notice.  During  the  treatment  we  must  care- 
fully collect  the  urine  passed  in  the  twenty-four  hours,  and  watch  the 
parallel  diminution  in  the  weight  of  the  patient.  The  reason  is  :  Under 
treatment  the  oedema  may  be  in  part  absorbed,  without  increase  in  the  urine, 
or,  in  other  words,  the  blood  stage  is  not  followed  by  polyuria.  The  serous 
fluid  is  absorbed  and  enters  the  circulation,  but  it  is  not  eliminated  by  the 
kidneys  in  due  course.  Serous  apoplexy  may  then  follow,  as  pointed  out 
by  Andral.  The  symptoms  are  coma,  convulsions,  and  dehrium.  Cheyne 
Stokes  breathing  may  or  may  not  be  present.  We  must  add  that  these 
troubles  are  chiefly  to  be  feared  in  patients  whose  kidneys  are  abeady 
affected.  In  any  case,  we  see  the  reason  for  associating  with  the  digitahs 
a  true  diuretic  in  order  to  favour  the  urinary  as  well  as  the  blood  stage. 

In  addition  to  the  troubles  above  noted,  the  patient  may  be  seized  with 
syncope  and  dyspnoea,  which  seem  to  herald  early  death.  We  may  then  ask 
whether  sudden  dilatation  of  the  heart  does  not  comphcate  an  already 
dangerous  situation.  In  this  case  cardiac  drugs  must  be  handled  with 
extreme  care.  Perhaps  it  is  better  to  omit  them.  It  has  long  been  my 
practice  to  place  an  ice-bag  over  the  heart,  and  patients  feel  such  reHef 
that  they  will  not  dispense  with  it.  Oxygen  should  be  given  in  large  doses. 
Ehxir  of  mate  may  be  given  in  drachm  doses.     Injections  of  oil  of  camphor 


DISEASES  OP  THE  ENDOCARDIUM  423 

are  useful,  and  strychnine  may  be  given  in  the  same  way  once  or  twice 
daily. 

When  the  patient  has  got  over  his  asystole,  when  the  excess  of  chlorides 
has  been  eliminated  in  the  urine,  when  the  dyspnoea,  anasarca,  and  ar- 
rhythmia are  better,  he  must  not  be  considered  as  cured,  for  the  cardiac 
lesion  persists,  and  may  at  a  given  moment  reproduce  the  same  effects.  For 
several  weeks  to  come  he  should  take  only  milk,  or  milky  foods,  eggs,  stewed 
fruit,  and  a  httle  bread.  Salt  (chloride  of  sodium)  should  be  proscribed, 
for  we  know  that  it  favours  the  production  of  oedema  (Widal,  Merklen). 
Alcoholic  drinks  and  tobacco  should  always  be  forbidden.  Local  treatment 
should  not  be  neglected.  It  consists  in  an  appUcation  of  Vienna  paste  to 
the  cardiac  region,  and  the  issue  is  allowed  to  suppurate  freely. 

Such  is  the  treatment.  It  often  dispenses  with  other  cardiac  tonics, 
such  as  strophanthin  and  spartein.  It  proves  clearly  that  in  the  cardiac 
Btorm  which  we  call  asystole  the  true  danger  lies,  not  only  in  the  heart,  but 
in  every  organ  and  at  the  periphery,  where  congestion  and  oedema  occur. 
The  proof  that  the  heart  is  worn  out  rather  than  degenerated  is  that,  when 
the  storm  is  over,  it  resumes  its  functions,  and  may  do  so  sometimes  for 
months  and  years  before  it  becomes  again  enfeebled.  We  see  daily  such 
cases  in  hospital. 

Amongst  other  examples  I  would  quote  the  case  of  a  moribund  woman  treated  in 
this  manner.  In  spite  of  her  mitral  lesion,  she  has  since  remained  in  a  very  satisfactorj' 
state  of  health.  I  would  mention,  top,  the  case  of  a  blacksmith,  also  cured  of  asystole 
for  four  years.  In  spite  of  a  mitral  lesion,  he  has  been  able  to  carry  on  his  heavy  work 
without  any  fresh  mishap.  He  reports  himself  at  the  hospital  every  four  or  five  months 
for  a  fresh  issue  to  be  made,  because,  he  says,  when  the  counter-irritation  no  longer  acts, 
he  experiences  slight  dyspncea  and  palpitation,  which  improve  when  the  free  issue  is 
employed.  I  have  thus  seen  a  large  number  of  asystolic  patients  resume  their  business 
for  years. 

The  attentive  study  of  all  these  cases  has  inspired  me  with  some  thoughts 
on  the  subject  of  prognosis  in  diseases  of  the  heart.  When  we  have  seen 
a  certain  number  of  cardiac  patients  triumph  once  or  several  times  over  the 
asystolic  storms,  and  practically  resume  their  work,  we  say  that  the  mitral 
disease  is  too  often  considered  as  a  very  grave  malady  of  almost  fatal  ter- 
mination, but  it  does  not  possess  such  a  gloomy  prognosis.  The  heart  is 
a  gallant  organ  ;  it  is  the  idtimum  moriens.  We  have  slandered  it  a  little, 
since  we  have  been  willing  to  assign  too  large  a  part  to  the  lesions  of  its 
vessels  and  its  myocardium.  We  must  treat  it  carefully  when  it  is  sick, 
assist  it  when  its  work  is  too  difficult,  but  we  must  avoid  forcing  and  weaken- 
ing it  with  cardiac  tonics. 

I  have  just  discussed  the  treatment  during  asystole,  but  what  treat- 
ment should  be  used  when  the  patient  only  complains  of  dyspnoea,  oedema, 
or  of  cardiac  angina  ?    In  the  first  place,  I  recommend  the  treatment  which 


424  TEXT-BOOK  OF  MEDICINE 

I  have  just  indicated,  for  it  succeeds  the  better  and  quicker  the  less  pro- 
nounced the  comphcations.  If  dyspnoea  is  the  cliief  symptom,  we  may 
also  employ  iodide  of  potash,  which  is  given  in  doses  of  10  grains  in  the 
twenty-four  hours. 

Lastly,  at  the  onset  of  the  mitral  disease,  if  there  is  no  notable  com- 
plication, and  if  the  disease  only  shows  itself  by  palpitation,  subcrepitant 
rales  from  pulmonary  oedema,  slight  dyspnoea,  or  some  oedema  over  the 
malleoli,  the  physician  should  not  remain  inactive,  but  should  foresee  and 
prevent  the  more  serious  complications,  and  attempt  to  stop  the  progress 
of  the  disease.  It  is  useful  to  produce  in  the  precordial  region  an  issue 
which  is  allowed  to  suppurate,  and  which  is  renewed  if  there  is  occasion. 

Heavy  meals,  alcoholic  drinks,  and  the  use  of  tobacco  should  be  forbidden. 
The  professions  which  entail  excitement,  such  as  gambhng  and  the  Stock 
Exchange,  furnish  a  marked  proportion  of  cardiac  cases.  Peter  has  seen 
many  politicians  in  whom  the  disease  made  rapid  progress.  A  life  free  from 
excitement  and  fatigue  should  be  advised  in  these  cases,  and  conduces  to 
longevity.  I  employ  the  above  treatment  in  a  systematic  manner,  but  I 
do  not  mean  that  other  treatment  may  not  give  good  results.  Thus,  digitalis 
may  be  given  as  a  tincture  or  maceration. 

Digitalin  is  prescribed  by  Potain  in  an  alcohohc  solution  (Nativelle's 
crystaUized  digitahn,  or  Homolle's  digitalin),  of  which  25  drops  corre- 
spond to  a  demimilhgramme.  This  drug  is  taken  at  one  dose  in  a  little 
water,  and  three  or  four  days  should  elapse  before  administering  a  fresh  dose. 

The  oily  solution  of  Nativelle's  digitalin  may  be  given  by  subcutaneous 
injection  in  doses  of  |  milhgramme  per  cubic  centimetre. 

Strophanthus  is  chiefly  indicated  as  a  cardiac  tonic.  It  does  not  slow 
the  heart-beats,  but  it  raises  the  contractile  power  of  the  myocardium. 
Five  to  twenty  drops  of  the  tincture  are  given.  Caffein  may  be  given  in 
daily  doses  of  from  7  to  30  grains,  either  in  solution  or  by  hypodermic 
injections. 

IjL  Distilled  water       . .  . .  . .  . .     5iii. 

Benzoate  of  soda  . .  . .  . .  . .     3i. 

Caffein     . .  , .  .  . .  . .     3i. 

A  Pravaz  syringe  of  this  solution  contains  3  grains  of  caffein. 
That  excellent  diuretic  theobromine  is  given  in  cachets,  in  doses   of 
from  7  to  15  grains.     The  dose  is  increased  or  repeated  if  necessary. 


DISEASES  OF  THE  ENDOCARDIUM  425 

V.  AORTIC  ORIFICE— INSUFFICIENCY  AND  STENOSIS. 

Aortic  insufficiency  is  present  when  the  sigmoid  valves  which  normally 
close  the  orifice,  in  order  to  prevent  the  backward  flow  of  blood,  do  not 
sufficiently  plug  it  to  prevent  the  blood  from  flowing  back  into  the  left 
ventricle.  Aortic  stenosis  occurs  when  the  lumen  of  the  orifice  no  longer 
has  its  normal  dimensions. 

The  aortic  orifice,  from  its  situation,  participates  in  lesions  of  the  aorta 
more  than  in  other  lesions  of  the  heart.  Thus,  inflammations  of  the  aorta 
and  their  most  usual  causes,  especially  syphilis,  are,  more  often  than  rheu- 
matic endocarditis,  the  origin  of  lesions  at  the  aortic  orifice.  According 
to  circumstances,  the  lesions  are  sometimes  those  of  chronic  aortitis,  at  other 
times  those  of  chronic  endocarditis.  Aortic  insufficiency  and  stenosis  are 
often  combined.  These  lesions  are  due  to  adhesions,  deformities  of  the 
sigmoid  valves,  vegetations,  or  calcareous  incrustations  of  the  valves  or  of 
the  walls.  Pure  insufficiency  is  frequently  associated  with  enlargement 
of  the  aorta,  which,  in  its  dilatation,  pulls  on  the  walls  of  the  orifice. 

The  stenosis  is  not  always  exactly  at  the  orifice.  Subaortic  narrowing 
(Vulpian,  Peter),  arising  from  the  contraction  of  the  portion  which  is  just 
in  front  of  the  opening  of  the  aorta,  has  been  described. 

Lesions  of  the  aortic  orifice,  and  especially  insufficiency,  cause  enormous 
hypertrophy  of  the  heart,  in  which  the  left  ventricle  takes  so  large  a  part 
(bovine  heart).  This  hypertrophy,  called  providential,  depends  upon  the 
hyperactivity  of  the  heart  muscle  ;  part  of  the  blood- wave  flows  back  into 
the  left  ventricle,  and  hypertrophy  takes  place  because  the  work  is  ex- 
aggerated. 

Examination  of  the  Heart  and  the  Pulse — 1.  Aortic  Insufficiency. 
— In  aortic  insufficiency  the  precordial  bulging  and  dullness  are  more 
extensive  than  in  mitral  lesions.  The  impulse  may  be  diffuse  and  the  apex- 
beat  is  in  the  sixth  or  seventh  space.  The  pulse  is  characteristic,  being 
regular,  bounding  (Corrigan)  and  falling  (Stokes) :  bounding,  because  the 
blood  is  violently  propelled  by  the  hypertrophied  ventricle  ;  faUing,  because 
the  pulse  vanishes  directly  after  the  beat,  the  aortic  blood-wave  being  pro- 
pagated in  two  directions  at  the  same  time — towards  the  periphery  and 
towards  the-  ventricle.  These  characters  are  seen  in  the  sphygmographic 
tracing  ;  the  line  of  ascent  is  sudden,  because  of  the  hypertrophy  of  tlie  ven- 
tricle, and  ends  in  a  notch,  wliich  coincides  with  the  return  wave  into  tlio 
ventricle.  The  force  of  the  systole  communicates  itself  to  the  great  arteries  ; 
their  pulsations  are  exaggerated,  and  often  yield  a  thrill.  It  is  in  aortic 
insuificiency  that  we  see  best  the  changes  of  colour  under  the  nails,  iso- 
chronous with  the  cardiac  systole.  This  phenomenon  has  been  called  the 
capillary  pulse. 


426  TEXT-BOOK  OF  MEDICINE 

We  hear  in  the  second  right  intercostal  space  a  diastolic  murmur,  due 
to  the  propagation  of  a  part  of  the  blood-wave  toward  the  left  ventricle. 
Tliis  diastolic  murmur  is  heard  in  the  great  vessels  of  the  neck  and  limbs. 
Thus,  when  the  stethoscope  is  applied  over  the  femoral  artery,  two  murmurs 
(double  crural  murmur)  are  heard  at  the  point  compressed — a  "  souffle 
d'aller,"  which  is  not  pathological,  but  due  to  the  vibration  of  the  blood- 
wave  launched  from  the  heart ;  and  a  reflux  murmur,  which  is  much  softer, 
and  due  to  the  vibration  of  the  blood- wave,  which  tends  to  flow  backwards. 
In  order  that  the  reflux  murmur  may  be  produced,  the  artery  must  be 
firmly  compressed  by  the  stethoscope,  but  not  too  much.  The  second 
murmur  is  sometimes  replaced  by  a  tone  which  has  the  same  value 
(Skoda). 

The  theory  of  flux  and  reflux  in  the  arteries  is  hardly  admitted  to-day. 
The  reflux  remains  absolutely  true  for  the  return  of  the  blood- wave  from  the 
aorta  into  the  left  ventricle,  but  the  backward  return  of  the  column  of 
blood  does  not  continue  in  the  arteries.  It  is  rather  admitted  that  the 
phenomena  described  above  result  from  the  lowering  of  the  arterial  tension, 
which  induces  an  exaggeration  in  the  vibrations  of  the  artery  and  a  rapidity 
of  the  waves  (Potain). 

The  reflux  murmur  and  the  water-hammer  pulse,  which  are  sometimes 
so  clear  in  pure  insufficiency,  are  naturally  less  marked  if  stenosis  is  also 
present,  because  the  blood- wave  no  longer  finds  so  free  a  passage.  Ausculta- 
tion at  the  aortic  orifice  also  reveals  the  disappearance  or  the  diminution 
of  the  second  sound,  which  normally  is  due  to  the  closure  of  the  sigmoid 
valves. 

2.  Aortic  Stenosis. — In  aortic  stenosis  hypertrophy  of  the  ventricle 
is  also  very  pronounced,  but  the  pulse  is  small,  and  shows  in  the  sphygmo- 
graphic  tracing  an  inclined  up-stroke,  because  the  blood-wave  passes  in  a 
threadlike  stream  through  the  constricted  orifice.  Auscultation  in  the 
second  right  space  reveals  a  systolic  murmur,  which  is  harsh  and  vibrating. 
This  murmur  is  propagated  into  the  great  vessels  which  arise  from  the  aorta, 
and  often  extends  along  the  descending  aorta  to  the  interscapular  region. 

General  Symptoms. — These  appear  more  slowly  than  those  of  mitral 
lesions,  because  aortic  lesions  are  better  compensated  by  the  hypertrophy 
of  the  left  ventricle,  and  because  they  have  a  less  direct  reaction  upon  the 
pulmonary  and  the  general  circulation.  The  patient  looks  anaemic,  because 
the  blood  in  part  returns  into  the  ventricle  and  does  not  all  reach  its  destina- 
tion. He  is  also  affected  by  cerebral  congestion,  due  to  the  exaggerated 
ventricular  contractions,  and  shown  by  epistaxis,  pulsations  in  the  tem- 
poral arteries,  dizziness,  ringing  in  the  ears,  etc. 

Some  patients  complain  of  angina  pectoris,  and  are  liable  to  faint.  In 
this  case  the  lesion  of  the  aortic  orifice  is  accompanied  by  aortitis,  and 


DISEASES  OF  THE  ENDOCARDIUM  427 

the  symptoms  of  aortitis  are  associated  with  those  due  to  the  insufficiency 
and  the  stenosis  (Peter). 

The  aortic  lesions  remain  a  local  malady  much  longer  than  the  mitral 
lesions,  and  it  is  only  at  a  remote  date  (degeneration  of  the  muscular  fibre 
or  mitral  comphcations)  that  the  invasion  of  the  economy  becomes  general — • 
that  congestion,  cedema,  and  the  symptoms,  which  precede  or  accompany 
asystole,  appear. 

The  patient  may,  however,  be  carried  off  suddenly  before  this  stage. 
Sudden  death  is  a  fairly  common  termination  in  aortic  lesions  (Aran, 
Mauriac),  while  it  is  exceptional  in  mitral  disease.  Writers  have  attributed 
it  to  endarteritis  obhterans,  insufficiency  of  circulation  in  the  coronary 
arteries  (Mauriac),  and  angina  pectoris,  which  is  often  associated  with  the 
aortic  lesions  (Peter). 

Treatment. — We  cannot  produce  much  action  on  the  lesions  of  the 
aortic  orifice.  The  cardiac  erethism  should  be  quieted  by  local  (leeches, 
cupping,  ice-bags)  or  general  treatment.  The  iodides  are  absolutely 
indicated.  We  shall  see  in  subsequent  chapters  the  treatment  for  lesions 
of  the  aortic  orifice  associated  with  aortitis  or  sypliilis. 

VI.  THE  TRICUSPID  ORIFICE— INSUFFICIENCY  AND 
STENOSIS. 

.flStiology. — Inflammatory  changes  in  the  tricuspid  valve  are  somewhat 
rare,  except  in  foetal  hfe.  They  nearly  always  affect  the  valves  on  both 
sides  of  the  heart.  Duroziez,  however,  maintains  that  they  are  less  rare 
than  is  generally  believed.  The  fibrous  and  atheromatous  lesions  of  chronic 
endocarditis  do  not  often  attack  the  right  heart.  On  the  other  hand, 
tricupsid  insufficiency  is  often  the  result  of  a  mechanical  cause — namely, 
dilatation  of  the  right  ventricle.  By  reason  of  the  exaggerated  blood- 
pressure  which  occurs  in  chronic  diseases  of  the  lung,  or  in  mitral  lesions, 
the  right  ventricle  allows  itself  to  be  distended.  It  also  becomes  distended 
through  dystrophy  of  its  muscular  fibres,  with  or  %vithout  adhesions  to  tlie 
pericardium  and  the  pleura,  and  drags  with  it  the  insertion  zone  of  the 
tricuspid  valve,  which  becomes  incompetent.  Some  authorities,  on  the 
other  hand  (Potain  and  Rendu),  refer  this  insufficiency  to  the  increase  in 
the  capacity  of  the  right  ventricle.  The  direction  of  the  ventricular  pillars 
is  altered  ;  the  chordae  tendinese  are  not  long  enough  to  permit  the  closure 
of  the  valves,  and  functional  insufficiency  results.  Dilatation  of  the 
fibrous  ring,  correctly  speaking,  is  quite  exceptional. 

Reflex  spasm  of  the  pulmonary  vessels  (Potain  and  Franck)  arising 
from  gastro-hcpatic  affections  leads  to  dilatation  of  the  right  ventricle  and 
fimctional  insufficiency  of  the  tricuspid  valve.     Lastly,  acute  and  chronic 


428  ■  TEXT-BOOK  OF  MEDICINE 

myocarditis  and  cardiac  degenerations  may  end  in  like  manner,  by  favouring 
paresis  of  the  right  ventricle. 

Pathological  Anatomy. — In  cases  of  inflammatory  insufficiency  the 
lesions  are  analogous  to  those  of  the  mitral  valves,  and  do  not  therefore 
require  further  details.  In  functional  incompetence  the  valves  are  healthy, 
but  the  size  of  the  right  auriculo-ventricular  orifice  and  ventricle  is  much 
increased.  The  ventricular  walls  are  rather  dilated  than  hypertrophied  in 
insufficiency  of  inflammatory  origin.  The  right  auricle  is  dilated,  and  its 
walls  are  thinned.  The  venae  cavse  and  the  jugular  veins  are  always  much 
distended  with  blood.  As  regards  the  chief  viscera,  such  as  the  Hver  and 
kidney,  more  or  less  marked  signs  of  blood-stasis  are  present. 

Description. — Tricuspid  insufficiency  is  characterized  by  a  systolic 
murmur,  with  its  maximum  at  the  xiphoid  cartilage,  while  its  tone  is  deeper 
and  less  whistHng  than  that  of  mitral  incompetence.  As  the  tricuspid 
valve  is  the  "  regulator  of  the  venous  circulation  and  of  the  general  venous 
tension  "  (Raynoud),  we  must  look  for  the  cliief  symptoms  of  this  lesion 
in  the  venous  system. 

Jugular  pulsation  first  attracts  attention.  On  inspection  and  with  the 
sphygmograph,  the  external  jugular  vein  shows  an  expansion  and  retraction, 
which  is  known  as  the  venous  pulse,  and  is  explained  in  the  following 
manner  :  During  the  systole,  part  of  the  blood- wave  flows  back  into  the  right 
ventricle,  and  thence  into  the  venous  system.  This  pressure  causes  dilata- 
tion of  the  veins,  and  the  valves  of  the  external  jugular  veins  become  in- 
competent. Accordingly,  at  each  ventricular  systole  the  blood  flows  back 
into  the  venous  system,  and  the  jugular  veins  show  a  true  systolic  and 
sometimes  dicrotic  venous  pulse,  synchronous  with  the  double  auricular 
and  ventricular  systole. 

The  reflux  of  blood  in  the  inferior  vena  cava  and  the  portal  vein  causes 
hepatic  pulsations,  which  may  be  felt  on  palpation. 

The  venous  pulse  may  be  present  in  the  veins  of  the  periphery,  especially 
in  the  saphenous  veins,  when  they  are  varicose. 

We  know  the  gravity  of  tricuspid  lesions,  for  "  they  form  the  bond  of 
union  between  lesions  of  the  lesser  and  the  greater  circulation  "  (Peter). 
Tricuspid  insufficiency  opens  the  door  to  asystole  (Raynaud)  ;  so  that 
the  murmur  has  been  rightly  called  the  symptomatic  murmur  of  asystole 
(Parrot). 

When  equilibrium  has  been  restored  by  appropriate  treatment,  the 
asystole  disappears  temporarily  or  finally,  and  with  it  the  functional  in- 
sufficiency. The  latter  may  appear  and  disappear  several  times  before 
being  finally  established.  The  disappearance  and  reappearance  of  the 
characteristic  signs  will  serve  as  a  guide  in  this  respect. 

In  some  cases  tricuspid  insufficiency  is  certainly  beneficial.      It  may 


DISEASES  OF  THE  ENDOCARDIUM  429 

eliminate  or  diniiiiish  the  excess  of  pressure  in  the  lesser  circulation, 
and  thus  prevent  vascular  ruptures.  Indeed,  the  general  condition  some- 
times improves  on  the  appearance  of  insufficiency.  Hence  the  tricuspid 
valve  has  been  called  the  safety-valve  of  the  pulmonary  circulation. 

Stenosis. — -Tricuspid  stenosis  may  be  congenital  or  acquired. 

Congenital  stenosis  is  due  to  foetal  endocarditis  or  to  faults  of  development. 

Acquired  stenosis  is  due  to  the  adhesion  of  the  valves,  to  stenosis  of  the 
tricuspid  orifice,  or  to  obstruction  of  this  orifice  by  vegetations.  Adhesions 
between  the  valves  is  the  most  usual  cause,  both  before  and  after  birth 
(Leudet).  Perforation  of  the  septa  and  stenosis  of  the  pulmonary  artery 
are  frequent  comphcations. 

Acquired  stenosis  is  chiefly  seen  in  women.  It  is  usually  due  to  rheu- 
matism, and  nearly  always  coincides  with  stenosis  of  the  mitral  or  other 
orifice.  The  chief  symptoms  are  cyanosis,  ascites,  oedema,  and  curving  of 
the  nails.  The  venous  pulse  in  the  jugular  veins  is  often  absent,  and  a 
diastolic  shock,  with  or  without  thrill,  is  found. 

The  prognosis  is  very  grave,  and  death  usually  occurs  between  the  ages 
of  twenty  and  twenty-five  years.  The  diagnosis  is  possible  when  stenosis 
of  the  tricuspid  orifice  occurs  without  lesions  of  other  orifices. 

VII.  PULMONARY  ARTERY— STENOSIS  AND  INSUFFICIENCY. 

Stenosis  of  the  pulmonary  ar-tery  may  be  congenital  or  acquired. 

Congenital  stenosis  usually  involves  the  sigmoid  valves,  which  are 
adherent  and  enclose  a  more  or  less  narrow  cleft.  As  they  are  in  close 
apposition,  they  obstruct  the  reflux  of  blood  into  the  right  ventricle.  Hence 
insufficiency  associated  with  congenital  stenosis  is  rare.  In  some  cases 
the  stenosis  affects  the  infundibulum,  and  has  been  called  "  prearterial " 
(C.  Paul).  The  valves  are  often  affected  in  such  cases.  The  stenosis  may 
involve  the  trunk  of  the  artery  in  exceptional  cases.  Acquired  stenosis, 
wliich  is  more  frequent  than  is  supposed,  nearly  always  affects  the  valves, 
but  cases  of  atheroma  and  of  gummata  (Schwalbe)  affecting  the  pulmonary 
artery  and  causing  constriction  have  been  pubhshed.  Apart  from  such 
exceptional  cases,  acquired  stenosis  of  the  valves  often  accompanies  dilata- 
tion of  the  pulmonary  artery  beyond  the  obstruction,  thus  forming  an 
exact  opposite  to  the  condition  in  aortic  stenosis.  Arterial  dilatation  is 
not  seen  in  cases  of  congenital  stenosis. 

The  right  ventricle  is  always  hypertrophied  and  dilated.  In  congenital 
cases  we  often  see  perforation  of  the  interventricular  or  interauricular 
septum,  and  sometimes  persistence  of  the  ductus  arteriosus.  Tiiis  perfora- 
tion may  also  be  seen  in  cases  of  acquired  stenosis  (C.  Paul)  resulting  from 
myocarditis,  wliich  often  accorapames  endocarditis  of  the  right  heart. 


430  TEXT-BOOK  OF  MEDICINE 

Congenital  stenosis  is  certainly  of  inflammatory  origin,  but  the  cause 
of  foetal  endomyocarditis  is  generally  obscure.  In  adults  rheumatism, 
perhaps  also  traumatism,  and  especially  infectious  diseases,  such  as  the 
eruptive  fevers,  puerperal  conditions,  broncho-pneumonia,  etc.,  have  been 
held  responsible. 

Stenosis  of  the  pulmonary  artery  may  long  pass  unnoticed.  In  other  cases 
the  patient  soon  becomes  breathless,  and  hable  to  frequent  fits  of  coughing, 
which  may  be  accompanied  by  bloody  sputum.  Chilliness  of  the  extremities 
and  sensations  of  numbness  and  anaesthesia  in  the  hmbs  are  common. 
Cyanosis  is  much  less  constant,  and  its  mechanism  has  received  a  different 
interpretation  (see  Morbus  Caeruleus).  It  often  appears  at  an  advanced 
period  of  the  disease,  or  as  the  result  of  some  broncho-pulmonary  complication. 

On  auscultation,  stenosis  of  the  pulmonary  artery  is  characterized  by 
a  systohc  murmur,  which  is  loudest  in  the  second  intercostal  space,  and  can 
be  traced  towards  the  clavicle.  Palpation  sometimes  reveals  the  existence 
of  a  systolic  thrill  at  the  same  spot,  and  percussion  shows  more  or  less 
hypertrophy  of  the  right  ventricle. 

The  sufferer  rarely  reaches  adult  age.  Death  frequently  results  from 
progressive  asystole  or  from  syncope,  but  the  striking  fact  is  that  pulmonary 
stenosis  appears  to  favour  the  development  of  phthisis  in  some  cases. 

Insufficiency  of  the  pulmonary  artery  rarely  exists  alone,  especially 
when  it  is  congenital.  It  is  nearly  always  associated  with  stenosis.  In  the 
acquired  form  it  results  from  the  same  causes  as  stenosis. 

It  is  characterized  by  a  diastolic  murmur,  wliich  is  loudest  in  the  second 
left  space,  and  can  be  traced  along  the  left  border  of  the  sternum.  Functional 
troubles,  chiefly  in  the  lesser  circulation,  are  present,  and  comprise  dyspnoea 
and  frequent  haemoptysis.  It  is  often  accompanied  by  hypertrophy  and 
dilatation  of  the  right  ventricle,  and  ends  in  death  from  asystole.  On  the 
other  hand,  the  development  of  tubercles  in  the  lung  is  exceptional  when 
there  is  no  coexistent  stenosis. 

VIII.  MORBUS  CiERULEUS— CYANOSIS. 

This  disease,  which  is  most  common  in  early  life,  is  characterized  by  a 
bluish  colour  of  the  skin  and  the  mucous  membranes,  with  dyspnoea,  attacks 
of  suffocation,  torpor,  inertia,  and  tendency  to  chilhness.  These  symptoms 
result  from  cardiac  and  vascular  lesions,  which  bring  about  the  mixture- of 
the  arterial  and  venous  blood,  and  do  not  allow  the  venous  blood  to  be 
sufficiently  arterialized. 

Pathology. — The  mixture  of  arterial  and  venous  blood  results  from 
abnormal  communication  between  the  arterial  and  venous  systems,  and  the 
abnormahties  which  make  this  communication  possible  affect  the  heart  and 


DISEASES  OF  THE  ENDOCARDIUM  431 

great  vessels.  The  abnormalities  of  the  heart  are  represented  by  the 
persistence  of  Botallo's  foramen  (52  out  of  69  cases,  Gintrac),  by  communica- 
tion between  the  two  ventricles  (33  cases,  Guillon),  and  by  fusion  of  the  cardiac 
cavities,  so  that  the  heart  may  show  only  one,  two,  or  three  cavities.  The 
vascular  abnormalities  comprise  abnormal  origin  of  the  vessels  and  per- 
sistence of  the  ductus  arteriosus  (30  cases,  Almagro).  Most  of  these  mal- 
formations are  congenital,  and  apparently  due  to  arrested  development  of 
the  heart,  to  endocarditis,  and  especially  to  stenosis  of  the  pulmonary 
artery  arising  during  intra-uterine  life. 

Raynaud  says  of  this  mechanism :  "  When  pulmonary  stenosis  is 
present,  the  consecutive  changes  in  the  heart  are  perfectly  intelUgible. 
The  right  ventricle  hypertrophies,  because  the  obstruction  demands  increased 
work,  but  the  dilatation  is  slight  or  absent,  because  the  imperfect  septum 
allows  blood  to  flow  back  into  the  left  cavities.  The  formation  of  the 
septum  becomes  arrested  as  a  result  of  the  reflux  in  question.  If  the  lesion 
has  arisen  before  the  development  of  the  ventricular  septum — that  is  to 
say,  before  the  end  of  the  second  month — -the  two  ventricles  continue  to 
communicate  with  one  another,  and  the  communication  is  the  larger,  as 
the  pulmonary  artery  remains  closed  at  a  time  more  closely  approaching 
that  of  conception.  If,  on  the  other  hand,  the  ventricles  are  already  shut 
off  from  one  another  when  obhteration  of  the  pulmonary  artery  takes  place, 
the  flow  of  blood  from  the  right  auricle  into  the  corresponding  ventricle  is 
prevented,  a  powerful  current  is- established  from  the  right  to  the  left  side 
of  the  auricular  chamber,  and  Botallo's  foramen  remains  open.  As  the 
aorta,  howevei,  is  from  this  time  the  only  channel  open  to  the  blood-stream, 
the  blood  can  only  reach  the  lungs  through  the  ductus  arteriosus,  which 
therefore  persists  after  birth  as  a  permeable  tube." 

These  lesions,  however,  although  they  allow,  more  or  less,  the  mingling 
of  arterial  and  venous  blood,  do  not  always  cause  symptoms  of  morbus 
caruleus.  Indeed,  there  are  many  examples  (Gelau,  Longhurst)  showing 
that  excellent  health  and  absence  of  cyanosis  have  for  many  years  been 
compatible  with  the  mixing  of  the  arterial  and  venous  blood.  Another 
factor  is  therefore  reqilired  to  produce  morbus  caeruleus,  and  the  lesions 
most  favourable  to  tliis  result  are  those  wliich  do  not  allow  the  mixed  blood 
to  be  properly  oxygenated  in  the  lung. 

Examination  of  the  blood  has  shown  an  increase  in  the  number  of  red 
corpuscles  (hyperglobulia),  which  may  reach  8,000,000  or  more.  This 
hyperglobulia  is  often  accompanied  by  an  increase  in  the  diameter  of  the 
red  corpuscles  (Vaquez).  These  phenomena  have  been  compared  to  the 
hyperglobulia  of  higli  altitudes,  and  have  also  been  looked  on  as  a  means  of 
defence  on  the  part  of  the  organism,  which  seeks  to  obtain  compensation 
for  the  difficulty  in  oxygenation  of  the  blood. 


432  TEXT-BOOK  OF  MEDICINE 

Description. — The  bluish  coloration  is  most  marked  in  the  lips,  the 
nostrils,  the  lobes  of  the  ears,  the  ends  of  the  fingers  and  toes,  and  the 
mucous  membrane  of  the  tongue  and  pharynx.  The  cyanosis  is  not  always 
of  the  same  intensity,  and  diminishes  during  sleep  or  after  a  long  rest,  while 
slight  effort  causes  it  to  return.  The  fingers,  in  addition  to  the  violet  tint, 
show  marked  deformity,  the  last  phalanx  being  swollen  and  rounded,  while 
the  nails  are  tliick,  broad,  and  curved. 

Respiration  is  short  and  painful,  the  voice  is  shrill  and  jerky,  and  the 
patient  cannot  take  exercise  without  feehng  short  of  breath  and  suffering 
from  palpitation,  angina,  and  syncope.  He  is  conscious  of  the  lowering 
of  his  temperature  (95°  F.,  Tupper),  and  the  slowness  of  his  movements 
somewhat  resembles  those  of  cold-blooded  animals. 

The  cyanosis,  dyspnoea,  somnolence,  apathy,  and  coldness  are  explained 
by  the  fact  that  the  blood  contains  too  much  carbonic  acid  and  not  sufficient 
oxygen.  The  duration  of  life  depends  upon  the  nature  and  gravity  of  the 
lesion.  Some  patients  die  from  asphyxia  or  syncope,  while  others  become 
tubercular. 

Examination  of  the  heart  gives  uncertain  information  as  to  the  precise 
site  of  the  lesion.  The  area  of  dullness  varies  with  the  hypertrophy  of  the 
ventricle,  and  palpation  sometimes  reveals  a  continuous  thrill  with  rein- 
forcement. 

The  murmurs  heard  on  auscultation  vary.  Perhaps  the  systolic  murmur, 
with  its  maximum  at  the  fourth  dorsal  vertebra,  indicates  tiie  persistence 
of  a  ductus  arteriosus. 


CHAPTER  III 

DISEASES  OF  THE  MYOCARDIUM 

Myocarditis,  or  carditis,  is  inflammation  of  the  heart.  Virchow  described 
two  varieties :  parenchymatous,  or  inflammation  of  the  muscle ;  and  in- 
terstitial, or  inflammation  of  the  connective  tissue. 

The  former  is  usually  found  in  acute  cases,  while  the  latter  obtains  in 
mo.st  of  the  chronic  cases.  At  the  present  day  the  general  term  of  fibrosis 
of  the  heart  is  more  often  used. 

I.  ACUTE  MYOCARDITIS— FATTY  DEGENERATION  OF  THE 

HEART. 

>Etiology. — Acute  primary  myocarditis  is  very  rare  (chill,  injury). 
The  causes  of  the  secondary  form  are  :  (1)  Rheumatism.  The  heart  alone 
may  be  affected,  or  may  be  involved  with  the  pericardium  and  endocardium. 
(2)  Infectious  diseases.  Amongst  these  we  must  quote,  as  of  primary  impor- 
tance, typhoid  fever,  variola,  scarlatina,  diphtheria,  erysipelas,  puerperal 
fever,  purulent  infection,  and  ulcerative  endocarditis.  AlcohoUsm,  syphihs, 
overwork,  and  previous  cardiac  lesions,  also  favour  its  development. 

In  certain  infectious  diseases,  such  as  diphtheria,  the  pathogenic  agent 
does  not  enter  the  blood,  and  yet  acute  myocarditis  is  fairly  frequent.  In 
these  cases  toxines  appear  to  play  the  chief  part,  just  as  in  acute  myocarditis, 
experimentally  produced  by  injection  of  a  filtered  culture  of  the  Bacillus 
pyoci/aneus  into  the  veins. 

In  other  affections,  however,  such  as  typhoid  fever,  the  pathogenic 
microbe  has  been  found  between  the  inflamed  muscular  fibres,  and  it  may 
then  be  asked  whether  the  micro-organism  acts  directly  on  the  myocardium, 
or  secondarily  by  its  secretory  products.  The  latter  explanation  is  more 
generally  accepted.  In  all  these  cases  a  certain  role  must  be  assigned  to 
waste  products  which  have  accumulated  in  the  blood,  and,  indeed,  they 
alone  (scurvy,  experimental  overwork)  may  be  capable  of  affecting  the 
vitality  of  the  heart  muscle. 

Pathological  Anatomy. — The  heart  is  generally  enlarged,  and  its  walls 
arc  llabby  and  pale.     (Ju  section  the  dead-leaf  tint  of  the  muscular  tissue 

433  li.S 


434  TEXT-BOOK  OF  MEDICINE 

is  very  clear.  The  tissue  tears  easily,  explaining  the  ruptures  of  the  musculi 
papillares  and  the  intracardiac  haemorrhages.  Under  the  microscope  the 
muscular  bundles  show  more  or  less  advanced  changes :  the  striation  is  less 
clear  than  usual,  and  we  find  in  the  fibre  fine  fatty  granules,  which  mask  its 
structure.  Vitreous  or  amyloid  degeneration  may  be  seen.  The  nuclei 
are  swollen  and  sometimes  increased  in  number.  Metchnikoi!,  however, 
says  that  this  nuclear  multiphcation  is  only  apparent,  and  the  increase  is 
simply  the  result  of  the  penetration  of  phagocytes  into  the  inflamed  fibres. 

In  some  cases  the  fibres  are  separated,  and  their  anastomoses  broken, 
as  though  the  cement  had  been  dissolved.  The  arterioles  present  clear 
traces  of  endarteritis  and  periarteritis. 

The  question  of  inflammation  or  of  degeneration  has  been  much  dis- 
cussed. Virchow,  Zenker,  and  Hayem  regard  the  condition  as  a  parenchy- 
matous inflammation.  Cohnheim,  Cornil  and  Ranvier,  and  Rindfleisch,  who 
base  their  opinion  on  the  almost  constant  integrity  of  the  interstitial  tissue, 
hold  that  the  lesions  are  degenerative.  Hanot  has  cleared  up  the  question 
by  showing  that  the  pathogenic  agents  may  affect  both  the  mucular  and 
the  comiective  tissue.  Each  element  reacts  in  its  own  way,  but  in  both 
cases  the  condition  is  due  to  an  inflammatory  process. 

Suppurative  myocarditis  is  rarer,  and  is  chiefly  seen  in  purulent  infection 
and  puerperal  conditions.  The  pus  may  infiltrate  the  tissue,  but  is  more 
often  collected  in  the  form  of  an  abscess.  The  abscess  may  open  into  the 
pericardium  or  into  the  ventricles,  and  cause  embohsms  in  the  lesser  or 
greater  circulation.  It  may  undergo  caseous  change  and  favour  the  forma- 
tion of  an  aneurysm. 

Description. — Acute  myocarditis  is  not  a  self-evident  affection,  and  its 
diagnosis  demands  careful  search.  Since  it  nearly  always  supervenes  as 
a  comphcation  of  some  other  disease,  it  often  passes  unnoticed.  Weakness 
and  irregularity  of  the  heart-beats  and  of  the  pulse  are  the  general  signs. 
We  also  find  disappearance  of  the  first  sound,  while  the  second  sound  persists, 
but  is  muffled  and  distant.  The  second  sound  may,  indeed,  be  replaced  by  a 
shght  rusthng.  When  the  myocarditis  is  less  severe,  the  first  sound  may 
be  replaced  by  a  soft  murmur,  which  is  limited  to  the  apex,  and  shows  a 
marked  tendency  to  alter  from  one  moment  to  another. 

Under  the  same  conditions  we  sometimes  hear  a  "  bruit  de  galop,"  due 
to  a  diastolic  shock,  indicating  the  ventricular  dilatation  which  accompanies 
the  change  in  the  myocardium.  Arrhythmia,  which  is  often  present,  has 
been  divided  into  regular  and  irregular.  In  the  former  the  cardiac  contrac- 
tion exists,  but  is  so  weak  that  it  cannot  be  recognized  either  by  ausculta- 
tion or  by  examination  of  the  pulse.  Sphygmographic  tracings  alone  show 
that  the  arrhythmia  is  only  ajDparent,  and  that  an  abortive  pulsation  really 
corresponds  to  the  interval  of  silence.     Lastly,  the  cardiac  rhythm  may 


DISEASES  OF  THE  MYOCARDIUM  435 

resemble   that   of   the   foetal   heart,  the  condition  being  called  embryo- 
cardia.     The  prognosis  in  these  cases  is  very  bad. 

Acute  myocarditis  is  generally  painless,  although  Peter  has  remarked 
that  pain  is  caused  by  percussion  of  the  third  and  fourth  intercostal  spaces, 
and  radiates  along  the  course  of  the  phrenic  nerve  and  the  cardiac  plexus. 
In  some  cases  of  typhoid  fever  painful  crises  resembhng  those  of  angina 
pectoris  have  also  been  observed. 

In  conjunction  with  the  troubles  affecting  the  power  and  rhythm  of  the 
heart-beats,  we  may  note  in  some  patients  tachycardia,  cyanosis,  oedema, 
and  chilhness  of  the  extremities — in  short,  all  the  signs  of  algid  collapse  ; 
in  others  the  phenomena  of  acute  asystole  predominate  (cardiac  form  of 
typhoid  fever).  Lastly,  we  may  see  repeated  attacks  of  syncope,  wliich  at 
times  prove  fatal.  In  typhoid  fever  in  particular,  some  authorities,  of  whom 
I  am  not  one,  have  attributed  sudden  death  to  acute  myocarditis.  This 
question  will  be  treated  in  detail  under  Typhoid  Fever. 

When  recovery  follows,  Landouzy  and  Siredey  think  that  the  myo- 
cardium may  preserve  some  rehcs  of  the  profound  change  which  it  has 
undergone,  and  that  this  change  may  ultimately  assist  in  the  development 
of  chronic  mischief. 

Counter-irritation  to  the  precordial  region  and  cardiac  tonics,  such  as 
digitaUs  and  caffein,  are  the  measures  generally  employed  for  feeble  action 
of  the  myocardium,  but  I  would  only  recommend  the  use  of  these  drugs 
with  reserve.  Degeneration  is  often  irregular,  especially  when  it  is  dependent 
upon  a  change  in  the  nutrient  vessels  of  the  heart.  In  these  cases  the  wall 
of  the  ventricle,  especially  at  the  apex,  is  often  thinned. 

The  symptoms  of  acute  fatty  degeneration  of  the  heart  resemble  those 
of  parenchymatous  myocarditis.  As  regards  chronic  fatty  degeneration, 
the  symptomatology  is  practically  that  of  fibrosis  of  the  heart,  with  this  differ- 
ence, however — that  the  phenomena  of  cardiac  excitation  are  wanting.  At 
first  the  striking  fact  is  the  weakness  of  the  heat-beats,  the  increase  in  the 
size  of  the  organ,  showing  its  dilatation,  and  lastly,  the  phenomena  of  peri- 
pheral and  visceral  stasis.  Accordingly,  after  some  time  asystole  follows 
unless  sudden  rupture  of  the  heart  causes  death. 

Fatty  Degeneration. — Fatty  degeneration  of  the  heart  has  more  in 
common  with  acute  myocarditis.  Ranvier,  indeed,  denies  the  latter 
disease,  which  would  therefore  be  characterized  solely  by  a  fatty  change  in 
the  muscles  of  the  heart. 

Many  conditions  give  rise  to  fatty  degeneration.  (1)  Certain  poisons 
(phosphorus,  arsenic^^tc.)  cause  complete  degeneration  in  a  few  days  (acute 
degeneration)  ;  (2)  alcoholism,  lesions  of  the  heart  and  of  the  valves  which 
impede  the  circulation  in  the  coronary  arteries,  gout,  and  old  age  cause 
chronic  degeneration. 

28—2 


436  TEXT-BOOK  OF  MEDICINE 

In  the  second  group  we  must  also  place  cachectic  conditions,  resulting 
from  chronic  diseases,  deep-seated  suppuration,  intense  anaemia  of  long 
duration  due  to  repeated  loss  of  blood,  chronic  diarrhoea,  and  athrepsia. 

It  is,  however,  important  to  distinguish  between  fatty  degeneration  and 
fatty  overgrowth.  The  latter  chiefly  occurs  in  obese  patients.  It  may 
exist  alone  for  a  long  while  before  the  malnutrition  of  the  heart,  due  to 
accumulation  of  fat  on  its  surface  and  between  its  muscular  bundles,  causes 
changes. 

Some  causes  (alcoholism),  however,  may  produce  simultaneous  over- 
growth and  degeneration. 

The  macroscopic  appearances  are  the  same  as  in  parenchymatous  myo- 
carditis, but  the  microscope  shows  that  the  nuclei  of  the  muscular  fibres  are 
intact,  while  the  interior  of  the  fibres  is  replaced  by  droplets  of  fat,  which  may 
be  large,  and  which  have  taken  the  place  of  the  sarcolemma.  Frequently, 
also,  a  certain  degree  of  granulo-pigmentary  degeneration  is  seen.  The 
coronary  vessels,  especially  in  chronic  affections  of  the  heart,  are  thickened, 
and  their  lumen  is  constricted  or  obliterated,  proving  the  joermanent  nature 
of  the  obstacle  opposed  to  the  nutrition  of  the  myocardium. 

II.  FIBROSIS  OF  THE  HEART. 

Fibrosis  of  the  heart,  or  inflammation  of  the  connective  tissue,  corresponds 
in  part  to  the  old  interstitial  myocarditis  of  Virchow. 

It  may  be  circumscribed  or  diffuse.  When  circumscribed  it  commences 
around  foreign  bodies  in  the  walls  of  the  heart — e.g^.,, hydatid  vesicles  or 
syphilitic  gumma ta. 

It  is  also  seen  in  areas  of  pericarditis  or  of  endocarditis.  In  adherent 
pericardium  the  fibrosis  may  extend  deeply  and  cause  pericardogenous 
myocarditis  (Brouardel,  Poulain).  Interstitial  endocardogenous  myo- 
carditis is  much  rarer.  In  children,  however,  we  see  constriction  of  the 
infundibulum  due  to  tliis  origin. 

The  diffuse  form  constitutes  fibrosis  of  the  heart  properly  speaking. 
It  has  lately  been  the  object  of  important  work,  which  has  profoundly 
modified  our  conceptions  of  the  diseases  of  the  myocardium.  It  nearly 
always  begins  with  arterio-sclerosis  of  the  arteries  of  the  heart,  and  occurs 
chiefly  in  persons  poisoned  by  alcohol,  lead,  and  tobacco  ;  in  arthritic,  gouty, 
or  syphilitic  patients  ;  or  in  those  who  suffer  from  Bright's  disease  and 
malarial  cachexia.  It  is  also  seen  in  elderly  or  overworked  persons.  It  is 
important  to  remember  that  in  all  these  cases  more  or  less  pronounced 
fibrous  change  is  also  present  in  most  of  the  organs.  Many  are  dependent 
upon  atheroma  or  on  arterio-sclerosis  (Gull  and  Sutton,  Debove,  etc.). 
It  may  also  be  seen,  as  a  secondary  lesion,  in  patients  suffering  from  valvular 


DISEASES  OF  THE  MYOCARDIUM  437 

affections.  According  to  Du  Pasquier,  the  large  fibroid  heart  is  associated 
with  blood-stasis  and  ischemia. 

The  fibroid  heart  is  increased  in  size,  of  a  brownish  colour,  and  firm  con- 
sistency. It  cuts  with  difficulty,  and  we  find  at  the  most  diseased  points 
greyish-white  patches,  due  to  the  inflammatory  process.  These  patches 
are  more  frequent  in  the  left  than  in  the  right  heart,  and  more  marked  in 
the  pillars  of  the  interventricular  septum,  and  especially  near  the  apex. 
In  some  hearts  these  islets  of  fibrosis  are  only  visible  under  the  microscope  ; 
they  then  appear  to  be  composed  of  fibrillary  connective  tissue  that  is  more 
or  less  dense,  according  to  the  age  and  interweaving  of  the  elastic  fibres 
(Letulle).  Some  develop  around  an  artery  affected  by  endoperiarteritis, 
while  others  are  situated  at  a  distance  from  the  arteries.  In  the  latter  case 
we  find  no  trace  of  periarteritis.  Endarteritis  exists  alone,  and  shows  itself 
at  first  sight  by  a  narrowing  in  the  calibre  of  the  vessel.  The  second 
variety  is  the  more  frequent.  Each  may  exist  alone,  but  they  are  sometimes 
found  together  in  the  same  patient,  the  fibrosis  being  mixed. 

The  muscular  bundles  situated  at  the  periphery  of  the  fibrous  islets  are 
atrophied  and  broken  up  ;  at  the  centre  of  the  islet  they  have  quite  dis- 
appeared. Those  situated  externally  to  the  inflammatory  or  degenerative 
process  are  enlarged,  but  their  contents  have  often  undergone  fatty  changes 
or  amyloid  degeneration  (Letulle). 

These  changes  may  lead  to  diminished  resistance  of  the  walls  of  the 
heart,  with  the  formation  of  aneurysms,  which  generally  develop  at  the 
spots  where  the  pressure  is  most  marked  and  the  lesions  in  the  muscle  are 
most  pronounced — namely,  near  the  apex  and  in  the  left  ventricle  (Pelvet). 

Symptoms. — When  the  fibrosis  has  caused  an  aneurysm,  sudden  death 
may  occur  from  rupture  of  the  heart.  In  some  cases  very  sharp  precordial 
pain,  due  to  the  tearing  of  some  deep  muscle  bundles,  precedes  the  rupture 
by  some  days  (Robin).  Sudden  death  has  also  been  noted  in  many  cases 
of  diffuse  or  circumscribed  gummatous  myocarditis  (Mauriac). 

In  general,  fibrosis  of  the  heart  is  of  slow  evolution  and  characterized 
by  no  pathognomonic  symptoms.  At  the  onset  the  patient  complains  of 
palpitation,  breathlessness,  dyspnoea,  and  sometimes  of  angina  pectoris. 
The  pulse  is  full  ;  the  impulse  is  forcible.  The  apex  of  the  heart  is  lowered 
and  carried  towards  the  axilla ;  the  first  sound  of  the  heart  is  dull ;  the 
second,  on  the  contrary,  is  ringing.  The  first  sound  is  often  reduplicated. 
This  gallop  rhythm,  however,  indicates  arterio-sclerosis,  rather  than  fibrosis 
of  the  myocardium.  The  pulse  gradually  becomes  weak  and  irregular,  the 
respiratory  troubles  increase,  stasis-phenomena  appear,  and,  after  repeated 
truces,  asystole  finally  results,  just  as  in  the  case  of  uncompensated 
valvular  lesions.  The  symptoms,  due  to  the  concomitant  fibrous  lesions 
in  the  kidneys,  are  often  present  as  well,  and  these  complex  cases  tax  the 


438  TEXT-BOOK  OF  MEDICINE 

skill  of  the  physician  in  recognizing,  from  the  symptomatology,  the  part 
belonging  to  each. 

Huchard  says  that  it  is  possible  to  distinguish  four  chief  forma  of 
cardio-fibrosis :  (1)  A  painful  form,  angina  pectoris  ;  (2)  an  arrhythmic 
form,  or  "  incurable  claudication  of  the  heart "  ;  (3)  a  tachycardiac  form 
often  associated  with  the  preceding  one ;  (4)  a  myovalvular  form  characterized 
by  mitral  or  aortic  murmur,  with  evident  fibrous  lesions. 

Treatment. — At  the  onset  we  must  employ  means  which  lower  the 
tension — e.g.,  milk  diet,  massage  and  passive  movements,  balneo-therapy 
at  Bourbon-Lancy,  Royat,  or  at  Evian.  An  alcohohc  solution  of  trinitrine, 
in  doses  of  from  2  to  10  drops  daily  in  water,  may  be  prescribed.  Tetra- 
nitrol  has  been  advised  in  doses  of  y^  to  ^  of  a  grain  several  times  daily. 

Iodide  of  sodium  is  especially  indicated.  Later  we  may  employ,  but  with 
great  care,  cardiac  stimulants,  such  as  caffein,  digitahs,  and  strophanthus, 
for  symptoms  of  asystole. 

We  must  never  forget  that  cardio-fibrosis  may  be  syphilitic  in  origin,  in 
wliich  case  injections  of  biniodide  of  mercury  are  indicated. 

III.  ANEURYSMS  OF  THE  HEART— INFARCTS  AND  FIBROUS 
PATCHES,  ETC.— RUPTURE  OF  THE  HEART. 

Aneurysms  of  the  heart  affect  chiefly  the  valves,  the  interventricular 
septum,  and  the  apex. 

1.  Valvular  aneurysms  result  from  acute  and  especially  from  infective 
endocarditis.  "  The  multiphcation  of  cells,  their  embryonic  condition,  the 
softening  of  the  intercellular  substance,  and  the  disappearance  of  the  elastic 
fibres — phenomena  which  are  associated  with  endocarditis — deprive  the  valve 
of  its  power  of  resistance."  As  a  result  of  this  inflammatory  process,  two 
things  may  happen  :  the  valve  is  perforated,  or  remains  distended,  and  forms 
an  aneurysm. 

Aneurysms  of  the  sigmoid  and  mitral  valves  always  have  their  opening 
at  the  side  upon  which  the  blood-pressure  acts.  A  sigmoid  aneurysm  opens 
on  the  upper  or  arterial  surface  of  the  sigmoid  valves,  because  the  blood- 
pressure  acts  on  this  surface,  while  a  mitral  aneurysm  opens  on  the  inferior 
or  ventricular  surface,  which  supports  the  pressure  of  the  blood  during 
systole,  when  the  valve  is  closed.  Valvular  aneurysms  rarely  preserve  their 
spherical  shape.  They  are  more  or  less  torn  by  the  blood-stream,  and  the 
valve  is  converted  into  shreds. 

This  rupture  may  show  itself  by  a  murmur  which  appears  suddenly  in 
the  course  of  infective  endocarditis.  The  murmur  is  due  to  insufficiency, 
and  is  therefore  systohc  if  the  mitral  valve  is  affected,  diastohc  if  the 
lesion  affects  the  aortic  valves.  Apart  from  these  exceptional  cases,  we  find 
during  hfe  no  indications  of  the  rupture  of  the  aneurysm. 

2.  Aneurysms  of  the  interventricular  septum  usually  have  the  same  origin 


DISEASES  OF  THE  MYOCARDIUM  439 

as  the  preceding  form,  and  are  often  simply  the  extension  of  a  valvular 
aneurysm.  As  a  rule,  they  are  found  by  chance  at  the  autopsy.  When  they 
burst  by  perforation,  communication  between  the  two  ventricles  allows 
arterial  and  venous  blood  to  mix. 

3.  Aneurysms  of  the  apex  of  the  heart,  also  called  partial,  are  quite 
different  in  their  pathogenesis.  They  are  due  to  fibrous  myocarditis,  or 
to  simultaneous  inflammation  of  the  myocardium  and  endocardium. 
The  fibrous  spots  have  no  reactive  power,  and  readily  yield  to  the  blood- 
pressure  ;  dilatation  and,  later,  aneurysm  result.  Some  authors  (Kundrat, 
Huchard)  regard  obUteration  of  the  coronary  arteries  as  important.  The 
area,  deprived  of  nutrient  vessels,  loses  its  resistance,  and  the  aneurysm  forms 
imperceptibly.  As  pericardial  adhesions  are  frequently  present  near  these 
aneurysms,  the  question  has  been  asked  whether  these  adhesions  may  not, 
by  repeated  traction,  facihtate  the  production  of  a  partial  aneurysm. 

These  aneurysms  are,  as  a  rule,  situated  in  the  left  ventricle,  near  the 
apex.  The  tumour  is  so  large  that  the  size  of  the  heart  is  doubled  (coBUr 
en  bissac).  The  aneurysm  generally  opens  into  the  ventricle,  and  the 
blood-stasis  within  the  sac  is  not  sufficiently  complete  to  bring  about  the 
formation  of  stratified  clots.  Cases  have,  however,  been  noted  in  which 
the  aneurysmal  cavity  was  filled  with  clots  of  this  nature.  The  limiting 
wall  is  sometimes  infiltrated  with  calcareous  salts. 

There  is,  so  to  say,  no  symptomatology  of  these  aneurysms.  Sometimes 
one  is  found  by  chance  post  moYtem ;  at  other  times  the  patient  dies  in 
asystole,  or  more  often  from  rupture  of  the  heart.  The  existence  of  a  diastolic 
murmur  at  the  apex,  independent  of  aortic  insufficiency,  has,  however,  been 
noted,  and  also  a  diastolic  sound  heard  over  the  middle  portion  of  the  heart, 
and  differing  from  the  gallop  rhythm  in  Bright's  disease  by  its  clearer  tone 
(Rendu). 

Infarcts  and  Fibrous  Patches  in  the  Myocardium. 

Post  mortem,  we  sometimes  find  on  the  surface  of  the  ventricles  depres- 
sions resembling  scars.  On  section  of  the  ventricle  we  see  that  these  de- 
pressions correspond  to  fibrous  tissue  which  has  replaced  the  myocardium 
to  a  more  or  less  large  extent.  Sometimes,  as  in  one  of  my  patients,  the 
muscle  of  the  wall  is  replaced  at  the  sclerosed  patch  by  fibrous  tissue,  which 
is  only  one-third  or  one- fourth  of  the  normal  thickness.  We  find  under 
the  microscope  simply  connective  tissue  and  dilated  vessels. 

They  are  called  fibrous  patches  in  the  myocardium.  Thoy  have 
long  been  known,  but  were  until  recent  years  looked  upon  as  the  result 
of  chronic  inflammation.  We  know  to-day  that  these  lesions  are  distinct 
from  localized  fibrosis  of  the  myocardium,  and  are  the  result  of  an  infarct ; 
they  are  true  cicatrices. 

The  myocardium  may  indeed  Ijc  the  scat  of  an  infarct,  just  as  all  organs 


440  TEXT-BOOK  OF  MEDICINE 

and  tissues  in  which  the  arterial  anastomoses  are  not  sufficiently  numerous. 
The  heart  answers  to  this  disposition,  for  the  coronary  arteries,  which 
anastomose  freely  at  the  base,  become  terminal  at  the  apex.  The  seat  of 
election  of  these  infarcts,  caused  by  obstruction  of  one  of  the  coronary 
arteries,  is  thus  explained.  This  obhteration  rarely  occurs  from  embohsm. 
It  is  in  the  majority  of  cases  a  thrombosis,  produced  by  the  lesions  of  arteritis 
obliterans. 

The  infarct  may  show  itself  either  as  a  hmited  yellow  or  red  focus,  the 
colour  being  due  to  necrosis  of  the  damaged  tissue,  or  as  a  haemorrhagic  focus. 
In  the  latter  case  it  has  been  supposed  that  the  blood  in  the  heart  cavity 
secondarily  inundates  the  focus  of  necrosis.  The  formation  of  some 
aneurysms  of  the  heart  may  be  thus  explained. 

If  the  patient  does  not  succumb,  the  infarct  changes  into  cicatricial  tissue, 
which  may  undergo  calcification,  and  form  the  fibrous  patch  in  the  myo- 
cardium. When  this  scar  is  extensive,  it  forms  a  weak  spot  in  the  wall  of 
the  ventricle,  and  may  lead  to  aneurysm  and  rupture  of  the  heart. 

Although  the  production  of  an  infarct  may  sometimes  be  revealed  by 
precordial  pain  and  tachycardia,  the  lesion  has,  as  a  rule,  no  clinical  history. 

Rupture  of  the  Heart. 

Rupture  of  the  heart  occurs  in  the  course  of  some  affections  of  the 
myocardium.  Partial  aneurysm  of  the  heart,  softening  of  the  heart  muscle 
by  rapid  obhteration  of  a  coronary  artery,  fatty  degeneration,  and  infective 
myocarditis,  are  the  most  frequent  causes  of  these  ruptures. 

The  rupture  may  take  place  from  without  inwards-,  but  it  more  often 
occurs  from  within  outwards,  and  is  then  due  to  the  pressure  of  the  blood 
upon  the  inner  surface  of  the  heart.  In  the  former  case,  on  the  con- 
trary, the  contraction  of  the  affected  muscle  produces  the  tear.  Both 
mechanisms  may  also  occur  together.  In  this  case  the  two  lines  of  rupture, 
instead  of  corresponding,  are  separated  by  unbroken  muscular  bundles. 
The  rupture  may  be  double  or  triple,  but  the  apex  of  the  left  ventricle  is 
the  seat  of  election.  At  this  point  the  wall  is  thinned,  especially  in  cases 
of  partial  aneurysm,  or  of  fibrous  myocarditis.  The  pericardium  is  usually 
full  of  dark  coagulated  blood. 

The  rupture  is  usually  caused  by  a  strain.  Cases  of  rupture  during  sleep 
have,  however,  been  quoted.  It  shows  itself  by  inexpressible  distress  and 
acute  precordial  pain,  which  may  radiate  to  the  back  and  to  the  left  shoulder. 
The  patient  utters  a  cry,  his  face  becomes  cyanosed,  the  beating  of  the 
heart  is  tumultuous,  the  pulse  is  small  and  cannot  be  counted,  the  breathing 
rapidly  becomes  embarrassed,  and  the  patient  dies  within  a  few  seconds. 
The  rupture  may  be  gradual,  and  may  only  become  complete  at  the  end  of 
several  days.  We  then  see,  in  addition  to  the  pain  and  vomiting  which 
marked  the  onset  of  the  rupture,  the  other  symptoms  just  enumerated. 


DISEASES  OF  THE  MYOCARDIUM  141 

IV.  SYPHILIS  OF  THE  HEART. 

vEtiology. — Syphilitic  lesions  of  the  heart,  first  noted  in  1859  by  Virchow, 
are  now  becoming  well  kno^vn.  They  are  chiefly  seen  during  the  tertiary 
period,  about  ten  years  after  infection  (JulUen),  though  they  may  appear 
earUer  or  later.  Parrot  has  pubhshed  several  cases  of  hereditary  syphihs 
of  the  heart  in  the  new-born.  Letulle  and  Nattan-Larrier  have  seen  miliary 
gummata  upon  the  valves  in  a  syphihtic  child  who  died  at  birth. 

Pathological  Anatomy.— S}T)hihs  affects  the  valves  more  rarely  than  the 
myocardium,  especially  the  left  ventricle.  The  interventricular  septum  and 
orifices  are  not  often  involved.  Gumma  or  fibrosis  is  the  usual  lesion. 
The  latter  is  recognized  by  its  clear  locahzation  to  one  part  of  the  heart,  the 
other  zones  being  free,  and  by  the  severity  of  the  arterial  lesions  at  this 
point,  the  arteries  of  the  other  regions  being  healthy.  These  characters, 
however,  are  not  specific,  and  at  most  allow  a  suspicion  of  syphiUs,  especially 
in  the  absence  of  other  visceral  manifestations. 

Syphilitic  gummata  in  the  heart,  as  in  other  organs,  constitute  the 
only  real  specific  lesion.  Their  yellowish  appearance,  their  elastic  consist- 
ency, their  well-defined  hmits,  their  multiphcity,  or  the  coexistence  of 
miliary  gummata  in  the  neighbourhood,  and  the  recognition  of  lesions  in 
the  liver,  kidneys,  etc.,  can  hardly  allow  any  mistake.  In  some  cases  they 
are  surrounded  by  healthy  muscular  tissue,  and  project  towards  the  endo- 
cardium, or  towards  the  pericardium.  The  serous  membranes  are  thickened  ; 
the  layers  of  the  pericardium  may  be  adherent.  In  other  cases,  on  the  con- 
trary, the  endocardium  is  not  thickened,  but  ulcerated,  the  gumma  having 
emptied  itself  into  the  ventricular  cavity,  while  the  blood  has  entered  the 
cavity,  hollowed  out  at  the  expense  of  the  myocardium.  The  possibihty 
of  partial  aneurysm  is  readily  seen. 

Description. — The  disease  often  remains  latent,  and  is  only  discovered 
post  mortem.  In  other  cases  we  find  all  the  .signs  of  a  chronic  affection  of 
the  myocardium — namely,  increased  precordial  dullness,  indistinct  and 
irregular  heart  sounds  (Semmola),  arrhythmic  pulse,  retro-sternal  pain, 
dyspnoea  on  effort,  oedema,  and  cachexia.  In  short,  we  see  the  evolution 
of  cardio-fibrosis  or  of  progressive  asystole. 

More  .striking  are  the  cases  in  which  a  syphilitic  person  previously  exempt 
from  cardiac  trouble  is  taken  ill  with  acute  asystole,  that  proves  fatal  in 
one  or  two  days  (Tessier).  Rapid  death  may  be  due  to  agonizing  dyspnoea, 
recalling  some  pulmonary  lesion  rather  than  a  cardiac  affection.  Lastly, 
sudden  death  may  be  consecutive  to  rupture  of  the  heart,  to  syncope,  or  to 
embolism.  The  pathogenic  diagnosis  of  cardiac  syphilis  is  a  matter  of 
supposition.  However,  in  a  patient  with  old  .syphilis,  wlio  suffers  from 
symptoms  of  cardio-fibrosis,  sypliilis  should  always  be  thought  of,  and  daily 
injections  of  biniodido  of  mercury  be  administered. 


442  TEXT-BOOK  OF  MEDICINE 

V.  TUMOURS  OF  THE  HEART  AND  TUBERCULOSIS  OF  THE 

MYOCARDIUM. 

Some  rare  cases  of  primary  spindle-celled  sarcoma  are  seen.  Epithe- 
lioma naturally  afEects  the  heart  only  as  a  secondary  growth.  Most  cases 
of  "  cancer  of  the  heart "  are  really  secondary  nodules  of  epithehoma,  and 
are  quite  exceptional.  These  nodules  are  secondary  to  cancer  of  the  ali- 
mentary canal,  the  lung,  etc.  ;  in  most  cases  they  coexist  with  secondary 
nodules  in  the  lung.  They  are  situated  in  the  myocardium,  and  chiefly 
in  the  right  heart  or  in  the  interventricular  septum.  Cancer  of  the  heart 
is  not  as  a  rule  recognized  during  hfe.  In  some  cases  it  may  give  rise  to 
dyspnoea,  tachycardia,  precordial  pain,  etc.  I  have  reported  the  case  of  a 
patient  suffering  from  pleuro-pulmonary  cancer,  whose  pulse-rate  was  ex- 
tremely quickened.  At  the  autopsy  I  found  a  cancerous  nodule  as  large 
as  a  hemp-seed  in  the  interventricular  septum. 

The  other  tumours  are  myxomata,  forming  pedunculated  swelHngs  on 
the  auricular  surface  of  the  mitral  valve,  and  hydatid  cysts,  which  may  be 
present  in  the  myocardium  as  in  other  muscles.  This  affection  is  exceptional, 
and  its  sole  clinical  interest  hes  in  the  possibility  of  hydatid  emboli,  when 
the  cyst  opens  into  the  cardiac  cavity. 

Tuberculosis  of  the  myocardium  is  a  rare  affection,  which  has  no  clinical 
history,  and  is  found  by  chance  post  mortem.  As  a  rule,  it  is  coexistent 
with  tubercular  pericarditis,  and  frequently  with  tubercular  lesions  of  the 
peritracheal  glands. 

We  may  find  miUary  tuberculosis,  but  more  often  we  see  large  isolated 
tubercles  in  which  Koch's  bacillus  has  been  found.  These  large  tubercles 
may  be  caseous  or  calcified.  Koch's  bacilli  have  been  found  by  Peron  even 
in  the  calcified  lesions.  Tubercular  lesions  of  the  myocardium  are  chiefly 
situated  in  the  ventricles,  and  are  most  often  seen  in  children. 

Tuberculosis  of  the  myocardium  is  frequent  in  domestic  animals  which 
have  become  tubercular  (dogs,  bovine  animals,  and  pigs),  while  it  is  rare 
in  laboratory  animals  inoculated  with  tubercular  products  (Peron). 

VI.  HYPERTROPHY  AND  DILATATION  OF  THE  HEART. 

Pathology. — A  muscle  hypertrophies  when  it  undergoes  increased 
work.  This  general  law  includes  the  heart,  which  hypertrophies  as  the 
result  of  excessive  or  repeated  contractions.  The  causes  of  this  hypertrophy 
may  be  divided  into  two  classes  (Jaccoud)  :  (1)  Simple  or  purely  functional 
hypertrophy  ;  (2)  hypertrophy  from  some  mechanical  obstacle. 

Simple  Hypertrophy. — This  form,  which  is  also  called  primary,  is  due 
to  nervous  palpitation,  and  consequently  to  the  causes  producing  this  palpi- 
tation   (adolescence,    hypertrophy    of    growth,    excesses    of   every    kind, 


DISEASES  OF  THE  MYOCARDIUM  443 

abuse  of  drink,  tobacco,  tea,  or  coffee,  hypertrophy  in  exophthalmic  goitre). 
The  whole  heart  is  affected,  and  the  hypertrophy  does  not  as  a  rule,  involve 
any  special  portion  of  the  organ. 

Hypertrophy  from  Mechanical  Obstacles. — The  causes  are  :  (1)  lesions 
of  the  heart ;  (2)  lesions  of  the  vascular  system  ;  (3)  lesions  or  abnormal 
conditions  of  more  or  less  distant  organs. 

1.  The  mechanism  by  which  valvular  lesions  of  the  heart  cause  hyper- 
trophy is  readily  understood.  When  an  obstacle  exists  at  one  of  the  orifices, 
whether  it  is  the  reflux  of  the  blood-wave,  as  in  insufficiency,  or  whether 
this  wave  pass  with  difficulty  through  the  orifice  and  the  cavity,  which  is 
in  front  of  the  diseased  opening,  in  order  to  overcome  the  excess  of  pressure, 
the  walls  of  the  cavity  are  subjected  to  exaggerated  functional  irritation, 
which  finally  produces  hypertrophy.  The  h}T)ertrophy,  which  is  at  first 
locaUzed  to  the  cavity  in  front  of  the  diseased  opening,  finally  extends  to 
the  other  cavities.  For  example,  lesions  of  the  mitral  orifice  increase 
the  blood-pressure  in  the  left  auricle,  which  hypertrophies  ;  the  blood-stasis 
in  the  left  auricle  increases  in  its  turn  the  blood-pressure  in  the  pulmonary 
veins,  the  pulmonary  artery,  and  the  right  cavities  of  the  heart ;  the  right 
ventricle  therefore  is  exposed  to  excess  of  work,  as  well  as  to  exaggerated 
functional  irritation,  which,  by  its  persistence,  produces  hypertrophy. 
This  hypertrophy  is,  within  hmits,  compensatory  to  the  mitral  lesions,  but 
the  excess  of  blood-pressure  in  the  right  ventricle  finally  reacts  on  the 
venae  cavse  and  the  capillaries  of  the  greater  circulation.  From  the  capil- 
laries the  excess  of  tension  reaches  the  arterial  system,  and  finally  the  left 
ventricle  shows  hypertrophy. 

The  lesions  of  the  aortic  orifice  produce  analogous  effects,  but  different 
in  degree.  The  power  of  the  left  ventricle  and  the  enormous  hypertrophy 
which  accompanies  aortic  stenosis  and  incompetence  protect  the  lesser 
circulation  for  a  long  while,  so  that  the  excess  of  tension  in  the  pulmonary 
vessels  and  the  right  cavities  of  the  heart  appears  later,  and  is  less  complete 
than  in  mitral  lesions. 

2.  Aneurysm  of  the  aorta  or  of  the  great  vessels,  acute  or  chronic  aortitis, 
endarteritis,  and  general  atheroma,  are  the  lesions  of  the  arterial  system 
which  may  produce  hypertrophy  of  the  left  cavities  of  the  heart.  How  do 
such  lesions  determine  hypertrophy  of  the  left  ventricle  ? 

In  the  normal  state  the  elasticity  of  the  arteries  diminishes  the  resist- 
ance experienced  by  the  blood  in  passing  from  the  heart  to  the  vessels 
(Marey).  Hence  diseases  which  abolish  or  diminish  this  elasticity  increase 
the  resistance  and  raise  the  blood-pressure,  the  result  being  hypertrophy  of 
the  left  ventricle. 

This  pathology  is  perfectly  applicable  to  chronic  aortitis  and  to  more 
or  less  general  atheroma,  though  it  does  not  sufficiently  explain  other  cases. 


444  TEXT-BOOK  OF  MEDICINE 

For  instance,  acute  aortitis  is  nearly  always  accompanied  by  hypertrophy 
of  the  left  ventricle,  which  must  not  be  set  down  to  a  concomitant  lesion 
of  the  aortic  orifice,  because  it  occurs  in  cases  in  which  acute  aortitis  exists 
without  comphcations.  Aneurysms  are  often  accompanied  by  hypertrophy 
of  the  left  ventricle.  In  fifty-eight  cases  of  aortic  aneurysm  hypertrophy 
of  the  ventricle  was  present  in  fifty-three.  This  hypertrophy  cannot  be 
set  down  to  excess  of  pressure,  for  physiological  experiments  have  proved 
that  the  presence  of  an  elastic  sac  in  the  course  of  a  vessel  does  not  interfere 
with  the  circulation.  Aneurysms  of  the  arch  of  the  aorta  are  by  no  means 
always  accompanied  by  hypertrophy  of  the  heart.  In  a  certain  number  of 
cases  (I  have  verified  this  fact  three  times  post  mortem)  the  heart  was 
normal  in  size,  although  the  aortic  aneurysms  were  large. 

Arterial  lesions  of  the  lesser  circulation  cause  hypertrophy  of  the  right 
ventricle.  Congenital  or  acquired  stenosis  of  the  pulmonary  artery 
leads  to  hypertrophy  and  dilatation  of  the  cavity  of  the  right  heart, 

Arterio-sclerosis  of  the  heart,  associated  with  sclerosis  of  the  myo- 
cardium will  be  discussed  under  Bright's  Disease. 

3.  The  morbid  condition  of  certain  organs  reacts  upon  the  heart  and 
determines  hypertrophy.  Chronic  diseases  of  the  lung  react  on  the  right 
ventricle,  which  dilates  and  hypertrophies  ;  chronic  pleurisy  and  costo- 
vertebral deformities  may  produce  the  same  result ;  interstitial  nephritis 
causes  hypertrophy  of  the  left  ventricle  (Traube,  Potain).  The  mechanism 
in  this  case  will  be  discussed  under  Bright's  Disease.  Transitory  hyper- 
trophy of  the  left  ventricle  during  pregnancy  is  generally  admitted. 
Potain  has  reported  cases  of  cardiac  hypertrophy  following  lesions  of  the 
brachial  plexus.  Chronic  lesions  of  the  liver  may  favour  dilatation  and 
slight  hypertrophy  of  the  right  ventricle  (Potain).  Cardiac  hypertrophy 
following  growth  is  said,  to  result  from  a  want  of  parallel  development 
between  the  heart  and  the  other  organs  (See).  Dilatation  of  the  cavities 
of  the  heart  nearly  always  accompanies  hypertrophy  (excentric  hyper- 
trophy). It  may  be  general  or  local,  and  as  it  depends  on  the  lessened 
resistance  of  the  walls,  it  is  more  marked  in  the  right  cavities  of  the  heart. 

Often  the  chief  lesion  is  dilatation,  and  is  seen  following  diseases 
which  lessen  the  resistance  of  the  heart- wall.  The  dystrophies  of  the  heart 
muscle,  described  under  Degeneration  and  Myocarditis,  belong  to  this 
class. 

Pathological  Anatomy. — In  true  hypertrophy  the  size  and  weight  of 
the  heart  are  increased.  The  weight  may  reach  as  much  as  1,000  grammes 
(the  normal  weight  is  300  grammes).  The  thickness  of  the  left  ventricle 
reaches  3  or  4  centimetres  (12  millimetres  being  the  normal)  ;  the  thickness 
of  the  right  ventricle  amounts  to  from  1  to  2  centimetres  (3  millimetres  bein» 
the  normal  thickness). 


DISEASES  OF  THE  MYOCARDIUM  445 

The  structure  has  given  rise  to  much  discussion  (LetuUe).  Some  hold 
that  the  hypertrophy  is  due  to  increase  in  the  number  of  the  primary 
bundles,  while  others  admit  increase  in  the  size  of  the  bundles,  or  both  of 
these  causes.  Hypertrophy  is  not  due  solely  to  the  change  in  the  muscle. 
Lesions  of  the  connective  tissue,  the  endocardium,  the  pericardium,  and 
the  vessels  are  present  in  a  hypertrophied  heart.  Nevertheless,  the  change 
in  the  muscular  fibre  is  most  important.  There  is  no  proof  of  the  multiplica- 
tion of  the  primary  bundles,  while  their  hypernutrition  is  admitted  by  all 
authorities,  and  each  primary  bundle,  instead  of  having  the  normal  diameter 
of  15  to  20  fjb,  reaches  one  of  25  to  30  /i. 

The  muscular  hypertrophy  is  dispersed  through  the  affected  regions, 
and  in  proportion  as  hypertrophy  gives  place  to  organic  decay,  the  heart 
is  invaded  by  diffuse  fibrosis,  by  endoperiarteritis  of  the  small  vessels,  and 
by  disseminated  fatty  degeneration. 

In  some  cases  more  or  less  general  cardiac  cirrhosis  is  seen.  The 
fibrous  tissue  appears  to  be  localized  around  the  small  arteries  in  the  heart 
muscle.  The  fibrosis  of  the  myocardium  is  said  to  be  consecutive  to  endo- 
periarteritis. 

The  shape  of  the  heart  shows  Uttle  change  when  the  hypertrophy  is 
general,  but  is  much  modified  in  cases  of  partial  hypertrophy.  In  this 
manner  local  hypertrophy  of  the  left  ventricle  increases  the  longitudinal 
diameter  of  the  heart,  giving  it  an  oval  shape  and  an  almost  horizontal 
direction.  The  septum  encroaches  on  the  cavity  of  the  right  ventricle,  and 
the  papillary  muscles  are  much  enlarged.  Hypertrophy  of  the  right  ventricle 
increases  the  transverse  diameter  of  the  heart,  and  tends  to  give  it  a  spherical 
shape. 

Description. — As  Jaccoud  has  observed,  care  must  be  taken  to 
distinguish  the  symptoms  proper  to  simple  hypertrophy  from  those  of 
hypertrophy,  accompanied  by  cardio-pulmonary  changes.  As  long  as  the 
muscle  has  not  undergone  fibro-fatty  degeneration,  hypertrophy  of  the  heart 
produces  neither  blood-stasis  nor  dropsy.  On  the  contrary,  the  hyper- 
trophied walls  sometimes  propel  the  blood  with  increased  vigour,  and 
cause  congestion.  Thus  the  enormous  hypertrophy  of  the  left  ventricle 
in  aortic  insufficiency  is  often  accompanied  by  cerebral  congestion,  with 
flushing,  dimness  of  sight,  ringing  in  the  ears,  headache,  vertigo,  and  epis- 
taxis.  The  impulse  of  the  blood-wave  is  shown  tliroughout  the  whole 
arterial  system  by  pulsation  in  the  carotids,  bounding  pulse,  dilatation 
and  elongation  of  the  arteries,  and  the  patient  complains  of  palpitation, 
precordial  distress,  and  dyspnrjca. 

When,  however,  the  hypertrophied  and  dilated  muscles  undergo  fibro- 
fatty  degeneration,  and  compensation  begins  to  fail,  the  train  of  symptoms 
which  we  have  enumerated  several  times  in  the  last  few  sections  appears. 


446  TEXT-BOOK  OF  MEDICINE 

The  physical  signs  of  hypertrophy  of  the  heart  are  as  follows :  The 
apex  of  the  heart  is  displaced  downwards  and  outwards,  and  the  impulse 
has  its  maximum  to  the  left  of  the  sternum  if  the  left  ventricle  is  afiected, 
and  in  the  epigastric  angle  if  the  right  ventricle  is  involved.  The  pre- 
cordial bulging  depends  on  the  extent  of  the  hypertrophy.  The  dullness 
is  increased  in  the  longitudinal  direction  by  hypertrophy  of  the  left  ventricle, 
and  in  a  transverse  one  by  that  of  the  right  ventricle.  Pure  hypertrophy, 
apart  from  valvular  lesions,  does  not  show  itself  by  any  abnormal  sound. 
The  gallop  rhythm  present  in  hypertrophy  of  renal  origin  will  be  studied 
under  Bright's  Disease. 

Diagnosis — Prognosis. — The  diagnosis  of  hypertrophy  of  the  heart 
is  made  from  the  symptoms  above  mentioned.  We  must  be  on  our  guard 
in  cases  where  the  size  of  the  heart  is  masked  by  the  exaggerated  percussion 
resonance  of  emphysema.  The  diagnosis  between  hypertrophy  and  peri- 
cardial effusions  has  been  discussed  under  Pericarditis.  Purely  functional 
hypertrophy  is  not  serious,  and  the  compensatory  form  is  favourable,  in 
that  it  diminishes  for  a  time  the  extreme  gravity  of  the  valvular  lesions. 
The  phenomena  of  congestion  due  to  excessive  cardiac  contractions  may 
produce  troublesome  results.  In  such  cases  it  is  necessary  to  diminish  the 
tension  in  the  arterial  system,  and  to  moderate  the  cardiac  erethism. 

VII.  ASYSTOLE. 

The  word  asystole  must  not  be  taken  literally,  for  the  absence  of  systole 
means  death.  In  coining  the  word  asystole,  Beau  supposed  that,  at  an 
advanced  period  in  valvular  lesions  of  the  heart,  the  contractions  of  the 
organ  are  so  faulty  that  they  open  the  road  for  congestion,  oedema,  and  all 
the  symptoms  of  cardiac  cachexia.  Beau's  description  remains  true,  but 
the  interpretation  of  asystole  must  be  modified.  Asystole  is  produced  by 
any  cause  which  interferes  with  the  contraction  of  the  heart  muscle.  This 
class  includes  excessive  fatigue,  overwork,  adherent  pericardium,  valvular 
lesions,  imperfectly  compensated  dilatation,  and  especially  degeneration 
of  the  muscular  fibre  (Stokes).  It  is  proper  to  add  that  these  causes  of 
cardiac  origin  may  be  reinforced  by  those  of  peripheral  or  vascular  origin, 
such  as  malnutrition  and  defective  resistance  of  the  small  vessels. 

The  symptoms  and  the  course  of  asystole  and  of  cardiac  cachexia  have 
been  described  under  Valvular  Lesions  of  the  Heart  and  their  Treatment,  so 
that  it  is  unnecessary  to  repeat  them. 


CHAPTER  IV 
NEUROSES  OF  THE  HEART 

I.  PALPITATION. 

According  to  many  authors,  palpitation  is  characterized  by  a  change  in 
the  frequency,  rhythm,  and  intensity  of  the  heart-beats.  This  view  of  the 
question  appears  to  me  incomplete.  The  pulse-rate  in  fever  exceeds  120, 
although  palpitation  is  not  present.  The  force  of  the  heart-beats  is  much 
increased  in  some  cases  of  hypertrophy  of  the  left  ventricle,  but  yet  palpita- 
tion may  be  absent  (Potain).  Intermittence  in  mitral  lesions  certainly 
does  not  entail  palpitation.  Palpitation,  then,  is  not  absolutely  associated 
with  changes  in  the  frequency,  rhythm,  and  intensity  :  it  often  accom- 
panies, but  is  not  the  consequence  of,  such  changes. 

"  Palpitations,"  says  Peter,  "  are  spasms  of  the  heart,"  and,  I  may 
add,  distressing  and  painful  spasms.  We  are  not  conscious  of  the  action  of 
the  organs  in  life  :  when  we  are  so,  we  recognize  it  by  discomfort  or  by  pain. 
In  the  normal  condition  the  stomach  and  intestine  execute  their  movements 
without  our  knowledge.  When  these  movements  change  in  character 
(spasms),  they  become  painful. 

The  heart  follows  the  same  law.  In  palpitation  the  heart- beats  are 
distressing  or  painful  to  a  variable  extent,  from  simple  discomfort  to  pain 
with  angina  and  tendency  to  syncope. 

Pathogenesis. — Whatever  is  the  initial  cause  of  palpitation,  some  trouble 
in  the  nervous  system  of  the  heart  must  finally  be  acknowledged.  In 
some  cases  this  nervous  trouble  appears  apart  from  any  material  change 
in  the  organ  ;  in  other  cases  a  material  change  is  manifest.  Between  these 
two  extremes  many  intermediate  forms  are  found,  but  their  classification 
is  impossible. 

Nervous  Palpitation. — The  physiology  of  the  innervation  of  the  heart 
has  been  examined  for  an  explanation  of  palpitation,  and  it  is  said  that 
the  pneumogastric  and  great  sympathetic  nerves  are  antagonists.  Inhibi- 
tion of  the  pneumogastric  or  excitation  of  the  sympathetic  produces  pnicti- 
cally  the  same  effect — namely,  the  acceleration  af  the  heart-beats.  Hence 
all  causes  which  lessen  the  action  of  tiie  former  or  increase  that  of  tlie  latter 

447 


448  TEXT-BOOK  OF  MEDICINE 

may  give  rise  to  palpitation.  Such  a  statement  appears  inexact,  because 
acceleration  is  not  sufficient  to  produce  palpitation,  and  consequently  it  is 
not  evident  how  causes  which  diminish  the  action  of  one  of  the  antagonistic 
nerves  may  not  at  the  same  time  enfeeble  the  action  of  the  other.  Ab- 
normal irritabihty  of  the  nervous  system,  cerebro-cardiac  neuropathy 
(Krishaber),  exophthalmic  goitre,  excesses  of  every  kind,  abuse  of  drink, 
coffee,  tea,  or  tobacco,  are  the  usual  causes  of  nervous  palpitation.  The 
so-called  palpitations  of  growth  and  of  reflex  origin  also  enter  into  this  class. 

Palpitation  with  Material  Lesions. — In  this  class  we  find  palpitation, 
which  accompanies  diseases  of  the  heart,  such  as  pericarditis  and  endocarditis, 
myocarditis,  hypertrophy  and  dilatation,  or  valvular  lesions.  Acute 
inflammation,  which  at  first  sight  would  appear  Ukely  to  irritate  the  nerve 
endings,  is  rarely  accompanied  by  palpitation,  while  valvular  lesions 
frequently  are,  and  it  remains  to  be  seen  what  is  the  mechanism  in  these 
cases.  Every  case  of  stenosis,  says  Peter,  is  accompanied  by  spasm.  Patho- 
logically constricted  tubes,  such  as  the  uretlira  or  the  oesophagus,  and  those 
normally  constricted,  such  as  the  glottis  or  the  biliary  ducts,  are  subject 
to  spasmodic  contraction,  and  stenoses  of  the  heart  also  provoke  spasms 
called  palpitations.  But  how  are  we  to  explain  palpitation  in  aortic  in- 
sufficiency, which  is  the  exact  opposite  of  stenosis  ? 

Palpitation  of  Mixed  Origin.— Marey  has  shown  that  lowering  of 
the  blood-pressure  increases  the  rate  of  the  heart-beats.  The  heart  beats 
more  quickly  when  its  load  is  lessened.  This  experimental  fact  has  been 
used  to  explain  palpitation  consecutive  to  haemorrhage,  high  temperature, 
or  violent  exercise,  the  blood-pressure  diminishing  as  the  result  of  haemor- 
rhage, or  of  dilatation  in  the  peripheral  vessels  (vasoinotor  nerves).  A 
fresh  element — namely,  the  quality  of  the  blood,  which  is  poorer  in  red 
corpuscles  and  in  oxygen — is  present  in  the  palpitation  of  anaemia. 

Description. — The  palpitations  may  be  isolated  or  grouped  in  attacks. 
In  sHght  attacks  the  heart-beats  are  troublesome  rather  than  painful,  and  are 
accompanied  by  precordial  discomfort.  In  violent  attacks  the  heart  "  beats 
as  if  it  would  burst  the  chest,"  its  movements  are  sometimes  tumultuous  and 
disordered  (arrhythmia),  the  pain  is  agonizing,  the  patient  suffocates,  his 
speech  is  interrupted,  his  face  is  pale  and  bathed  in  sweat,  and  his  hands  are 
cold  ;  he  is  threatened  with  faintness  and  syncope. 

Examination  during  an  attack  yields  various  results.  In  some  cases 
the  heart-beats  are  tumultuous  and  disordered,  but  in  others  they  preserve 
their  regularity.  The  pulse  is  not  always  in  exact  relation  with  the  heart- 
beats. The  pulsation  in  the  radial  artery  may  remain  normal,  in  spite  of 
the  apparent  intensity  of  the  ventricular  contraction. 

Palpitation  is  often  brought  on  by  trifling  causes  :  emotion,  movement, 
or  a  heavy  meal. 


NEUROSES  OF  THE  HEART  449 

The  diagnosis  of  the  cause  is  the  most  important  feature,  and  it  is  neces- 
sary to  know  whether  the  palpitations  are  purely  nervous  or  are  associated 
with  some  cardiac  lesion.  The  treatment  depends  upon  the  recognition  of 
the  cause.  The  first  indication  is  to  eUminate  anything  which  may  produce 
palpitation  (excesses  of  every  kind — tea,  coffee,  tobacco,  emotion,  heavy 
meals).  The  preparations  of  digitaUs  are  the  more  indicated  in  proportion 
as  the  arterial  tension  is  but  little  raised  and  the  pulse  is  weak  and  com- 
pressible (Jaccoud). 

Bromide  of  potassium,  valerian,  the  application  of  ice-bags  to  the  pre- 
cordial region,  and  hydrotherapy  yield  good  results. 


II.  PAROXYSMAL  TACHYCARDIA. 

Bouveret  in  1889  applied  the  term  "  paroxysmal  tachycardia  "  to  a 
disturbance  of  the  cardiac  rhythm,  characterized  by  crises  during  which 
the  pulse  beats  from  180  to  220  times  a  minute.  These  crises  come  on 
suddenly  without  appreciable  cause  at  various  intervals,  and  cease  just  as 
suddenly,  after  a  duration  varpng  from  a  quarter  of  an  hour  to  some  days. 
Since  Bouveret's  article  many  cases  have  been  published,  and  I  have 
had  a  patient  under  observation  for  two  years.  His  history  will  serve  as 
my  type,  because  all  cases  of  paroxysmal  tachycardia  are  a  replica  of  one 
another. 

One  day,  without  apparent  reason,  he  felt  as  though  his  heart  were  beating  with 
extraordinary  quicknes.a  and  violence.  The  attack,  which  lasted  an  hour  and  a  half, 
wa.s  painless,  and  passed  otf  suddenly.  Next  month  a  second  attack.  The  crises  have 
since  recurred  once  or  twice  a  month,  and  lately  almost  daily.  The  attack  may  be 
thus  described  :  Something  appears  to  get  loose  in  the  chest,  and  the  heart  beats  violently. 
After  a  period,  varying  from  a  quarter  of  an  hour  to  four  hours,  the  attack  ends  as 
suddenly  as  it  began.  On  examination  during  a  crisis  nothing  special  is  to  be  noted 
in  his  appearance  ;  no  distress,  no  angina  ;  he  talks  and  is  often  able  to  carry  on  his 
work.  During  the  attack  a  tremor  of  the  chest- wall  is  seen,  and  on  placing  the  hand 
over  the  heart,  as  many  as  200  beats  a  minute  may  be  counted.  This  condition  lasts 
from  one  to  three  hours.  At  the  end  of  the  attack  the  patient  feels  a  sudden  shock 
due  to  a  beat  of  exceptional  force,  and  the  normal  rhj'thm  is  then  re-estabhshed. 

It  is  curious  that  the  patient  can  sometimes  stop  the  crisis  by  fixing  the  chest  in 
forced  expiration  and  holding  his  breath  ;  he  becomes  cyanosed,  and  the  jugular  veins 
swell.  He  remains  for  a  moment  in  this  condition,  and  is  sometimes  obliged  to  take 
another  breath  without  having  strangled  the  crisis,  but  at  other  times  he  says:  "It 
has  stopped."     The  tremor  ceases,  and  the  pulse  suddenly  falls  to  70  or  80. 

In  all  published  cases  the  crisis  has  beeij  practically  identical. 

Sharp  emotion,  blows  upon  the  epigastrium,  abuse  of  cofEee  or  of  tobacco, 
digestive,  pulmonary,  or  uterine  troubles,  and  physical  or  mental  strain  have 
been  in  turn  invoked  to  explain  this  paroxysmal  tachycardia.  As  a  matter 
of  fact,  we  do  not  know  its  aetiology.  In  the  patient's  previous  history, 
hysteria,  neurasthenia,  and  hereditary  nervous  diseases  are  wanting. 

29 


450  TEXT-BOOK  OF  MEDICINE 

As  a  rule,  no  valvular  lesion  is  found,  Bouveret  accordingly  called  the 
disease  "  essential  paroxysmal  tachycardia,"  in  order  to  distinguish  it  from 
ordinary  tachycardia  seen  in  cardiac  affections.  There  are  cases,  however, 
in  which  the  disease,  while  remaining  identical  from  the  semeiological  point 
of  view,  coexists  with  mitral  or  aortic  endocarditis.  The  patient  of  whom 
I  have  just  spoken  was  suffering  from  aortic  incompetence. 

The  disease  may  last  for  an  indefinite  period.  If  the  crisis  only  lasts  a 
few  hours,  it  is  perfectly  bearable.  When  it  lasts  several  days,  haemoptysis, 
indicative  of  pulmonary  stasis,  may  occur.  If  the  crisis  lasts  still  longer, 
the  hver  becomes  large  and  painful,  the  urine  is  suppressed,  the  right  heart 
dilates,  oedema  and  serous  effusions  form,  and  the  patient  appears  dying. 
But  as  soon  as  the  crisis  ceases,  the  circulation  is  re-established,  the 
oedema  is  absorbed,  the  urine  becomes  abundant,  and  the  patient,  who 
appears  moribund,  recovers. 

The  prognosis,  however,  is  grave,  for  the  patient  may  succumb  in  a 
prolonged  attack.  The  disease  may  remain  stationary  and  be  prolonged 
indefinitely,  or  it  may  improve  and  end  in  recovery.  In  my  patient  the 
attacks,  which  occurred  daily,  have  become  less  frequent,  and  he  has  only 
one  crisis  every  week  or  fortnight. 

Post-mortem  examinations  have  been  performed  in  fatal  cases.  Dilata- 
tion of  the  right  heart  and  venous  stasis  in  every  organ  have  been  found ; 
the  lesions  are  evidently  secondary  and  terminal.  The  primary  lesions 
have  not  been  found ;  the  neuromotor  system  of  the  heart  has  always 
appeared  healthy  ;  the  bulb,  the  spinal  cord,  the  pneumogastric,  and  the 
sympathetic  nerves  are  free  from  disease,  and  the  heart  itself  only  shows 
commonplace  lesions. 

The  characters  of  the  disease  are  so  specific  that  it  is  not  necessary  to 
dwell  upon  the  diagnosis.  The  crises  of  paroxysmal  tachycardia  resemble 
neither  the  ordinary  palpitation  in  heart  disease  nor  the  reflex  palpitation 
of  dyspeptic  or  hepatic  origin,  etc.  Tachycardia  in  Basedow's  disease 
may  supervene  in  crises,  but  does  not  show  the  sudden  passage  from  the 
state  of  crisis  to  that  of  absolute  calm  and  vice  versa. 

Treatment  has  so  far  been  powerless  to  influence  this  disease. 

III.  PERMANENT  BRADYCARDIA. 

The  pulse-rate  in  health  is  from  70  to  72.  As  a  result  of  different  in- 
fluences (intoxication,  jaundice),  the  rate  may  fall  below  50 ;  but  in  this  case 
the  fall  is  transitory,  while  this  section  deals  with  permanent  slowness  of 
the  pulse. 

The  slowing  is  so  great  that  the  pulse  falls  to  20  beats,  or  even  less.  In 
one  of  my  patients  the  pulse-rate  fell  to  14  per  minute  for  some  days. 


NEUROSES  OF  THE  HEART  451 

The  pulse  preserves  its  regularity.  The  sphygmographic  tracing  stows 
a  short  upstroke  and  a  long-drawn-out  downstroke.  The  arterial  pressure 
is  usually  higher  than  normal. 

The  heart-beats  are  well  marked.  The  duration  of  the  first  pause  is 
not  increased,  and  it  is  the  increase  of  the  second  pause  that  causes  the 
slowness  of  the  cardiac  rhythm.  In  short,  each  heart-beat  is  normal,  but 
the  interval  between  the  beats  is  much  increased.  This  interval  may  not 
be  completely  silent.  After  the  diastohc  sound,  muffled  rumbhng  sounds 
are  heard.  Vaquez  has  shown  that  they  are  due  to  an  abortive  contrac- 
tion of  the  auricles,  and  radiography  has  confirmed  his  interpretation. 

Bradycardia  may  be  associated  with  perfect  health,  or  may  be  accom- 
panied by  morbid  phenomena,  caused  in  several  ways. 

Any  lesion  that  affects  the  cardiac  innervation  may  result  in  brady- 
cardia, either  by  stimulating  the  system  that  slows  the  rate  (bulb  and 
vagus),  or  by  inhibiting  the  system  that  quickens  it  (spinal  cord  and  great 
sympathetic). 

Lesions  may  be  present  in  the  heart,  and  affect  the  intracardiac  gangha 
(syphihtic  gumma  of  the  interventricular  septum  and  upper  part  of  the  left 
ventricle,  in  Rendu  and  Massary's  case).  They  may  affect  either  pneumo- 
gastric  nerve,  which  is  compressed  in  its  intrathoracic  course  either  by  the 
dilated  aorta  (Stackler's  case)  or  by  enlarged  mediastinal  glands  (Lannois' 
case).  The  pneumogastric  may  also  be  injured  in  its  intracranial  course 
(compression  by  a  gummatous  tumour  of  the  cerebellum).  Many  lesions 
may  affect  the  cardio -inhibitory  nucleus  in  the  bulb  (injury,  cervical  caries, 
syphihtic  or  tubercular  tumours,  infectious  myelitis). 

Lesions  of  the  accelerator  system  are  less  often  in  evidence,  yet  the 
presence  of  unilateral  dilatation  of  the  pupil  has  shown  the  lesion  to  be  in 
the  cardio-spinal  centre,  which  is  near  the  centre  for  dilatation  of  the  pupil. 

All  these  cases  of  bradycardia  depend  upon  such  gross  lesions  that  there 
can  be  no  possible  doubt  as  to  their  existence  ;  but  the  case  is  different  in  the 
syndrome  which  Charcot  has  called  "  Permanently  slow  pulse,  with  syncopal 
or  epileptiform  crises,"  and  for  which  Huchard  has  proposed  the  name 
of  "  Stokes-Adams  disease."  The  patients,  who  are  of  advanced  years, 
often  show  signs  of  renal  insufficiency  ;  their  arteries  are  hard  and  tortuous, 
and  the  tension  is  high.  They  are  subject  to  attacks  of  syncope,  which  in 
one  of  my  cases  had  the  following  characters  : 

The  syncope  was  ushered  in  by  a  kind  of  aura  :  gonerai  malaise,  feeling  of  weight  in 
tlie  chest,  buzzing  in  the  ears,  cold  sweat,  pallor,  and  chilliness.  The  patient  lost 
consciousness  and  looked  almost  dead,  with  dull  eyes  and  cadaveric  tint.  Aft«r  two 
or  three  minutes  the  colour  returned,  the  eyes  opened,  and  she  rapidly  recovered  con- 
sciousness. She  had  no  involuntary  emission  of  urine,  no  epileptiform  movements. 
After  the  crisis  she  comi)laincd  of  feeling  bruised,  as  though  her  body  had  been  racked  ; 
she  sometimes  felt  sick,  but  did  not  vomit. 

29—2 


452  TEXT-BOOK  OF  MEDICINE 

The  syncope  may  be  immediately  followed  by  an  epileptiform  attack. 
Whether  the  attacks  are  syncopal  or  epileptiform,  they  are  often  ushered  in 
by  very  marked  slowing  of  the  pulse. 

The  attacks  succeed  one  another  at  variable  intervals  ;  the  more  fre- 
quent they  become,  the  more  grave  the  prognosis.  The  patient  finally  dies 
during  an  attack  of  syncope  which  is  more  prolonged  than  the  others,  and 
the  duration  of  the  disease  does  not  exceed  three  or  four  years. 

No  grave  lesions  are  found,  as  a  rule.  The  kidneys  and  myocardium  often 
show  fibrous  change  ;  the  arteries  of  the  nerve  centres  are  atheromatous ; 
arterio-sclerosis  of  the  vessels  in  the  bulb  appears  to  be  the  chief  cause  of  the 
disease. 

No  treatment  has  any  efiect  upon  permanent  bradycardia.  Milk  diet 
gives  some  benefit  in  cases  of  renal  insufficiency  (Debove).  Rest  is  abso- 
lutely indicated  (Hirtz).  During  an  attack  of  syncope  the  patient  must 
keep  his  bed. 


IV.  EXOPHTHALMIC  GOITRE— BASEDOW'S  DISEASE. 

Medical  and  Surgical  Treatment. 

**  Many  patients  will  consult  you  for  palpitation  of  the  heart,  but  you 
will  at  once  be  struck  by  their  strange  look  and  their  prominent  eyes,"  and 
you  will  find  hypertrophy  of  the  thyroid  gland. 

These  patients  are  suffering  from  exophthalmic  goitre,  Graves'  or 
Basedow's  disease,  characterized  in  a  typical  case  by  the  following  troubles, 
wliich  are  mostly  of  nervous  origin  :  (1)  cardiac  troubles  ;  (2)  ocular  troubles ; 
(3)  hypertrophy  of  the  thyroid  gland  ;  (4)  motor  troubles  ;  (5)  psychical 
troubles.  According  to  the  case,  these  various  symptoms  may  appear  in 
succession  or  in  combination.  In  some  cases  they  are  predominant ;  in 
others  they  are  indefinite. 

Description — 1.  Cardiac  Troubles. — Acceleration  of  the  heart-beats 
is  the  essential  symptom  of  Basedow's  disease.  This  symptom  is  never 
lacking ;  it  is  found  in  early  cases,  and  even  after  all  the  other  symptoms 
have  disappeared,  the  acceleration  of  the  heart-beats  persists  for  some  time 
longer.  This  symptom  is  due  to  paralysis  of  the  nucleus  of  the  vagus 
nerve.  In  some  cases  the  patient  does  not  notice  the  tachycardia,  but  in 
others  the  beats  are  distressing  and  cause  palpitation.  This  palpitation 
becomes  gradually  more  severe,  and  supervenes  in  the  form  of  attacks  ; 
120  to  150  beats  per  minute  may  be  counted  during  the  paroxysms.  The 
palpitation  is  often  violent,  and  the  cardiac  impulse  so  strong  that  it  raises 
the  chest-wall,  while  the  heart  "  beats  as  though  it  would  burst."  In 
spite  of  this  disturbance,  the  beats  may  not   be   irregular.      In   another 


NEUROSES  OF  THE  HEART  453 

variety  the  beats  are  irregular  ;  the  heart  seems  feeble,  and  its  pulsations  are 
hurried,  uneven,  and  abortive.  During  the  paroxysms  the  arrhythmia  and 
cardiac  weakness  may  lead  to  acute  asystole,  with  dyspnoea,  angina,  and 
cyanosis.  In  some  cases  the  symptoms  of  angina  pectoris  have  been 
recorded.     The  symptoms  of  asystole  disappear  between  the  paroxysms. 

Lastly,  in  some  patients  the  troubles  of  innervation  are  comphcated  by 
hypertrophy,  dilatation  of  the  cavities,  or  insufficiency  of  the  tricuspid  and 
mitral  valves.  The  hypertrophy  is  attributed  to  the  functional  hyper- 
activity of  the  heart,  or  to  an  excess  of  tension  consecutive  to  lesions  of  the 
valves.  These  valvular  lesions  (insufficiency  of  the  auriculo-ventricular 
and  aortic  valves)  are  sometimes  entirely  mechanical  in  origin.  They  may 
be  caused  by  dilatation  of  the  ventricles  ;  the  heart  muscle,  weakened  bv 
the  strain,  allows  overdistension.  These  lesions  are  usually  transient,  and 
cease  with  the  disease,  though  they  may  become  permanent. 

The  carotid  arteries  are  tortuous  and  enlarged.  The  pulsation  raises 
the  tissues  of  the  neck.  These  beats  are  not  the  contre-coup  of  the  cardiac 
impulse,  but  the  vessels  in  the  neck,  both  arteries  and  veias,  beat  on  their 
own  account,  and  appear  to  participate  in  the  overgrowth  and  pulsation 
which  affect  the  vessels  of  the  thjToid  gland.  The  sphere  of  vascular 
excitation  appears  limited  to  this  region,  for  violent  pulsation  is  not  found 
in  the  abdominal  aorta,  the  radial  artery,  or  elsewhere.  In  spite  of  these 
vascular  troubles,  the  blood-pressure  remains  normal.  Inequality  of  the 
two  radial  pulses  has  been  found. 

2.  Ocular  Troubles. — Spasms  of  the  upper  eyelid  may  precede  or  accom- 
pany the  exophthalmos  (Wecker).  When  the  glance  is  directed  downwards, 
the  upper  eyelid  no  longer  follows  the  ball  of  the  eye,  but  remains  fixed  above 
it  (de  Graefe).  The  exophthalmos  is  double,  and  may  be  so  extreme  that 
the  eyeUds  can  scarcely  cover  the  ball,  giving  to  the  physiognomy  a  strange 
expression  of  astonishment  and  terror,  which  Marchal  de  Calvi  called  the 
"  tragic  eye."  This  appearance  is  partly  due  to  retraction  of  the  levator 
palpebrse  superioris,  which  causes  considerable  enlargement  of  the  palpebral 
aperture  (Stellwag). 

During  the  paroxysms  the  exophthalmos  increases  to  such  a  degree  that 
luxation  of  the  eyeball  has  often  been  seen  (Pain).  The  conjunctiva  is 
often  injected,  and  the  cornea,  being  continually  exposed,  may  become 
infected  and  ulcerated.  The  sight  is  unaffected,  and  it  is  rare  to  see  myopia 
or  j)resbyopia.  The  ophthalmoscope  may  reveal  congestion  of  the  choroid 
and  dilatation  of  the  retinal  vessels.  Galezowski  and  the  wTitcr  have  seen 
retinal  haemorrhages. 

In  patients  suffering  from  Basedow's  disease,  with  or  without  hysteria, 
we  sometimes  see  bilateral  paralysis  of  the  motor  muscles  of  the  eyeball, 
in  which  case  the  voluntary  movements  are  chiefly  affected,    while    the 


454  TEXT-BOOK  OF  MEDICINE 

reflex  ones  are  in  part  preserved.  The  whole  external  musculature — namely, 
the  recti  and  the  obHqui,  innervated  by  the  third,  fourth,  and  sixth  pairs — 
is  paralyzed.  In  addition,  the  movements  of  the  eyeball  are  abohshed,  and 
only  elevation  of  the  upper  eyehd  is,  as  a  rule,  preserved.  This  inability 
to  move  the  eyes  gives  a  strange  fixed  look,  and  the  patient  cannot  see  an 
object  to  his  right  or  his  left  without  turning  his  head.  The  name  "  ex- 
ternal ophthalmoplegia  '*  has  been  given  to  this  paralysis  of  the  external 
musculature.  The  internal  musculature,  i^hich  comprises  the  cihary 
muscles  and  the  radial  or  circular  fibres  of  the  iris,  and  governs  accom- 
modation and  the  dilatation  or  contraction  of  the  pupil,  is  unaffected  in 
Basedow's  disease.  External  ophthalmoplegia  maybe  seen  in  patients  suffering 
from  both  exophthalmic  goitre  and  hysteria,  or  from  either  malady  alone. 

3.  Thyroid  Body. — The  enlargement  of  the  thyroid  body  results  from 
dilatation  of  its  numerous  vessels.  Auscultation  of  the  gland  therefore 
reveals  simple  or  double  blowing  murmurs,  which  are  louder  during  diastole, 
as  in  a  cirsoid  aneurysm.  On  palpation,  we  feel  expansile  pulsation,  as  in 
an  aneurysm.  The  right  lobe  is  more  often  invaded  than  the  rest  of  the 
organ,  and  although  the  tumour  is  not  as  large  as  an  ordinary  goitre,  it 
may,  by  compression  of  the  trachea  or  by  the  excitation  of  the  recurrent 
nerves,  produce  voice  changes,  spasm  of  the  glottis,  and  paroxysmal  attacks 
of  suffocation. 

4.  Motor  Troubles. — Tremors,  paralysis,  and  choreiform  movements 
may  appear  at  the  onset  or  during  the  course  of  Basedow's  disease. 

Tremor  is  almost  constant,  but  may  be  so  shght  that  care  is  required 
to  discover  it.  The  tremor  is  most  frequent  in  the  upper  limbs.  The 
arms  and  hands,  even  during  rest,  show  tremors,  which  hamper  writing  and 
all  the  delicate  functions  of  the  hand  and  fingers.  In  the  lower  hmbs  the 
tremor  is  also  present  during  repose,  as  well  as  in  walking.  During  repose 
the  limbs  show  a  kind  of  pedal  movement.  In  exceptional  cases  the  tremor 
may  invade  the  whole  body,  including  the  face  and  the  tongue.  Fibrillary 
movements  are  usually  seen  in  all  the  muscles. 

In  some  cases  tremor  opens  the  scene,  and  attracts  so  much  notice  as  to 
constitute  a  defaced  form  of  Basedow's  disease.  On  closer  inspection, 
however,  we  usually  find  other  symptoms,  such  as  tachycardia,  palpitation, 
peculiar  look,  pulsation  of  the  carotids,  diarrhoea,  rapid  wasting,  diminished 
electrical  resistance,  etc.  (Vigouroux).  Although  these  symptoms  may  only 
be  present  to  a  partial  extent,  they  assist  in  forming  a  diagnosis.  The 
syndrome  may  be  reconstructed  from  the  recognition  of  some  one  symptom. 
Hence  we  are  not  liable  to  confound  this  tremor  with  that  due  to  alcoholism, 
mercurial  poisoning,  neurasthenia,  or  morphinomania.  Lastly,  we  may  add 
that  the  tremor  in  Basedow's  disease  shows  its  special  tracing  (Marie),  and 
gives  about  eight  or  nine  oscillations  a  second. 


NEUROSES  OF  THE  HEART  455 

Paralytic  troubles  are  manifold  (Ballet).  Without  mentioning  external 
ophthalmoplegia,  the  paralyses  of  Basedow's  disease  may  show  the  most 
varied  forms — monoplegia,  hemiplegia  (Teissier),  weakness  of  the  upper 
Umbs  (Drejrfus-Brisac),  diplegia,  paralysis  of  the  nuchal  muscles  (Chwos- 
teck),  paresis  of  the  lower  Umbs  (Heyden),  and  complete  paraplegia  (Charcot). 

These  paralyses,  whether  shght  and  transient  or  severe  and  prolonged, 
have  been  set  down  to  hysteria.  As  hysteria  is  sometimes  associated  with 
exophthalmic  goitre,  it  is  reasonable  to  admit  that  paralyses  which  are 
hysterical  in  nature  may  coexist  with  Basedow's  disease.  Due  allowance, 
however,  being  made  for  the  possible  paralyses  of  hysteria,  which,  moreover, 
have  their  own  characteristics,  certain  paralyses  are  inherent  to  Basedow's 
disease,  without  the  need  for  invoking  the  intervention  of  another  factor. 
Thus,  my  patient,  who  showed  no  signs  of  hysteria,  was  a  perfect  example 
of  Basedow's  paralysis. 

As  regards  the  upper  hmbs,  the  paralysis  diminishes  or  aboHshes  the 
functions  of  the  hands.  My  patient  could  neither  seize  an  object  nor  hold 
it.  She  was  incapable  of  dressing  herself,  or  of  feeding  herself,  so  that  for 
some  time  she  had  to  be  fed  by  others. 

Paraplegia,  varying  in  degree  from  paresis  to  total  paralysis,  is  very 
common  in  Basedow's  disease.  Its  prominent  features  have  been  given  by 
Chevaher  :  "  In  the  upright  position,  or  in  walking,  although  the  patient 
experiences  no  feeUng  of  vertigo,  the  limbs  give  way  and  bend  suddenly. 
Sometimes  during  a  walk  he  may  fall  forward  upon  his  knees.  At  other 
times,  though  more  rarely,  the  motor  weakness  takes  months  to  become 
complete,  as  in  a  case  quoted  by  Charcot,  where  the  impossibility 
of  maintaining  the  upright  position  and  of  walking  lasted  nearly  a  whole 
year.  These  paraplegic  troubles  do  not  remain  stationary  ;  they  improve 
from  time  to  time  and  grow  worse  again,  and  tliis  relapse,  which  is 
followed  by  improvement,  shows  a  certain  analogy  with  the  evolution  of 
the  disease.  In  the  intervals  the  legs  frequently  collapse  while  walking,  so 
that  crutches  may  be  needed." 

If  we  do  not  understand  these  cases,  the  idea  of  paraplegia  consecutive 
to  myeUtis  at  once  enters  our  mind  ;  but  we  should  not^  confound  the  para- 
plegia of  Basedow's  disease  with  myelitis,  for  in  the  former  case  bladder 
troubles  are  absent,  the  sphincters  are  intact,  and  we  sen  no  trophic  troul)les, 
no  bed-sores  on  the  sacrum.  Moreover,  we  should  not  confound  tliis  para- 
plegia with  that  duo  to  hysteria,  because,  in  addition  to  the  numerous 
stigmata  of  hysteria,  such  as  hemianajsthesia,  narrowing  of  the  \isual  field, 
aboUtion  of  the  pharyngeal  and  ovarian  reflexes,  hysterogenous  zones,  etc, 
hysterical  paraplegia  is  soft,  and  accompanied  by  anaesthesia  of  tlio  paralyzed 
parts,  with  complete  loss  of  the  muscular  sense,  while  the  muscles  do  not 
present  the  diminution  of  electrical  resistance  seen  in  Basedow's  disease. 


456  TEXT-BOOK  OF  MEDICINE 

Choreiform  movements  complete  the  triad  of  motor  troubles  in  Base- 
dow's disease.  They  were  very  marked  in  my  patient  at  the  Hotel-Dieu, 
and  a  cursory  examination  revealed  choreiform  movements  in  the  hands, 
arms,  shoulders,  trunk,  neck,  and  face.  It  has  been  asked  whether  chorea 
and  Basedow's  disease  are  two  associated  maladies,  or  whether  Basedow's 
disease  may  not  be  capable  of  causing  choreiform  movements,  just  as  it 
causes  tremors  and  paralysis.  In  1864  L.  Gros,  comparing  exophthalmic 
goitre  with  chorea,  described  a  case  of  Basedow's  disease,  with  choreiform 
movements  which  affected  the  upper  and  lower  Umbs,  the  neck,  and  the  face. 

In  1876,  at  the  Congress  of  Clermont-Ferrand,  Gagnon,  while  studying  the  rela- 
tions between  exophthalmic  goitre  and  chorea,  quoted  the  case  of  a  neurotic  young  girl 
who  never  had  rheumatism.  For  a  month  this  child  had  wasted,  her  character  had 
changed,  and  she  had  palpitation.  Tliis  picture  marked  the  onset  of  Basedow's 
disease.  At  this  time  the  pulse-rate  was  130,  and  hypertrophy  of  the  thyroid  body 
was  evident.  The  disease  followed  its  course,  and  two  years  later  she  showed  choreic 
movements,  which  finally  became  general. 

In  1881  Gueneau  de  Mussy  pubUshed  a  case  of  a  young  girl  suffering  from  Base- 
dow's disease,  with  choreiform  movements.  For  some  weeks  the  locomotor  functions 
had  been  so  affected  that  the  patient  could  not  walk.  She  used  to  make  some  regular 
steps  forwards  or  backwards,  showing  that  the  muscular  power  was  much  enfeebled, 
in  addition  to  the  incoherence  of  her  movements.  The  cerebral  functions  were  not 
spared.  The  young  girl  was  strange,  her  memory  was  not  reUable,  she  had  troubled 
dreams,  and  even  delirium.  At  the  end  of  eight  or  ten  months  the  choreiform  and 
paralytic  troubles  disappeared,  as  well  as  the  mental  aberration. 

Raymond  and  Serieux,  in  a  paper  on  Basedow's  disease  and  mental  degeneration, 
found  in  one  patient  permanent  choreiform  spasms  of  the  external  obhque  muscle. 
Deleage,  in  1894,  communicated  to  the  Societe  des  Sciences  Medicales  of  Gannat  a  case 
of  exophthalmic  goitre  with  tremors,  paralytic  troubles,  and  choreiform  movements. 

Is  it  a  question  of  choreiform  movements  or  of  true  chorea  in  these 
patients  ?  Kohler  is  incHned  to  look  on  this  symptom  as  a  choreiform 
motor  trouble  ;  Dach  states  his  opinion  that  it  is  only  met  with  in  children, 
which  is  wrong  ;  and  Mobius  thinks  that  it  is  a  question  of  chorea  super- 
vening as  an  accidental  complication.  For  my  part,  I  cannot  compare 
this  condition  with  Sydenham's  chorea.  I  beheve  that  it  is  only  a  question 
of  choreiform  movements,  and  my  reasons  for  this  opinion  are  as  follows  : 
If  exophthalmic  goitre  and  chorea  are  indeed  two  associated  diseases,  as 
some  authors  think,  why  does  Basedow's  disease  always  precede  chorea  ? 
We  do  not  see  exophthalmic  goitre  during  the  course  or  during  the  decline 
of  true  chorea.  Hundreds  of  children  who  are  affected  by  chorea  never 
develop  exophthalmic  goitre.  I  think,  therefore,  that  choreiform  move- 
ments are  a  part  of  Basedow's  disease,  just  as  are  tremors  and  paralysis. 

The  choreiform  movements,  with  the  tremor  and  paralysis,  constitute 
a  triad  of  motor  troubles.  The  triad  may  be  incomplete  or  complete,  and 
we  can  understand  how  great  is  the  disturbance  in  a  muscular  system 
affected  at  the  same  time  by  paresis,  tremor,  and  choreiform  movements. 


NEUROSES  OF  THE  HEART  457 

5.  Other  Nervous  Troubles.  —  The  sensory  troubles  in  Basedow's 
disease  consist  in  trigeminal  neuralgia,  intercostal  neuralgia,  racliialgia, 
and  hemiansesthesia,  which  is  usually  associated  with  hysteria. 

In  most  patients  vasomotor,  trophic,  and  secretory  troubles  are  seen. 
Albuminuria,  glycosuria,  and  polyuria,  which  indicate  disturbance  in  the 
bulb,  have  been  noted. 

Many  patients  complain  of  an  exaggerated  sensation  of  heat.  They 
open  the  windows,  and  often  complain  of  being  too  heavily  clad  (Basedow, 
Teissier).  This  increase  in  temperature  is  appreciable  with  the  thermo- 
meter, and  sometimes  reaches  one  degree  higher  than  normal. 

Changes  in  the  skin,  sweating,  purpura,  pigmented  patches,  discrete  or 
confluent  vitiligo,  alopecia,  and  chronic  urticaria  have  often  been  observed, 
I  have  frequently  seen  pigmentation  of  the  neck,  shoulders,  and  arms,  in  the 
form  of  more  or  less  large  and  discrete  patches.  (Edema  is  frequent,  and 
chiefly  affects  the  lower  hmbs.  Trousseau  has  seen  hypertrophy  of  the  breasts. 

We  may  also  find  the  following  series  of  symptoms  : 

Dyspnoea,  which  may  be  associated  with  palpitation,  is  frequent.  It 
may  be  continuous,  intermittent,  or  paroxysmal,  and  is  the  chief  symptom 
in  some  cases.     It  is  probably  due  to  changes  in  the  nucleus  of  the  vagus. 

The  digestive  functions  suffer  in  Basedow's  disease.  I  have  found 
hypertrophy  of  the  Uver  and  jaundice;  bouhmia  succeeds  anorexia,  and 
violent  pulsations  are  seen  in  the  epigastric  angle.  We  may  see  vomiting 
and  diarrhoea  in  the  form  of  crises  lasting  one  or  more  days.  In  spite  of 
the  increased  appetite,  patients  waste  and  pass  into  a  condition  of  exophthal- 
mic cachexia.  The  general  wasting  contrasts  in  a  singular  manner  with 
the  exaggerated  development  of  the  eyes  and  neck.  Wasting  may  be  the 
first  apparent  symptom.  I  have  seen  a  patient  who  rapidly  lost  over  a 
stone  in  weight ;  wasting  and  tachycardia  were  here  the  only  appreciable 
symptoms  for  some  months.  At  first  sight  such  wasting  leads  us  to  think 
of  tuberculosis  or  of  diabetes,  and,  as  glycosuria  is  often  present,  the  diagnosis 
must  be  carefully  considered  in  order  to  avoid  mistakes. 

Menstruation  is  nearly  always  affected.  It  may  be  irregular  or  sup- 
pres.sed,  and  the  amenorrhoea  is  often  accompanied  by  leucorrhoea.  Re- 
estabhshment  of  the  menstrual  functions  is  one  of  the  most  favourable  signs 
in  prognosis.  Pregnancy  has  sometimes  a  beneficial  effect.  In  men  im- 
potence is  usually  associated  with  Basedow's  disease. 

Haemorrhages  are  sometimes  seen.  I  have  observed  purpura,  haemop- 
tysis, and  retinal  haemorrhages  in  the  same  patient.  Cerebral  hioniorrhago 
and  death  from  apoplexy  have  been  noted.  I  saw  one  case  of  this  nature 
with  Jaccoud. 

Vigouroux  and  Kohler  have  noted  diminished  resistance  to  electric 
currents. 


458  TEXT-BOOK  OF  MEDICINE 

In  some  cases  Basedow's  disease  and  myxoedema  have  been  associated ; 
no  antagonism  exists  between  them. 

6.  Psychical  Troubles — Mental  Condition. — As  a  general  rule,  few 
patients  escape  psychical  troubles.  Trousseau  was  the  first  to  describe 
them  :  "  The  changes  of  character  are  such  that  Ufe  becomes  difficult  for 
the  entourage  of  these  patients,  who  are  irritable  and  exacting  to  such  a 
degree  that  the  disease  forms  their  only  excuse.  In  addition  to  these  changes 
in  character  we  may  note  insomnia — a  cruel  comphcation  which  reduces 
patients  to  extreme  despair."  Trousseau  mentions  psychical  troubles  in 
most  of  his  cases,  and  assigns  such  importance  to  them  that  he  gives  them 
a  prominent  place  in  his  wonderful  description  of  exophthalmic  goitre. 
All  authors  who  have  studied  exophthalmic  goitre  have  laid  stress  upon 
the  psychical  troubles.  "  In  nearly  all  patients  suffering  from  exophthalmic 
goitre,"  says  Ball,  "  there  exists  a  certain  degree  of  exaltation.  They  nearly 
all  have  strange  ideas,  and  these  morbid  manifestations  may  end  in  the  most 
acute  mania."  According  to  JofEroy,  "  the  patient  is  restless,  often  a 
prey  to  exaggerated  activity,  and  yet  incapable  of  methodical  work  or  of 
prolonged  mental  effort.  Among  the  first  changes  which  exophthalmic 
goitre  imprints  upon  the  character  of  patients,  we  find  in  some  cases 
depression ;  or  in  others  excitation."  Boeteau  thus  describes  the  psychical 
troubles  :  "  The  chief  symptom  is  profound  melancholy,  which  more  and 
more  enters  into  every  one  of  the  patient's  thoughts,  so  that  he  entertains 
ideas  of  suicide.  At  the  same  time  the  victims  become  impatient,  surly, 
and  remarkably  emotional.  Their  will-power,  when  not  quite  absent,  is 
often  very  feeble  ;  they  are  incapable  of  fixing  their  -attention  upon  any 
subject,  even  for  a  minute  ;  they  cannot  remember  next  day  what  they  did 
the  day  before.  They  show  complete  indifference  not  only  to  what  concerns 
them,  but  to  everything  which  affects  their  family,  even  to  those  who  are 
most  dear  to  them ;  and  this  indifference  may  sometimes  amount  to 
aversion." 

Psychical  troubles  may  exist  from  the  first — sometimes,  indeed,  as  the 
initial  symptom — so  that  the  diagnosis  remains  in  doubt  until  forcible 
beating  of  the  heart,  exophthalmos,  goitre,  tremors,  etc.,  appear.  The 
interpretation  of  the  psychical  troubles  is  not  decided.  Some  authors 
consider  them  to  be  a  direct  part  of  the  disease  ;  others,  on  the  contrary, 
look  upon  them  as  due  to  hysteria  and  neurasthenia.  To  those  who  make 
these  psychical  troubles  subordinate  to  hysteria,  we  may  answer  that  there 
are  cases  of  exophthalmic  goitre  in  which  hysteria  is  absent,  and  cannot, 
therefore,  be  the  cause.  Neurasthenia  appears  to  be  open  to  the  same 
objections.  It  is  undeniable  that  individuals  may  suffer  at  once  from 
exophthalmic  goitre  and  from  neurasthenia  or  hysteria,  but  this  is  no  reason 
to  bring  in  neurasthenia  in  every  case. 


NEUROSES  OF  THE  HEART  459 

It  is  perhaps  more  logical  to  admit  that  Basedow's  disease,  like  chorea, 
awakens  psychical  troubles  in  predisposed  persons.  The  psychical  troubles 
of  chorea  show  very  great  analogy  with  those  of  Basedow's  disease.  We 
find  the  same  intellectual  depression,  the  same  inaptitude  for  work,  lapses 
of  memory,  changes  in  character,  melancholy,  indifference,  and  irascibihty. 
Must  we  say  that  neurasthenia  or  hysteria  has  for  some  weeks  been  associated 
with  chorea  ?  I  think  not.  We  must  say  (omitting  cases  in  which  the 
association  does  exist)  that  chorea  can  extend  to  the  whole  cerebro-spinal 
system,  and  excite  slight  or  severe  psychical  troubles.  The  same  reasoning 
appHes  to  Basedow's  disease.  Are  we  to  say  that,  at  the  onset,  neurasthenia 
comes  to  our  rescue  by  bringing  in  its  contingent  of  psychical  troubles  ? 
I  think  not.  We  must  say  that  Basedow's  disease  can  extend  to  the  whole 
nervous  system,  and  excite  psychical  troubles  ju^t  as  it  excites  nervous 
troubles  of  every  kind.  Further,  as  Toulouse  has  remarked,  "  neuras- 
thenia has  succeeded  in  donning  the  mental  troubles  which  formerly  belonged 
to  exophthalmic  goitre  alone." 

These  psychical  troubles  are  usually  transitory,  and  tend  to  recover. 
I  shall  now  deal  with  certain  serious  mental  troubles  or  true  psychoses 
"  running  crescendo  through  the  whole  gamut  from  transitory  or  fugitive 
deUrium  to  inveterate  mania  "  (Boeteau).  These  psychoses  include  acute 
and  chronic  mania,  delirium  with  ideas  of  persecution,  melancholia,  irresistible 
impulses,  and  apprehensive  madness,  and  have  been  repeatedly  discussed 
(Raymond  and  Serieux,  Joffroy). ' 

Resume  of  cases : 

Young  woman,  -without  nervous  antocedonts,  taken  ill  with  acute  mania  during 
Basedow's  disease.  She  became  violent  and  refused  all  food ;  excitation  gave  way 
to  depression  ;  her  mental  condition  improved,  but  she  died  from  cachexia. — A  young 
woman,  without  personal  or  hereditary  antecedents,  had  Basedow's  disease  compUcated 
by  melanohoha.  She  refused  food,  tried  to  throw  herself  out  of  the  window,  and 
suffered  from  delusions.  She  recovered  some  months  later. — A  woman,  suffering 
from  typical  exophthalmic  goitre,  was  seized  with  irresistible  impulses  and  delirium. 
She  felt  an  impulse  to  kill  her  children,  but  she  was  able  to  resist  the  impulse,  though 
she  feared  the  greatest  misfortunes.  Her  insomnia  was  persistent,  and  her  distress 
was  intolerable.  A  year  later,  however,  recovery  was  complete. — My  patient,  with 
exoj)hthalniic  goitre,  had  hallucinations  of  sight  and  hearing,  was  liaunted  with  ideas  of 
persecution,  and  imagined  that  j^eople  hid  in  her  room  in  order  to  kill  her. 

The  psychosis  in  Basedow's  disease,  therefore,  may  assume  very  different 
forms.  Difficulties  begin  when  we  have  to  interpret  its  intimate  nature. 
Some  authors  say  that  these  mental  troul)les  form  an  integral  part  of  tlie 
disease.  Whether  the  cerebral  symptoms  are  slight,  as  is  usually  the 
case,  or  whether  they  are  severe,  with  hallucinations,  impulses,  maniacal 
excitement,  or  delirium  of  every  kind,  it  is  none  the  less  true  tliat  they  are 
symptoms  of  a  cerel)ral  nature,  and  form  part  of  Basedow's  disease,  in  the 
same  way  as  the  other  nervous  troubles.     This  conception  of  Basedow's 


460  TEXT-BOOK  OF  MEDICINE 

disease  makes  it  a  morbid  entity,  a  neurosis,  or  a  neuropsychosis,  in  which 
every  part  of  the  nervous  system  is  more  or  less  affected. 

Other  authors  enunciate  a  different  opinion  and  divide  up  the  disease. 
They  say  that  the  mental  troubles,  melancholia,  delirium,  or  delusions — 
in  short,  every  form  of  mental  ahenation — must  be  set  down  as  psychoses 
which  do  not  spring  directly  from  the  disease,  but  are  associated  with  it, 
just  as  the  same  authors  would  associate  hysteria  and  neurasthenia  with  it. 
These  morbid  conditions  which  evolve  in  the  same  patient  are  not,  therefore, 
hybrids  in  the  true  sense  of  the  word  ("in  neuropathology,"  says  Charcot, 
"  hybrids  do  not  exist "),  but  are  associated,  each  association  preserving 
its  autonomy,  characters,  degree  of  gravity,  and  therapeutic  indications. 
Tliis  grouping  of  morbid  conditions,  neuroses,  and  psychoses,  is  said  to  have 
heredity  as  its  cause. 

This  opinion  is  seductive,  although  it  is  far  from  agreeing  with  the  facts 
of  heredity,  and  though  it  forms  an  incomplete  explanation  of  the  fact  that 
heredity  is  sometimes  direct,  sometimes  intermittent,  and  that  there  may 
be  heredity  of  transformation,  and  also  homologous  heredity.  According 
to  some  neuropathologists,  persons  affected  with  psychoses  in  Basedow's 
disease  are  really  degenerates.  "  In  many  cases,"  say  Raymond  and 
Serieux,  "  Basedow's  disease  may  be  only  a  special  locahzation  of  functional 
troubles  which  supervene  in  degenerates,  or  in  predisposed  persons,  in  some 
part  of  the  cerebro-spinal  axis.  Magnan's  theory  of  this  failure  of  equiU- 
brium  in  the  centres  of  the  cortex  or  of  the  spinal  cord  (paralysis,  or  erethism 
of  these  centres)  may  be  apphed  to  these  different  manifestations. 

Toulouse,  in  a  critical  review  of  the  relations  betw-een  exophthalmic 
goitre  and  mental  alienation,  discusses  this  question,  and  shows  us  the 
defects  of  too  hasty  conclusions.  "  At  this  time,"  says  he,  "  the  tendency 
evident  in  psychiatry,  thanks  to  the  works  of  Morel  and  Magnan,  is  to 
refer  mental  diseases  to  some  distant  hereditary  cause,  and  to  overlook 
the  closer  causes.  This  psychopathic  predisposition  cannot  be  denied,  but 
it  is  too  general  an  idea,  although  it  forms  the  basis  of  all  mental  ahenation. 
The  hypothesis  of  predisposition  does  not  suffice  to  explain  the  appearance 
of  mental  disorders  in  exophthalmic  goitre,  as  in  other  maladies  in  which 
psychoses  appear." 

The  discussion,  therefore,  takes  this  form.  There  is  a  question  of  fact 
and  of  theory.  Chnical  facts  show  that  many  persons  suffering  from  Base- 
dow's disease,  especially  women,  may  have  psychical  troubles  and  mental 
disorders  as  well  as  motor  troubles  (tremor,  paralysis,  choreiform  movements) 
and  nervous  troubles  of  every  kind  (crises  of  diarrhoea,  sweating,  albuminuria, 
glycosuria,  and  visceral  congestions),  all  of  which  depend  upon  the  nervous 
system.  Is  it  necessary  to  isolate  these  groups  and  claim  for  them  an 
autonomous  or  hereditary  origin  in  every  case,  independent  of  Basedow's 


NEUROSES  OF  THE  HEART  461 

disease  ?  I  do  not  think  that  we  need  go  so  far.  The  question  of  soil  and 
of  acquired  or  hereditary  disposition  play,  not  only  in  neuropathology,  but 
in  the  whole  domain  of  pathology,  too  large  a  part  for  me  to  attempt  to 
belittle  their  importance.  I  think,  on  the  contrary,  that  heredity  in  all 
its  forms  is  the  conducting  wire  which  helps  us  to  assign  things  to  their 
proper  place  ;  but  it  does  not  furnish  sufficient  reason  for  cutting  up  a  morbid 
entity  and  disjoining  the  pieces.  Here,  as  elsewhere,  I  repeat,  acquired  or 
hereditary  predisposition  plays  a  leading  part  in' the  production  of  psychical 
symptoms  and  mental  troubles.  These  cerebral  troubles,  however,  have 
undoubtedly  arisen  in  persons  who,  neither  in  personal  nor  hereditary 
antecedents,  have  had  anything  which  could  explain  the  appearance  of  a 
psychosis  apart  from  their  Basedow's  disease.  Sometimes  psychical  troubles 
and  mental  disorders  begin  with  this  disease,  increase  during  its  paroxysms, 
and  then  disappear  with  the  other  symptoms,  or  even  before  them.  There 
is,  indeed,  under  these  conditions,  such  affinity  or  agreement  in  the  evolution 
of  the  different  symptoms  which  comprise  Basedow's  disease,  that  it  is  very 
difficult  in  this  case  to  see  only  the  coupling  of  morbid  conditions,  and  it 
appears  to  me  more  reasonable  to  admit  the  development  of  a  series  of  nervous 
troubles  of  various  kinds,  assuming  the  form  of  neuroses  or  of  psychoses, 
but  having  indeed  a  common  origin.  However  this  may  be,  the  appear- 
ance of  mental  troubles  is  always  of  ill  omen. 

Course — Termination. —  Basedow's  disease  is  rarely  quite  t5rpical. 
One  of  the  cardinal  symptoms  may  be  absent  or  sHght,  while  other  nervous 
troubles  or  symptoms  are  prominent.  Sometimes  the  disease  is  more  or 
less  abnormal  in  appearance. 

The  course  is  usually  slow  and  progressive,  and  the  disease  may  last 
for  ten  or  twelve  years,  or  even  more.  In  some  cases  it  runs  an  acute 
course.  The  symptoms  follow  one  another  rapidly,  and  the  clinical  picture 
is  complete  in  a  few  weeks — indeed,  it  may  be  so  in  the  space  of  twenty-four 
hours.  My  patient  at  the  Hotel-Dieu,  after  terrible  emotion,  developed 
in  a  single  night,  tremor,  paralysis,  exophthalmos,  hypertrophy  of  the 
thyroid  gland  and  cardiac  palpitation,  and  the  mental  condition  appeared 
later.     Trousseau  quotes  the  following  typical  example  of  this  sudden  onset : 

A  woman  lost  her  father.  She  was  much  upset,  and  cried  during  the  night.  Next 
day  she  suddenly  felt  that  her  eyes  swelled  and  the  eyelids  became  raised,  while  the 
thyroid  gland  enlarged  and  showed  unusual  pulsation.  She  also  felt  violent  palpita- 
tion of  the  heart.  Four  days  later  she  came  and  consulted  Desmarcs,  who  found  ex- 
ophthalmic cachexia. 

Terrible  paroxysms,  described  by  Trousseau,  may  supervene  in  the 
course  of  the  disease.  After  some  prodromata,  or,  indeeti,  suddenly,  the 
patient  has  an  acute  attack  of  dysjmcea;  the  tliyroidghiiid  bocoiiies  eiihirged; 
palpitation  is  severe ;  the  eyes  start  from  their  sockets ;  the  face  is  bathed  in 


462  TEXT-BOOK  OF  MEDICINE 

sweat ;  the  vessels  in  the  neck  show  rapid  pulsation ;  the  dyspnoea  is  accom- 
panied by  stridor  and  sucking-in,  and  death  sometimes  appears  imminent. 
Quiet  is,  however,  re-estabHshed,  and  the  paroxysm  ends.  Acute  paroxysms 
are  much  more  serious  than  chronic  ones.  In  a  case  quoted  by  Trousseau 
the  patient  was  seized  with  such  terrible  attacks  of  suffocation  that  prepara- 
tions were  made  for  tracheotomy.  The  paroxysms  may  only  recur  at  in- 
tervals of  months  or  years.  They  show  infinite  variation  in  their  duration 
and  gravity,  and  may  even  reappear  every  month  or  every  few  days. 

Exophthalmic  goitre  is  a  grave  malady,  for  the  mortahty  amounts  to 
20  per  cent.  Death  results  from  cachexia  or  from  intercurrent  trouble, 
such  as  paroxysms,  pulmonary  hsemorrhage,  intestinal  and  ^cerebral  haemor- 
rhage (Hirsch),  multiple  gangrene,  mental  alienation,  angina  pectoris,  or 
pulmonary  tuberculosis. 

etiology. — Exophthalmic  goitre  is  a  disease  of  the  middle  period  of 
life.  It  is  much  more  frequent  in  women  than  in  men,  and  is  often 
associated  with  a  nervous  temperament,  hysteria,  epilepsy,  chorea,  mental 
ahenation,  diabetes,  chlorosis,  or  pathological  conditions  of  the  genital 
system.  It  may  appear  after  moral  or  physical  shock,  accident,  emotion, 
fright,  violent  anger,  or  injury  (De  Graefe).  Pregnancy  has  sometimes  a 
beneficial  influence  on  the  progress  of  the  disease,  but,  on  the  other  hand, 
the  goitre  may  appear  during  pregnancy. 

Heredity  plays  the  chief  part  in  its  aetiology,  and  the  parents  may 
themselves  be  sufferers  from  goitre,  or  from  one  of  the  nervous  diseases 
above  quoted. 

As  regards  direct  heredity,  I  do  not  know  a  more  interesting  or  conclu- 
sive case  than  that  of  the  family  of  Les ,  natives  of  a  place  near  Soissons, 

where  goitre  is  endemic.  I  have  seen  several  members  of  this  family,  which 
in  three  generations  has  furnished  six  cases  of  Basedow's  disease. 

I  could  quote  cases  in  which  the  children  of  parents  suffering  from 
Basedow's  disease  were  born  with  a  goitre.  For  many  years  the  goitre 
remained  the  only  sign  of  the  disease,  and  ten  or  fifteen  years  later  other 
symptoms,  such  as  exophthalmos  and  palpitations,  appeared  as  the  result 
of  acute  emotion,  menstruation,  or  pregnancy. 

A  more  singular  fact  is  that,  in  countries  where  goitre  is  endemic,  we 
see  goitre  in  persons  who  are  not  descended  from  parents  affected  with 
Basedow's  disease,  and  yet  at  some  period  of  their  Uves  exophthalmos 
and  tachycardia  appear  in  addition  to  the  goitre. 

Diagnosis. — At  first  the  diagnosis  is  very  difficult,  especially  when  the 
disease  is  abnormal,  because  we  may  only  have  a  single  symptom.  Mistakes 
are  rare  when  the  chief  symptom  is  goitre  or  exophthalmos ;  but  when  the 
patient  only  complains  of  pulsation,  tremor,  rapid  wasting,  or  attacks  of 
dyspnoea,  we  must  be  able  to  reconstruct  the  disease  by  grouping  certain 


NEUROSES  OF  THE  HEART  463 

symptoms,  or  traces  of  the  more  or  less  important  symptoms  above 
enumerated. 

In  women  the  general  symptoms  may  simulate  chlorosis,  but  the  accelera- 
tion of  the  pulse,  the  pecuUar  look,  the  prominent  eyes,  the  tremor  of  the 
hands  and  feet,  the  pigmented  spots,  the  pulsation  of  the  cervical  vessels, 
and  the  shght  sweUing  of  the  thyroid  body  should  indicate  the  diagnosis. 

As  the  exophthalmos  in  Basedow's  disease  affects  both  eyes,  and  is  not 
accompanied  by  squint,  it  shows  no  resemblance  to  unilateral  exophthalmos 
of  orbital  or  of  cranial  origin.  The  prominence  of  the  eyeball  in  myopic 
patients  will  be  readily  distinguished. 

The  origin,  appearance,  and  progress  of  exophthalmic  goitre  do  not 
allow  confusion  with  goitre,  properly  so  called.  Many  cases  will  call  for  a 
minute  inquiry  into  the  symptoms  present. 

Nature  of  the  Disease. — Exophthalmic  goitre  is  a  cardio- vascular 
neurosis,  resulting  doubtless  "  from  profound  disturbance  in  the  vasomotor 
nerves  "  (Trousseau).     It  is  a  neurosis  of  bulbar  origin  (See). 

We  may,  I  think,  be  satisfied  with  Ballet's  conclusions  :  The  possible 
association  of  external  ophthalmoplegia,  of  paralysis  of  the  facial,  the  hypo- 
glossal or  the  motor  branch  of  the  trigeminal  nerves,  with  exophthalmic 
goitre  forms  an  argument  in  favour  of  the  theory  which  refers  Basedow's 
disease  to  some  trouble  in  the  central  nervous  system,  and  particularly  in 
the  bulb. 

The  common  troubles  of  the  disease  depend  on  nuclear  paralysis  of  the 
vagus,  wliich  causes  tachycardia,  dyspnoea,  and  gastric  troubles;  and  on 
paralysis  of  the  vasomotor  centres,  which  gives  rise  to  flusliing  of  the  face 
and  neck.  The  goitre  and  the  exophthalmos  result  from  the  coexistence  of 
vasomotor  paralysis  and  tachycardia.  These  paralyses  do  not  depend  upon 
a  material  lesion,  but  are  simply  functional  troubles,  capable  of  improve- 
ment, aggravation,  recovery,  or  relapse. 

It  follows  from  the  preceding  statements  that  Basedow's  disease  is 
especially  a  bulbar  neurosis.  Troubles  of  medullary  or  of  cortical  origin 
may  also  appear,  and  therefore  Basedow's  disease  is  often  associated  with 
other  neuroses,  such  as  unsoundness  of  mind,  epilepsy,  and  especially 
hysteria. 

Treatment. — I  will  give  here  the  treatment  of  Basedow's  disease  described 
in  my  lectures  at  the  Faculte.  Let  us  consider  this  treatment  from  two 
different  points  of  view — (1)  during  the  paroxysms,  and  (2)  during  the 
course  of  the  disease. 

In  dealing  with  an  acute  paroxysm,  in  which  the  thyroid  and  cardiac 
trouble  are  most  severe,  we  must  at  once  act  because  the  paroxysm  will 
last  for  half  an  hour  or  more,  and  may  cause  death,  if  we  do  not  intervene 
immediately.     Distress  and  dyspna^a  are  extreme.     The  excessive  swelhng 


464  TEXT-BOOK  OF  MEDICINE 

of  the  thyroid  body  compresses  the  trachea,  causing  stridor  and  preventing 
the  free  passage  of  air.  In  such  conditions  tracheotomy  appears  imperative, 
and,  indeed,  it  would  be  indicated  but  for  the  danger  arising  from  the 
dilatation  of  the  vessels  of  the  neck,  which  are  gorged  with  blood,  and  the 
fatal  haemorrhage  which  might  result,  as  in  a  case  quoted  by  Trousseau. 

How,  then,  are  we  to  reheve  the  thyroid  and  cardiac  troubles  ?  The 
first  indication  is  fulfilled  by  the  application  of  ice-bags  to  the  thyroid  until 
the  crisis  disappears.  We  should  treat  the  cardiac  excitation  by  digitahs, 
in  large  doses,  as  advised  by  Trousseau — e.g.,  2  grains  of  the  dried  leaves  in 
powder  every  half-hour  for  two  or  three  hours,  according  to  the  severity 
and  duration  of  the  attack,  while  an  ice-bag  is  applied  to  the  precordial 
region. 

If  this  gives  no  relief,  we  must  resort  to  bleeding,  to  the  apphcation 
of  leeches  to  the  neck,  and  to  careful  inhalations  of  ether  or  of  chloroform. 
The  paroxysm  ends  more  or  less  rapidly,  and  the  patient  is  for  the  time 
being  saved. 

We  must,  however,  not  forget  that  the  disease  remains,  that  it  is  dan- 
gerous in  these  cases,  that  other  crises  will  appear,  and  that  one  or  other  of 
them  will  be  fatal.  Therefore  we  must  be  on  our  guard,  and  ready  to 
act  in  a  similar  manner.  It  is,  above  all,  necessary  to  prevent  them^ — that 
is,  to  direct  our  attention  to  the  disease  itself.  The  physician  must  adopt 
the  same  course,  although  the  patient  has  shown  no  paroxysms,  because 
great  improvement  in  the  symptoms  can  be  effected  by  rational  and  well- 
directed  treatment. 

Many  drugs  have  been  extolled  in  exophthalmic  goitre,  and  the  chief 
among  these  are  iodine  and  the  iodides.  Cheadle  prescribes  tincture  of  iodine, 
taken  internally.  This  drug  is  certainly  efficacious  in  simple  goitre,  but 
renders  no  service  in  exophthalmic  goitre.  Trousseau  has  even  given  his 
opinion  against  this  method  of  treatment,  and  most  writers  agree  with  his 
advice. 

Bromides  are  indicated  for  the  cardio- vascular  excitation  and  erethism. 
Although  this  drug  does  not  act  directly  on  the  disease,  it  at  least  has  a 
favourable  effect  upon  the  symptoms,  when  given  in  large  doses. 

Extract  of  valerian,  or  valerianate  of  ammonia,  produces  manifest 
improvement  in  the  palpitation  and  the  dyspnoea. 

All  authors  are  unanimous  in  advising  digitahs  in  the  treatment  of 
exophthalmic  goitre.  While  it  has  the  disadvantage  of  raising  the  blood- 
pressure,  it  has  the  advantage  of  slowing  the  heart-beat  in  severe  tachy- 
cardia ;  therefore  its  disadvantages  must  be  passed  over,  and  we  must  only 
think  of  reheving  the  patient.  The  dose  varies  according  to  the  suscepti- 
bihty  of  the  patient.  In  some  patients  1  or  2  grains  of  the  dried  leaves  will 
be  sufficient,  while  in  others  it  will  be  necessary  to  increase  the  dose,  the 


NEUROSES  OF  THE  HEART  465 

whole  point  being  to  estimate  the  susceptibility  of  the  patient.  Except  in 
rare  cases,  fligitalis  is  an  excellent  drug. 

The  use  of  belladonna  has  in  some  cases  caused  improvement  of  all  the 
symptoms,  except  the  hypertrophy  of  the  thyroid  gland. 

Hydrotherapy,  in  spite  of  unfavourable  criticism,  is  none  the  less  an 
excellent  method.  The  cold  douche  should  not  be  given  at  first,  but  shower- 
baths  at  a  temperature  of  75°  F.  should  be  first  given,  and  the  temperature 
of  the  water  should  be  gradually  reduced. 

Electricity  is  certainly  very  efficacious.  The  continuous  current  appears 
to  have  given  the  best  results.  The  following  procedure  is  usually  adopted  : 
Two  rheophores  are  applied  on  either  side  of  the  neck  over  the  superior 
cervical  ganghon,  then  over  the  vagi,  and  a  current  of  from  3  to  8  miUi- 
amperes  is  allowed  to  flow  for  eight  or  ten  minutes.  A  daily  sitting  is  given 
for  three  to  four  weeks  ;  the  treatment  is  then  stopped  and  resumed  at  the 
end  of  a  week.  For  some  time  past  the  faradic  current  has  met  with  some 
credit  (Vigouroux).  This  rapid  survey  of  the  different  methods  of  treat- 
ment shows  that  digitahs,  valerian,  bromides,  the  continuous  current,  and 
hydrotherapy  give  the  best  results. 

As  regards  treatment  with  thyroid  extracts,  opinions  are  much  divided. 
Voisin  has  quoted  a  case  in  which  sheep's  thyroid  gland  gave  excellent 
results.  In  answer  to  Voisin's  communication,  Dreyfus-Brisac  and 
Beclere  declare  that  thyroid  treatment  for  exophthalmic  goitre  has  always, 
in  their  experience,  increased  the  symptoms,  and  they  are  not  alone  in  this 
opinion. 

For  my  part,  I  have  for  a  long  time  used  ipecacuanha.  The  idea  of 
giving  ipecacuanha  in  Basedow's  disease  occurred  to  me  on  seeing  the 
success  obtained  in  haemoptysis. 

These  patients  have  erethism  of  the  cardio- vascular  and  vasculo-pulmonary 
systems.  The  pulse  is  hard  and  vibrating  during  the  haemoptysis.  In 
such  cases  we  give  ipecacuanha  in  emetic  doses  if  we  desire  to  arrest  abundant 
haemoptysis,  or  in  fractional  doses  so  as  to  cause  nausea  if  we  are  treating 
more  chronic  bleeding.  The  pulse  diminishes  in  frequency  and  force,  and 
the  haemoptysis  improves  or  ceases.  In  Basedow's  disease  the  treatment 
of  cardio-vascular  erethism  is  also  one  of  the  indications  to  be  fulfilled. 

I  have  therefore  given  ipecacuanha  with  digitahs  and  opium  in  pills  : 

I^  Powdered  ipecacuanha     . .  . .  •  •     gi'-  iV 

Powdered  digitalis  leaves . .  . .  • '     S^-  s^ 

Extract  of  opium  . .  . .  •  •     g^-  ^V 

To  make  one  pill.     Take  four  pills  at  equal  intervals  in  the 
twenty-four  hours. 

In  giving  ipecacuanha  we  should  not  cause  vomiting,  but  only  very 
shght  nausea.     We  must  then  diminish  the  number  of  pills  to  three,  or  even 

30 


466  TEXT-BOOK  OF  MEDICINE 

two,  in  the  twenty-four  hours,  and  gradually  increase  the  dose  up  to  the 
limit  of  tolerance.  With  ipecacuanha  I  am  fond  of  giving  valerianate  of 
ammonia  in  a  daily  dose  of  2  or  3  teaspoonfuls,  and  I  also  employ 
hydrotherapy. 

I  have  treated  many  cases  of  exophthalmic  goitre  in  this  manner,  and 
marked  improvement,  especially  in  the  dyspnoea,  has  been  the  rule.  It 
was  particularly  striking  in  two  cases,  and  I  do  not  think  that  any  other 
method  of  treatment  would  have  given  a  better  result.  The  effect  of 
this  treatment  is  shown  by  the  appreciable  improvement  after  a  few  days, 
and  very  marked  benefit  after  some  months.  The  only  inconvenience 
of  this  treatment  is  diarrhoea,  which  disappears  as  soon  as  tolerance 
conmaences. 

Surgical  Treatment. — Surgical  treatment  consists  in  operations  upon 
the  goitre  or  upon  the  cervical  sympathetic  nerves.  Let  us  first  consider 
operations  upon  the  goitre.  The  idea  of  partial  or  total  removal  of  the 
gland  or  of  enucleation  by  drawing  it  out  of  the  wound  and  allowing  it  to 
waste  (exothyropexia)  arises  from  the  somewhat  erroneous  conception  that 
the  hyperthyroidization  is  the  chief  cause  of  the  symptoms  and  complica- 
tions of  Basedow's  disease. 

According  to  this  theory,  the  goitre  produces  too  much  secretion,  poisons 
the  nerve  centres,  and  produces  auto-intoxication  from  functional  hyper- 
activity. This  theory,  to  be  accepted,  should  be  appHcable  to  every  case. 
We  find,  however,  nothing  of  the  kind.  The  exophthalmos,  tachycardia, 
etc.,  may  be  already  marked,  while  the  goitre  is  absent  or  slight.  These 
defaced  forms  are  far  from  rare,  and  we  cannot,  under  such  conditions, 
invoke  primary  hyperactivity  of  the  thyroid  gland.  Abadie  has  quoted 
cases  in  which  the  exophthalmos  was  so  marked  that  complete  loss  of  both 
eyes  had  resulted,  while  the  enlargement  of  the  thyroid  body  was  scarcely 
appreciable. 

In  order  to  appreciate  the  question  better,  let  us  consider  the  operations 
upon  the  thyroid  body  and  their  results.  Allen  Starr  gives  statistics  of 
190  cases  of  thyroidectomy  in  Basedow's  disease,  with  the  following  results  : 
Recovery  in  74,  improvement  in  45,  failure  in  3,  and  death  in  33  cases. 
As  a  rule  death  was  not  expected,  and  occurred  soon  after  the  operation, 
or  two  or  three  days  later.  Whatever  theory  be  used  to  explain  the 
deaths,  the  patients  succumbed  with  nervous  symptoms — viz.,  excessive 
tachycardia  (pulse-rate  180  to  200),  sudden  rise  of  temperature,  angina, 
restlessness,  profuse  sweating,  and  collapse. 

Brissaud  published  a  case  in  which  Poncet  performed  exothyropexia, 
which  is  a  benign  operation,  and  consists  in  exposing  the  thyroid  gland. 
The  patient  died  without  any  warning. 

Lejars  witnessed  the  following  accident : 


NEUEOSES  OF  THE  HEART  467 

A  girl  eighteen  years  of  age  had  tachycardia,  slight  exophthalmos,  tremor,  etc. 
The  goitre  was  very  moderate  ;  the  right  lobe  of  the  thyroid  body  appeared  to  be  the 
larger.  It  was  firm,  could  be  depressed,  and  showed  neither  nodules  nor  induration. 
The  right  lobe  was  removed  en  masse,  after  freeing  the  upper  and  lower  cornua  and 
ligaturing  the  vessels.  The  operation  was  satisfactory,  and  the  patient  rested  well 
during  the  day.  About  eleven  o'clock  at  night  she  was  suddenly  seized  with  intense 
dyspnoea  and  considerable  acceleration  of  the  respiratory  movements.  No  flushing  of 
the  face,  no  asphyxia.  She  died  in  three-quarters  of  an  hour.  The  autopsy  revealed 
no  operative  lesion ;  the  recurrent,  vagus,  and  sympathetic  nerves,  with  their  cervical 
branches,  were  absolutely  intact.  The  fact,  says  Lejars,  remains  that  a  simple 
operation,  performed  A^ithout  mishap,  was  followed  by  sudden  death,  which  could  not 
be  explained  at  the  autopsy,  but  appeared  to  be  related  to  acute  bulbar  trouble. 

Jaboulay,  in  one  of  his  cases,  adds  : 

Diminution  of  the  mass  remaining  after  partial  extirpation  of  the  goitre  usually 
follows  when  the  case  is  one  of  ordinary  goitre.  Section  of  the  isthmus,  for  example, 
may  cause  atrophy  of  both  the  hypertroiahied  lobes,  and  unilateral  thyroidectomy 
produces  diminution  in  the  size  of  the  remaining  lobe.  I  have  seen  the  opposite  result 
in  a  case  of  Basedow's  disease.  Acting  on  the  theory,  which  subordinates  the  other  symp- 
toms to  perversion  of  the  secretion,  I  have  several  times  operated  upon  her  thyroid 
gland,  and  have  left  it  exposed  on  two  consecutive  occasions.  As  each  intervention 
was  only  followed  by  temporary  improvement,  I  decided  last  year  to  remove  the  right 
lobe.  Three  months  later  the  left  lobe  was  enlarged,  and  quite  recently  the  middle 
lobe  formed  a  goitre  as  large  as  a  small  orange.  After  each  operation  upon  the  thyroid 
itself  the  symptoms  showed  genuine  improvement,  and  the  tremor  in  particular  speedily 
disappeared  ;   but  relapses  occurred,  with  palpitation,  tremor,  and  fresh  goitre. 

Poncet  sums  up  the  matter  thus  : 

After  various  operations  which  I  Have  performed  in  exophthalmic  goitre,  including 
simple  exothyropexia,  I  have  seen  a  fatal  result.  Such  results,  and  also  the  frequent 
return  of  symptoms  which  had  yielded  for  a  very  short  while  before  the  operation,  have 
made  me  very  circumspect.  For  my  part,  I  shaU  not  again  meddle  with  the  thyroid 
body  in  a  case  of  Basedow's  disease. 

It  must  be  admitted  that  the  results  just  quoted  are  hardly  encouraging, 
but  for  a  correct  decision  let  us  also  take  into  account  the  successes  obtained. 
Tillaux  has  reported  a  case  of  cure  : 

At  the  Societe  de  Chirurgie,  Tuffier  presented  two  young  women  suffering  from 
exophthalmic  goitre,  both  treated  by  partial  thyroidectomy,  involving  the  right  lobe 
and  tlio  isthmus.  The  first  patient  had  been  under  medical  treatment  for  two  years 
at  the  Salpet^lere,  with  no  result.  After  thyroidectomy  the  exophthalmos  and  the 
nervous  troubles  were  cured.  Later  the  tachycardia  and  the  tremor  ceased,  so  that 
two  and  a  half  years  after  the  operation  the  patient  was  in  good  health.  The  left  lobe 
of  the  th3Toid  gland  remained  larger  than  normal,  but  had  not  increased  in  size  since 
the  operation. 

The  second  patient  was  a  young  woman  whose  condition  was  very  grave  when 
TufBer  operated.  She  had  taken  tabloids  of  thyroid  gland  for  six  months,  instead 
of  tabloids  of  thymus  glands.  Symptoms  of  acute  thyroidism,  which  demanded  re- 
moval of  the  gland,  appeared.  Before  the  operation  her  contUtion  was  very  grave  : 
Enormous  exophthalmos,  violent  dyspmca,  incessant  palpitation,  pul.se  1-44,  tliyroid 
gland  double  its  normal  size  and  showing  marked  pulsation,  insomnia,  tremor,  (i-doma 
of  the  lower  Umbs,  and  profuse  diarrhrx-a.  The  results  of  the  operation  were  remark- 
able.    Next  day  the  erethism  of  the  vessels  disappeared,  the  diarrha'a  ceased,  and  tho 

30—2 


468  TEXT-BOOK  OF  MEDICINE 

pulse  fell  from  125  to  72.  Condition  quite  satisfactory  a  month  after  operation.  Ex- 
ophthalmos still  present,  although  less,  tremor  cured,  no  trace  of  dyspncea,  sleep  good, 
no  nervous  symptoms.     The  future  will  show  the  ultimate  worth  of  the  operation. 

In  spite  of  the  successes  above  set  down,  as  well  as  two  other  cases 
reported  by  Doyen,  it  is  none  the  less  true  that  operations  in  exophthalmic 
goitre  expose  the  patient  to  very  grave  danger. 

We  may  therefore  form  a  judgment  upon  the  advantages  or  disadvantages 
of  such  operations  in  Basedow's  disease.  It  seems,  however,  well  estab- 
lished that  the  disadvantages  outweigh  the  advantages.  Operation,  even 
when  performed  under  the  most  favourable  conditions,  does  not  protect 
the  patient  from  very  grave  risks,  nor  the  surgeon  from  terrible  surprises. 
The  results  obtained  are  temporary  or  incomplete.  For  these  reasons  I 
should  be  very  loth  to  advise  this  operation. 

Another  operation — viz.,  double  section  of  the  great  cervical  sympathetic 
— was  first  performed  by  Jaboulay.  Trousseau  had  seen  that  the  chief 
symptoms  and  vascular  troubles  in  Basedow's  disease  do  not  extend  beyond 
the  area  of  the  cervical  sympathetic.  The  carotid  arteries,  with  the  thyroid 
vessels  and  their  branches,  are  alone  affected  by  the  expansive  pulsation, 
wliile  the  other  vessels,  such  as  the  radial,  the  femoral,  or  the  abdominal 
aorta,  beat  normally.  Accordingly,  the  great  sympathetic  nerve  has  been 
considered  as  the  cause,  and  theories,  some  based  upon  excitation,  others 
upon  paralysis  of  its  branches,  have  been  brought  forward.  None  of  these 
theories,  however,  were  applicable  to  all  the  symptoms.  The  brilhant 
discovery  of  Dastre  and  Morat  has  thrown  much  light  upon  this  ques- 
tion. These  physiologists  showed  that  the  vasodilator  fibres  of  the  cervical 
sympathetic  have  a  distinct  origin,  and  upon  this  fact  Abadie  has  built 
up  an  ingenious  theory. 

Be  this  as  it  may,  it  is  none  the  less  true  that  double  section  of  the  great 
sympathetic  nerve  has  given  remarkable  results.  Out  of  six  cases  published 
by  Jaboulay,  one  is  absolutely  characteristic  : 

A  woman  fifty -five  years  of  age  had  for  three  months  suffered  from  exophthalmos, 
tachycardia,  and  tremor.  Hypertrophy  of  the  thyroid  gland  was  absent.  She  had 
gained  no  benefit  from  thyroid  extract.  When  she  came  under  Jaboulay's  care, 
"  her  look  was  indeed  alarming  from  the  exophthalmos,  which  had  al&ost  dislocated 
the  left  eye  from  the  orbit,  and  the  tremor  was  excessive.  She  suffered  from  tachy- 
cardia and  from  such  intense  dyspncBa  that  the  possibihty  of  surgical  intervention  was 
discussed."  Double  ablation  of  the  superior  cervical  ganglion  was  performed.  The 
result  was  immediate.  Three  days  later  her  face  had  lost  its  terrible  expression,  while 
the  eyes,  and  the  left  eye  in  particular,  had  almost  regained  their  normal  position. 
Tremor,  dyspnoea,  and  precordial  pain  completely  disappeared,  but  the  tachycardia 
persisted,  and  the  pulse  varied  between  100  and  120. 

In  his  communication  of  October  21,  1896,  at  the  Congres  de  Chirurgie, 
Jonnesco  (of  Bucharest)  brought  forward  two  cases  of  exophthalmic  goitre, 
treated  by  double  resection  of  the  cervical  sympathetic. 


NEUROSES  OF  THE  HEART  469 

Reclus  and  Faure's  case  is  comparable  to  that  of  Jaboulay.  The 
result  of  the  operation  was  remarkable,  but  it  is  necessary  to  see,  as  Reclus 
says,  what  will  become  of  the  patient,  for  it  may  be  only  a  case  of  transient 
improvement. 

The  following  case  was  pubUshed  by  Gerard-Marchant  and  Abadie  : 

A  young  woman  suffered  from  a  defaced  form  of  Basedow's  disease,  characterized 
chiefly  by  exophthalmos.  Tachycardia  absent  ;  thyroid  body  showed  very  slight  hyper- 
trophy of  the  right  lobe  ;  exorbitism  was  so  marked  that  the  lids  did  not  cover  the  eye. 
Gerard-Marchant  performed  resection  of  both  cervical  sj'mpathetic  nerves.  The 
exophthalmos  gradually  diminished,  but  did  not  quite  disappear.  "  This  rdsult," 
say  the  authors,  "  was  not  maintained.  Under  the  influence  of  emotion  and  fatigue, 
exophthalmos  reappeared,  although  in  a  less  degree  than  before  the  operation.  It  is 
right  to  add  that  there  is  no  trace  of  goitre,  and  that  her  physical  and  moral  condition 
has  remained  excellent." 

Chauffard  and  Quenu  have  published  the  following  case  : 

A  man,  aged  twenty-five,  admitted  with  the  classical  symptoms  of  Basedow's  disease. 
Eyes  very  prominent,  complete  closure  of  the  eyelids  impossible.  Goitre  bilateral  and 
pulsatile.  Heart-beats  very  forcible,  and  rate  110  a  minute  ;  dyspnoea  and  palpita- 
tion on  the  least  effort.  Carotids  showed  marked  pulsation.  Marked  tremor  of  the 
hands  and  limbs.  Patient  irritable,  unstable,  and  showed  stigmata  of  hysteria. 
Quenu  performed  bilateral  resection  of  the  cervical  sympathetic.  After  the  operation, 
aggravation  of  the  tachycardia  and  appearance  of  arrhythmia,  which  did  not  exist 
before,  became  manifest.  Some  days  later  heart  showed  a  rate  of  110.  As  regards 
the  heart  the  benefit  has  therefore  been  nil,  the  goitre  has  been  slightly  affected,  and  the 
circumference  of  the  neck,  which  before  the  operation  was  38  centimetres,  varies  from 
36|  to  37  centimetres,  since  the  operation.  The  eyes  may  be  less  prominent,  but  this 
is  very  doubtful.  In  short,  the  benefit  obtained  has  been  nil.  We  may,  indeed,  ask 
whether  the  patient  has  not  rather  suffered  than  profited  by  operation,  since  in  two 
months  he  has  lost  6  pounds  in  weight. 

In  short,  the  results  obtained  by  bilateral  resection  of  the  cervical 
sympathetic  are  so  far  too  much  at  variance  to  yield  definite  information 
as  to  the  value  of  this  intervention.  Besides  the  truly  remarkable  results 
(Jaboulay  and  Reclus'  cases)  there  are  others  in  which  the  good  results  are 
doubtful  (Gerard-Marchant  and  Abadie's  cases)  or  absent  (Chauffard  and 
Quenu's  case). 

It  is  therefore  impossible  at  present  to  give  surgical  treatment  the 
preference  over  medical  means.  Both  of  them  show  defects  and  are  often 
ineffectual,  but  medical  treatment  at  least  does  not  endanger  the  patient's 
life  (I  allude  to  operations  on  the  goitre),  and  may  result  in  recovery. 


CHAPTER  V 
DISEASES  OF  THE  VESSELS 

I.  PHLEBITIS— PHLEGMASIA  ALBA  DOLENS. 

Phlebitis  is  inflammation  of  a  vein.  This  question  is  in  part  surgical ; 
thus  phlebitis  consecutive  to  injury  of  veins,  operations,  inflammation,  etc., 
is  of  traumatic  or  external  origin.  This  variety  was  thoroughly  described 
by  Hunter  (1795),  Ribes  (1816),  and  Dance  (1828),  who  divided  the  condition 
into  suppurative  and  adhesive  phlebitis.  This  side  of  the  question  does  not 
concern  us,  and,  further,  it  is  no  longer  of  interest,  since  aseptic  procedures 
are  employed  in  surgery.  The  phlebitis  which  now  occupies  our  attention 
arises  from  internal  causes,  and  infectious  phlebitis  figures  in  the  first  rank. 
Sometimes  the  deep  tissue  of  organs  is  the  seat  of  phlebitis,  at  other  times 
the  miscliief  develops  in  the  veins  of  the  trunk  and  the  limbs.  Phlebitis 
may  pass  unnoticed  when  deeply  hidden  in  the  splanchnic  cavities,  or  show 
itself  by  symptoms  depending  upon  its  locahzation  (portal  vein,  sinuses  of 
the  meninges) ;  at  other  times  it  produces  embolisms  described  under 
pulmonary  embolisms. 

When  phlebitis  affects  the  veins  of  the  limbs,  it  shows  itself  as  phleg- 
masia alba  dolens.  The  word  phlegmasia  is  derived  from  (f)\iyfjia, 
(^Xe'yixaro'i,  which  in  old-time  medicine  signifies  phlegm  (oedema).  The 
literal  translation  of  phlegmasia  alba  dolens  is  painful  white  oedema. 
I  shall  here  describe  the  different  kinds  of  phlebitis  and  phlegmasia  alba 
dolens. 

Pathological  Anatomy. — We  have  to  study  a  double  lesion  :  the  one 
affecting  the  walls  of  the  vein,  or  phlebitis ;  the  other  affecting  the  blood, 
which  forms  a  clot  inside  the  vein — i.e.,  the  obturator  clot  or  thrombus. 
The  name  thrombosis  is  given  to  the  process  which  ends  in  obliteration  of 
the  vein  by  a  thrombus. 

1.  Phlebitis — Mechanism  of  Thrombosis. — A  vein,  when  affected  by 
phlebitis,  is  often  obliterated  by  a  blood-clot.  Ancient  theories  considered 
phlebitis  the  initial  phenomenon,  and  thrombosis  the  consecutive  one. 
Later,  at  the  instigation  of  Virchow,  an  entirely  opposite  theory  has  been 
admitted  :  thrombosis  is  the  initial  phenomenon,  and  phlebitis  the  secondary 

470 


DISEASES  OF  THE  VESSELS  471 

one.  In  spite  of  the  infatuation  for  German  researches,  Vulpian  fought 
against  the  too  exclusive  doctrine  of  Virchow,  and  taught  that  the  coagula- 
tion of  blood  in  the  veins  is  preceded  by  a  change  in  the  vascular 
epithelium. 

Modern  researches  prove  that  Vulpian  was  right.  In  some  cases  the 
primary  lesion  of  the  vein  is  self-evident  (varices,  injury) ;  in  other  cases  it 
is  at  first  sight  less  apparent.  What  do  histology  and  bacteriology  teach 
us  ?  In  the  great  majority  of  cases  phlebitis,  Uke  endocarditis,  is  due 
to  microbic  agents.  Widal  has  found  the  streptococcus  of  puerpural 
infection  in  the  clots  of  phlegmasia.  Bacteriological  examination  must  be 
made  with  material  from  the  uterine  veins,  because  coagulation  starts  in 
them,  and  gradually  reaches  the  femoral  veins,  although  we  may  not  be 
able  to  find  any  trace  of  characteristic  streptococci  in  the  clot  which  ob- 
literates them.  Chantemesse  and  Vaquez  have  found  Koch's  bacillus 
in  phlebitis  among  tubercular  patients.  More  often  in  the  lesions  of  phlebitis 
we  find  not  one  specific  bacillus,  but  the  ordinary  micro-organisms  of  sup- 
puration— viz.,  staphylococci  or  streptococci.  In  the  latter  case  phlebitis 
supervenes  as  a  secondary  infection.  In  this  manner  the  cases  of  phlebitis 
in  influenza,  typhoid,  cancer,  tuberculosis,  cachexia,  and  possibly  also 
chlorosis,  are  explained.  The  microbic  agents  are  often  present  in  the 
vessel  wall  and  in  the  clot.  Whether  these  agents  penetrate  the  walls  of 
the  vein  by  the  vaso  vasorum,  or  whether  the  microbes  circulating  in  the  blood 
directly  cause  irritation  of  the  vascular  endothelium,  matters  Httle.  The 
essential  fact  is  that  phlebitis  precedes  thrombosis. 

How  does  tluombosis  arise  ?  Different  interpretations  have  been  given 
as  to  the  formation  of  the  thrombus :  (1)  An  increase  of  the  plasmin 
(spontaneously  coagulable  fibrin) ;  (2)  sloAving  of  the  blood-stream.  In- 
crease of  plasmin  is  associated  with  cachectic  conditions  (cancer  and  phthisis), 
the  puerperal  state,  and  chlorosis.  Slowing  of  the  blood-stream  is  due  to 
the  pressure  of  aponeurotic  laminae,  situated  in  the  course  of  certain  veins 
(crural),  to  compression  caused  by  the  foetus,  to  degeneration  of  the  heart 
muscle,  and  to  cardiac  paresis  (Jaccoud)  in  severe  fevers  and  cases  of  p}Texia. 
According  to  Hayem  and  Bizzorero,  the  haematoblasts,  or  blood- platelets, 
play  a  considerable  part  in  the  coagulation  of  the  blood. 

However  this  may  be,  the  lesion  commences  with  granulo-fatty  degenera- 
tion of  the  endothelial  cells;  the  tunica  intima  becomes  thickened,  and 
granular  and  stratified  layers  of  fibrin  are  deposited  upon  this  granular 
tissue.  This  is  the  origin  of  the  thrombus.  The  fibrinous  clot  is  adherent. 
"  All  attempts  to  break  down  this  adhesion  are  useless,  and  it  is  difficult 
to  delimit  exactly  the  wall  of  the  vein  which  undergoes  progressive  thicken- 
ing. At  the  central  point  of  the  clot  the  wall  presents  a  reddish  bud, 
which  arises  from  the  deep  tissue  of  the  vein,  and  becomes  lost  in  the 


472  TEXT-BOOK  OF  MEDICINE 

coagulum  "  (Vaquez).    After  these  preparatory  changes  the  partial  or  total 
obUteration  of  the  vein  by  coagulation  of  the  blood  is  readily  understood. 

2.  Thrombus. — We  may  now  consider  the  clot  itself.  The  clot  fills 
the  cavity  of  the  vein  more  or  less,  and  may  be  parietal  or  obhterating. 
The  portion  in  contact  with  the  vein  is  whitish  and  very  adherent — "  the 
clot  of  pulsation  "  (Hay em) — while  the  portion  which  obhterates  the  vessel 
is  reddish,  "  the  clot  of  stasis."  The  central  end  of  the  clot  sometimes 
ends  in  a  tapering  manner.  This  end,  struck  by  the  current  of  blood,  or 
detached  by  the  stream  from  a  collateral  vein,  may  become  an  embolus. 

The  thrombus  may  undergo  one  of  the  following  changes  :  (1)  Its 
elements  may  become  disaggregated  and  disappear  by  absorption ;  (2)  it 
may  be  invaded  and  broken  up  by  vasculo-connective  vegetations  of  the 
tunica  intima,  and  the  vein  is  sometimes  converted  into  a  cord  of  cavernous 
tissue  ;  (3)  the  peripheral  portions  of  the  clot  may  alone  undergo  fibrous 
change  and  retract,  so  that  the  circulation  is  re-estabUshed  through  the  centre; 
and  (4)  the  thrombus  may  be  broken  up,  and  the  detached  fragment  may 
cause  embolism  in  the  right  heart  or  in  the  lung.  The  clot  sometimes 
softens  at  its  centre,  and  presents  a  puriform  appearance  which  has  been 
wrongly  taken  for  suppuration,  but  is  really  a  disintegration  of  the  clot 
with  granulo-fatty  change.  If  the  particles  enter  the  blood-stream,  they 
may  cause  infarcts  in  the  lung ;  and  if  bacteria  are  present  in  the  thrombus, 
the  capillary  embohsms  are  also  septic,  and  lead  to  septic  infarcts  and  miUary 
abscesses  in  the  lungs  or  in  the  heart. 

Description. — I  shall  give  a  general  description  of  phlegmasia  alba 
dolens,  and  return  later  to  the  pecuharities  which  each  phlebitis  may  present, 
according  to  the  cause  which  has  given  rise  to  it.  Phlegmasia  alba  dolens  may 
affect  the  veins  of  the  upper  and  lower  limbs,  the  neck  and  the  face,  but  shows 
a  remarkable  predilection  for  the  veins  of  the  leg,  and  usually  begins  in  the 
veins  of  the  calf.  It  has  an  insidious  onset,  which  is  rarely  febrile,  and  shows 
itself  by  pain,  which  is  at  first  diffused  through  the  whole  Kmb,  and  later 
is  locaHzed  in  certain  points.  In  the  leg,  wliich  is  the  ordinary  seat  of  the 
lesion,  the  pain  is  more  marked  in  the  calf  and  the  groin  ;  the  limb  is  heavy 
and  swollen,  and  the  hypersesthesia  is  at  times  excessive.  In  some  cases 
the  patient  complains  of  joint  pains,  simulating  rheumatism  ;  in  other  cases 
pain  may  be  completely  absent.  The  bluish  network  under  the  skin  shows 
that  the  circulation  is  impeded  in  the  deep  veins,  and  tends  to  re-estabhsh 
itself  by  the  superficial  ones.  The  deep  veins  are  sometimes  transformed 
into  a  hard,  tortuous  cord,  which  may  be  felt  in  the  calf  and  followed  up- 
wards, as  far  as  the  ring  of  the  adductor  magnus.  The  knee-joint  is  some- 
times filled  with  fluid  ;  the  movements  of  the  leg  are  difficult,  as  though  the 
muscles  were  affected  with  paresis.  Transient  loss  of  power  in  the  Kmb,  with 
or  without  muscular  atrophy,  has  also  been  noted. 


DISEASES  OF  THE  VESSELS  473 

The  obliteration  of  the  veins  causes  oedema  which  has  special  charac- 
ters :  white,  because  the  skin  is  bloodless  ;  smooth  and  hard,  because  the 
areolae  of  the  skin  are  distended  by  serous  fluid ;  painful,  from  the  com- 
pression of  the  nerve  endings.  It  does  not,  therefore,  resemble  the  oedema 
of  cachexia,  or  of  diseases  of  the  heart  and  kidney.  In  some  cases,  however, 
it  may  be  shght,  or  its  absence  may  make  an  error  in  diagnosis  easy.  It 
may  only  appear  days,  or  even  weeks,  after  the  pain.  In  some  patients  it 
is  almost  the  only  symptom  of  the  lesion.  The  oedema  often  begins  in  the 
foot  and  leg,  and  later  reaches  up  to  the  thigh.  In  puerperal  phlegmasia, 
however,  the  oedema  often  begins  at  the  root  of  the  Hmb,  and  spreads  from 
above  downwards. 

Phlegmasia  has  a  variable  duration.  We  see  sUght  forms,  as  in  a  tuber- 
cular patient  in  whom  the  trouble  only  lasted  about  twelve  days ;  as  a  rule, 
it  lasts  four  or  five  weeks.  Patients  feel  the  effects  of  the  disease  for  a  long 
time.  For  months  and  years  walking  tires  them,  and  severe  exercise  causes 
the  oedema  to  reappear.  The  cellular  tissue  and  the  skin  are  often  the  seat 
of  ill-defined  induration. 

Venous  thrombosis  fer  se  very  rarely  causes  gangrene,  which  more 
usually  supervenes  in  the  course  of  phlegmasia,  because  the  inflammation 
extends  from  the  vein  to  an  artery. 

In  rare  cases  the  clot  breaks  up,  and  is  carried  away  by  the  blood-current ; 
the  thrombus  becomes  an  embolus,  which  gets  stranded  in  the  right  heart, 
or  passes  through  into  the  lung.  Disastrous  complications  are  the  result : 
cardiac  emboUsm  may  produce  fatal  syncope,  while  pulmonary  embolism, 
according  to  its  extent,  produces  rapidly  fatal  asphyxia,  attacks  of  dyspnoea, 
pulmonary  gangrene,  and  mechanical  or  septic  infarcts  in  the  lung.  These 
complications,  described  under  Pulmonary  Embohsm,  show  how  great  may 
be  the  gravity  of  the  prognosis. 

It  is  of  interest  to  know  at  what  period  embolism  is  most  to  be  feared. 
It  is  rightly  admitted  thar  the  accident  in  question  is  no  longer  to  be  feared 
six  weeks  after  the  appearance  of  phlebitis.  The  exceptions,  however, 
must  be  reckoned  with,  as  in  the  case  quoted  by  Trousseau,  where  fatal 
embohsm  supervened  three  months  after  the  onset  of  phlebitis. 

The  diagnosis  is  generally  easy.  It  must  not  be  forgotten,  however, 
that  pain  and  oedema,  which  are  the  chief  symptoms,  may  be  absent.  Cases 
have  been  quoted  in  which  the  disease  was  almost  latent,  and  yet  the  patients 
succumbed  rapidly  from  pulmonary  embohsm.  On  the  other  hand,  phleg- 
masia may  be  of  value  in  diagnosis. 

When  we  hesitate,  for  example,  between  ulcer  and  cancer  of  the  stomach, 
the  appearance  of  phlegmasia  confirms  the  existence  of  cancer.  Trousseau, 
who  brought  this  fact  so  clearly  to  hght,  was  able  to  apply  the  senieiological 
value  of  phlegmasia  to  his  own  case.     The  appearance  of  painful  oedema 


474  TEXT-BOOK  OF  MEDICINE 

in  the  leg  led  him  to  diagnose  the  gastric  cancer  from  which  he  died  six 
months  later. 

Varieties. — After  this  general  description,  let  us  consider  special  cases  : 

1.  In  puerperal  women  phlebitis  appears  some  days  after  accouche- 
ment, rarely  later  than  two  weeks.  It  is  often  ushered  in  by  fever.  Puer- 
peral phlebitis  is  usually  absent  when  the  accouchement  has  been  normal, 
and  is  generally  seen  only  in  cases  in  which  the  patient  has  shown  some 
infectious  phenomenon,  foetid  lochia,  difficult  or  artificial  deUvery,  slight 
fever,  etc.  In  other  cases,  after  accouchement  or  miscarriage,  no  sign  of 
infection  may  occur,  and  yet  phlegmasia  develops  three  or  four  weeks  later. 
Phlegmasia  of  puerperal  origin  improves  after  three  or  four  weeks,  but  may 
last  much  longer.  I  cannot  direct  too  much  attention  to  a  variety  of 
phlebitis  which  also  has  a  uterine  origin,  although  it  may  not  be  puerperal. 
I  allude  to  the  cases  of  deep  phlebitis  or  of  phlegmasia  alba  dolens  which 
supervene  after  operations  for  diseases  of  the  ovaries  and  uterus,  and 
especially  fibroids. 

2.  Phlegmasia  in  typhoid  fever  usually  supervenes  during  the  decline 
of  the  disease  or  during  convalescence.  Its  onset  is  often  febrile.  It  may 
afEect  the  veins  of  the  upper  Hmbs  and  the  neck,  and  may  be  associated  with 
arteritis. 

3.  Painful  phlebitis  occurs  in  influenza,  and  recent  epidemics  have 
provided  material  for  its  careful  study.  In  the  pubhshed  cases  the 
phlebitis  affected  the  veins  of  the  lower  hmbs  or  of  the  arm. 

4.  Phlegmasia  is  frequently  associated  with  tuberculosis.  It  usually 
supervenes  in  the  cachectic  stage.  In  some  cases,  however,  it  may  appear 
early. 

5.  I  would  make  the  same  remark  concerning  cancer.  In  most  cases 
phlegmasia  supervenes  in  the  stage  of  cachexia,  but  in  other  cases  (Trousseau 
was  himself  a  memorable  example)  it  appears  during  the  first  stage  of  cancer, 
before  other  positive  symptoms.  It  is  therefore  a  typographical  error 
which  states  that  Trousseau  diagnosed  cancer  of  the  stomach  a  month 
before  his  death,  on  the  appearance  of  phlegmasia.  It  was  several  months 
before  liis  death  that  the  appearance  of  phlebitis  in  the  calf  led  Trousseau 
to  diagnosw  cancer,  although  no  other  positive  signs  of  organic  disease  were 
present.     1  am  able  to  state  this  fact  because  I  saw  the  case. 

6.  Phlegmasia  associated  with  chlorosis  presents  pecuhar  interest. 
Possibly  this  phlebitis,  hke  so  many  other  cases,  is  due  to  a  superadded 
infection.  Certainly  phlegmasia  of  chlorotic  origin  is  far  from  being  rare, 
and  in  some  cases  has  been  followed  by  pulmonary  embohsm  and  death. 
In  several  cases  death  has  supervened  from  phlebitis  of  the  pulmonary 
veins. 

7.  Phlebitis  has  been  noted  in  acute  articular  rheumatism  and  in  pneu- 


DISEASES  OF  THE  VESSELS  475 

raonia  (Obrecht).     The  importance  of  gouty  phlebitis  will  be  considered 
under  Gout. 

8.  Phlebitis  of  the  limbs  may  occur  in  the  course  of  blennorrhagia. 

9.  Appendicular  phlebitis  is  not  uncommon.  I  have  seen  it  in  a  woman 
suffering  from  appendicitis,  which  was  operated  on  later  by  Segond.  The 
phlebitis  usually  affects  the  left  leg.  It  may  appear  as  an  infectious  com- 
pUcation,  even  though  the  appendicitis  be  slight. 

Treatment. — In  a  patient  suffering  from  phlegmasia  we  must  avoid 
massage,  and  movement  of  every  kind  which  may  favour  the  displacement 
of  a  clot  and  the  formation  of  an  embolus. 

The  affected  hmb  should  be  placed  in  a  trough-spHnt  in  order  to  obtain 
complete  immobiUty.    The  pains  may  be  reheved  by  the  following  ointment : 

VaseUne,  10  parts  ;  methyl  saHcylate,  3  parts.  Salt  must  be  excluded 
from  the  diet.  Since  Widal  showed  that  the  oedema  in  Bright's  disease 
disappears  by  excluding  salt,  Chantemesse  has  apphed  this  treatment 
successfully  to  phlegmasia  in  enteric  fever.  I  have  seen  the  good  effects 
of  milk  diet  in  women  suffering  from  post-operative  phlebitis.  The  cure 
at  Bagnols  (Department  of  Orne)  is  of  much  service. 

II.  SYPHILITIC  PHLEBITIS. 

Description. — Although  sj^hiHtic  phlebitis  may  not  appear  tiU  some 
one  or  two  years  after  infection,  i€  is  usually  a  much  earUer  manifestation 
of  the  disease.  In  one  of  Roussy's  cases  it  appeared  five  months  after 
the  chancre.  In  one  of  my  cases  it  supervened  two  and  a  half  months  after 
the  chancre.  Thibierge  has  recorded  phlebitis  of  the  internal  saphenous 
and  cephahc  veins  two  months  after  the  chancre.  Fournier  noted  its  appear- 
ance in  the  internal  saphenous,  median  basiUc,  and  median  cephaUc  veins 
six  months  after  the  primary  sore.  Phlebitis,  therefore,  may  appear  witliin 
a  few  weeks  or  months  of  the  chancre  ;  it  may  precede  or  coincide  with  the 
roseola  and  the  mucous  patches.  Le  Noir  and  Girdwood  state  that  the 
sldn  rash  may  not  appear  until  several  days  after  the  onset  of  superficial 
phlebitis.  Fournier  and  Loeper  have  recorded  the  fact  that  in  one  case 
phlebitis  appeared  two  days  before  the  papules  in  the  skin.  The  disease 
does  not  always  begin  in  the  same  way.  A  sensation  of  weight,  formication, 
or  cramp  may  be  noticed  in  the  Umb  ;  on  the  other  hand,  prodromata  may 
be  absent,  the  pain  is  acute  from  the  first,  iind  oedema  appears. 

In  one  patient  the  phlebitis  had  a  sudden  onset.  He  was  returning 
liome  when  he  felt  acute  pain  in  the  left  thigh,  along  the  course  of  the 
saphenous  vein,  in  the  popliteal  space,  and  in  the  leg.  Next  day  the  wliolc 
limb  was  oedematous.  Mauriac's  patient  was  in  hospital  when  he  felt  a 
sharp  pain  in  the  right  calf  ;  phlebitis  had  just  commenced.     Charcot  speaks 


476  TEXT-BOOK  OF  MEDICINE 

of  a  syphilitic  patient  who  felt  acute  pain  on  the  inner  side  of  the  left  thigh  ; 
phlebitis  had  just  begun  in  the  internal  saphenous  vein. 

Fever  is  exceptional  or  slight,  and  throughout  the  disease  "  the  symp- 
toms," as  Fournier  says,  "  begin  Hke  those  of  a  subacute  phlebitis,  which 
almost  at  once  becomes  of  the  apyretic  variety,  in  which  the  affection  com- 
prises simply  a  plastic  induration  of  the  venous  trunk." 

The  veins  of  the  leg  are  more  often  affected  than  those  of  the  arm.  We 
find,  in  order  of  frequency,  the  internal  saphenous,  the  external  saphenous, 
the  basihc,  and  the  cephahc  veins. 

The  vein  is  not  always  involved  along  its  whole  course  :  the  phlebitis  is 
often  partial.  In  one  of  Fournier's  cases  induration  was  noticeable  over 
the  internal  malleolus,  and  did  not  appear  again  until  above  the  knee, 
whence  it  extended  to  the  groin. 

This  segmentation  has  often  been  noted  in  the  median  cephahc  and 
basihc  veins.  It  is  also  common  in  syphihtic  arteritis,  where  healthy  and 
diseased  segments  alternate. 

We  must  note  the  multipUcity  of  phlebitis  in  the  same  patient.  Other 
diseases  besides  syphihs  cause  multiple  phlebitis,  but  this  pecuHarity 
is,  I  think,  nowhere  more  marked  than  in  sypliihs.  In  thirty-six  cases 
twenty-two  patients  had  multiple  phlebitis.  In  my  patient  both  legs  were 
affected.  In  Fournier's  patient  the  left  leg,  the  right  leg  and  arm  were 
involved.  In  Fournier  and  Loeper's  case  phlebitis  was  present  in  the  left 
leg  and  in  the  right  leg  and  arm. 

Syphihtic  phlebitis  is  fairly  often  symmetrical.  It  is  prone  to  relapse. 
A  patient  who  thinks  he  is  cured  has  a  fresh  attack  some  weeks  or  months 
after  the  first  attack. 

Phlebitis  is  far  more  common  in  the  superficial  than  in  the  deep  veins. 
Mauriac,  however,  has  seen  a  case  of  deep  phlebitis  with  thrombosis.  Andry 
and  Constantin  have  seen  phlebitis  of  the  pophteal  vein,  resembhng  in  every 
way  phlegmasia  alba  dolens. 

Pain  and  oedema  are  not  as  a  rule  as  severe  in  the  syphihtic  as  in  the  other 
forms  of  phlebitis.  Nevertheless,  when  my  patient  was  admitted  to  the 
Hotel-Dieu,  the  oedema  extended  from  the  foot  to  the  trunk. 

Recovery  occurs  in  a  few  weeks,  and  the  veins  regain  their  elasticity. 
This  is  the  reason  why  specific  phlebitis  does  not  leave  behind  it,  as  the 
other  forms  do,  interminable  oedema,  which  reappears  on  the  least  provoca- 
tion, and  obstinately  resists  all  treatment,  including  massage  and  the  cure 
at  Bagnoles.  We  must  not,  however,  suppose  that  syphihtic  phlebitis  is 
always  of  short  duration  ;  in  some  cases  the  disease  lasts  five  or  six  months, 
owing  to  the  multiplicity  of  the  lesions  and  to  the  relapses  which  occur. 

But  a  capital  difference,  which  would  alone  suffice  to  distinguish  the 
syphilitic  from  the  other  forms  of  phlebitis,  is  that  it  is  not  complicated 


DISEASES  OF  THE  VESSELS  477 

by  emboKsm.  In  phlebitis  due  to  puerperal  or  typhoid  fever,  to  pneumonia, 
influenza,  appendicitis,  cancer,  tuberculosis,  gout,  etc.,  the  chief  danger 
lies  in  emboHsm  and  infarcts.  Nothing  of  the  kind  is  found  in  syphihtic 
phlebitis,  fatal  embolism  or  infarcts  having  never  been  noted. 

The  diagnosis  comprises  two  stages.  We  must  diagnose  phlebitis  and 
prove  that  it  is  syphilitic.  The  signs  of  phlebitis  include  pain  in  the  course 
of  a  vein,  the  transformation  of  the  vein  into  a  rigid  and  at  times  indurated 
cord,  and  the  appearance  of  oedema,  which  may  be  sUght,  in  the  subjacent 
region  of  the  Umb!  We  must  not,  however,  confuse  it  with  syphihtic 
lymphangitis,  which  also  forms  a  superficial  rigid,  painful  cord,  with  or 
without  reddish  tracks  in  the  skin.  Lymphangitis  gives  rise  to  enlarged 
and  painful  glands.  Further,  the  rigid  cord  in  lymphangitis  does  not  coincide 
with  the  course  of  the  vein.  The  decision  as  to  the  specific  nature  demands 
a  survey  of  all  the  causes  which  may  engender  phlebitis.  If  we  find  no  such 
cause,  and  if,  on  the  other  hand,  the  phlebitis  appears  a  few  weeks  or  months 
after  the  chancre,  but  especially  at  the  same  time  as  the  secondary  symp- 
toms, the  lesion  is  specific. 

I  have  so  far  coasidered  early  phlebitis.  The  tertiary  forms  are  (^uite 
exceptional.  They  may  appear  as  gummatous  tumours  of  the  vein,  or  as 
generalized  phlebosclerosis  with  dilatation  of  the  veins. 

Pathological  Anatomy. — This  question  has  been  worked  out  upon  the 
living  subject,  because  no  one  has  died  of  the  malady.  Mendel  reports  a 
case  in  which  Lion  found  a  clot  totally  obhterating  the  resected  segment 
of  the  vein. 

Darier  and  Civette  have  published  the  following  conclusions  on  the 
pathological  anatomy  of  phlebitis.  Among  the  manifestations  of  severe 
secondary  syphiUs  we  may  find  hard,  movable  nodules  under  the  skin. 
Their  anatomical  situation  is  in  the  walls  of  the  subcutaneous  veins,  their 
structure  is  that  of  a  syphiloma,  and  they  give  rise  secondarily  to  ordinary 
thrombo-phlebitis.  Mercurial  treatment  brings  about  their  disappearance, 
with  an  apparent  return  of  the  tissues  to  their  normal  integrity. 

The  recognition  of  the  spirochsete  in  the  lesions  of  the  vessel  wall  is  the 
specific  hall-mark  of  syphihtic  phlebitis.  Benda  has  outUned  the  findings 
in  a  case  of  syphihtic  arteritis,  while  Nattan-Larrier  and  Brindeau  have 
given  a  complete  description  of  the  lesions  in  a  case  of  specific  arteritis  and 
phlebitis.  These  authors  systematically  examined  eighteen  syphihtic 
placentae,  which  showed  such  multiple  vascular  lesions  as  endophlebitis  and 
endarteritis  obliterans  aut  vegetans. 

In  five  placenta)  they  found  stainable  spirochaetae  in  the  vascular  layers 
of  the  veins  and  arteries,  which  correspond  to  the  tunica  media.  This 
finding  shows  the  importance  and  the  action  of  the  spirocha}tc. 

The  first  point  in  treatment  is  to  immobihze  the  hmb.     I  know  that  this 


478  TEXT-BOOK  OF  MEDICINE 

procedure  may  appear  somewhat  umiecessary  after  the  statement  that 
syphiUtic  phlebitis  has  never  caused  embohsm.  I  would  not,  however, 
depend  on  it,  because  the  unexpected  may  happen,  and  I  therefore  kept  my 
patient  at  absolute  rest  in  bed  in  the  Saint-Christophe  ward. 

Specific  treatment  must  be  employed.  Iodide  of  potassium  is  not  of 
much  use  in  my  opinion,  and  I  prefer  injections  of  a  watery  solution  of 
biniodide  of  mercury  daily  for  ten  days,  the  dose  being  |  grain.  The  treat- 
ment can  be  suspended,  and  then  repeated  if  occasion  arise. 


III.  ARTERITIS— ATHEROMA— ARTERIO-SCLEROSIS. 

Anatomy. — Before  undertaking  the  important  question  of  diseases  of  the  arteries,  I 
will  briefly  describe  their  normal  structure.  The  arteries  are  made  up  of  elastic,  muscular, 
and  connective  tissue,  an  endotheUal  layer,  nutrient  vessels,  and  nerves.  These  tissues 
vary  in  extent  according  to  the  size  of  the  artery  and  its  functions,  just  as  the  arterial 
lesions  vary  according  to  the  size  of  the  vessel. 

An  artery  is  composed  of  three  coats  :  (1)  The  tunica  externa,  or  adventitious  coat, 
is  composed  of  bundles  of  connective  tissue,  mixed  with  elastic  fibres,  and  receives  the 
vaso  vasorum,  which  do  not  penetrate  into  the  tunica  media,  except  in  pathological 
conditions.  (2)  The  tunica  media  is  the  characteristic  portion  of  the  artery.  In  the 
large  arteries  (aorta,  carotid,  pulmonary  arteries)  the  elastic  tissue  predominates, 
and  the  muscular  elements  are  scanty.  The  elastic  fibres  and  laminae  form,  as  it  were, 
a  felting,  whence  the  name  fenestrated  membrane. 

These  elastic  elements  are  supported  upon  the  internal  elastic  lamina,  which  is 
more  important  than  the  external  one.  In  arteries  of  medium  size  the  tunica  media  is 
less  rich  in  elastic  tissue  and  more  rich  in  muscular  tissue  ;  the  elastic  felting  is  less  impor- 
tant ;  the  internal  lamina  persists,  but  the  external  lamina  has  disappeared.  The  smooth 
muscle  fibres  form  bundles  which  are  transverse  in  direction,,  and  are  inserted  into  the 
network  of  the  tunica  externa.  In  the  arterioles  the  elastic  tissue  is  only  represented  by 
the  internal  elastic  lamina,  which  appears  festooned  in  transverse  sections,  because  the 
muscular  fibres  contract  and  the  elastic  lamina  undergoes  retraction.  The  connective 
tissue  has  disappeared.  The  nerves  of  the  artery  belong  to  the  tunica  media.  (3)  The 
tunica  intima  varies  according  to  the  artery :  the  endothelial  layer,  formed  by  endotheUal 
cells,  is  everywhere  the  same  ;  but  in  the  large  arteries  of  the  elastic  type  we  find  a  fibro- 
elastic  layer,  which  is  divided  into  two — the  one  showing  longitudinal,  the  other  trans- 
verse striation  (the  lesions  of  atheroma  begin  in  the  fibro-elastic  layer).  In  arteries 
of  the  muscular  type  the  longitudinal  layer  alone  persists  ;  in  the  arterioles  the  tunica 
intima  is  formed  by  the  endothelium  alone. 

History — Discussion. — Since  the  commencement  of  the  century, 
arteritis  has  been  more  or  less  intimately  allied  with  questions  of  doctrine, 
Pinel,  in  his  classification  of  fevers,  gave  the  name  of  angiotenic  to  a  tran- 
sient fever  which  originated,  as  he  thought,  in  inflammation  of  the  arteries. 
He  said  that  this  inflammation  was  shown  post  mortem  by  the  redness  of 
these  vessels. 

Bouillaud  did  not  agree  with  Pinel's  narrow  classification.  In  his 
opinion  inflammation  of  the  vessels  and  of  the  heart  is  not  only  a  cause  of 
fever,  but  represents  fever  taken  in  its  widest  sense.     This  forms  the  famous 


DISEASES  OF  THE  VESSELS  479 

angiocarditic  fever,  the  anatomical  proof  of  which  Bouillaud  also  found  in 
the  redness  and  phlogosis  of  the  hning  membrane  of  the  heart  and  vessels. 
At  this  time,  moreover,  medicine  was  dominated  by  the  doctrine  of  inflam- 
mation, gastroenteritis  according  to  Broussais,  angiocarditis  according  to 
Bouillaud,  or,  in  other  words,  gastro-intestinal  inflammation,  on  the  one 
hand,  and  cardio-vascular  inflammation  on  the  other  ;  but  it  was  always 
inflammation  causing  slightly  different  types,  according  to  the  intensity  of 
the  inflammatory  process.  Two  renowned  men  had  been  brought  to  this 
pass  by  adhering  to  system. 

Reaction,  however,  occurred.  Trousseau  and  Rigot  had  abeady  shown 
that  the  redness  of  the  arteries,  the  so-called  phlogosis,  was  only  the  result 
of  cadaveric  imbibition,  and  Bretonneau,  in  his  memorable  work,  partly 
destroyed  the  doctrine  of  inflammation,  and  replaced  it  by  the  admirable 
doctrine  of  specificity,  which  has  in  our  day  been  rejuvenated  and  confirmed 
by  the  discovery  of  microbes.  Whilst  medicine  was  led  astray  as  to  inflam- 
mation of  the  arteries  and  its  consequences,  surgeons  pubhshed  excellent 
works,  and  Frangois  proclaimed  that  arteritis  causes  obhteration  of  the 
arteries  and  spontaneous  gangrene.  The  German  school  next  took  the  field 
with  the  doctrine  of  embohsm  (Virchow),  and  from  that  time  two  causes  of 
arterial  obliteration  were  recognized — the  one  by  thrombosis,  the  other  by 
embolism. 

From  this  time  two  fines  of  study  were  estabfished  :  the  one  studied 
chiefly  arterial  degeneration,  and  it  appears  that  the  active  process  was 
rather  neglected ;  atheroma  was  found  in  every  case — "  this  vital  rusting," 
according  to  Peter's  happy  expression  ;  "  a  man  is  as  old  as  his  arteries," 
according  to  the  dictum  of  CazaUs.  On  the  other  hand,  the  active  process 
was  especially  studied,  endarteritis  and  periarteritis,  obliterating  endar- 
teritis and  dilating  arteritis,  being  described.  Small  mihary  aneurysms  of 
the  brain,  associated  with  cerebral  haemorrhage,  were  discovered  (Bouchard, 
Charcot),  and  descriptions  were  given  of  the  small  aneurysms  in  pulmonary 
cavities,  resulting  in  fulminant  lia3moptysis  (Rasmussen),  while  ectasia  of 
the  vessels  in  bronchial  dilatation  and  the  profuse  haemorrhage  which  they 
jjroduced,  were  proved  (Hanot). 

Our  knowledge  of  these  lesions  has  gradually  progressed  up  to  the 
present  time,  when  we  consider  chiefly  the  pathogenesis  of  arteritis  and  the 
part  played  by  infectious  diseases  and  their  agents.  I  must  now,  however, 
deal  with  another  important  question,  that  of  arterio-sclerosis. 

In  1S72  Gull  and  Sutton  described  a  kind  of  fibroid  change  in  tlio 
arterioles  and  capillaries  under  the  name  of .  arterio-capillary  fibrosis. 
They  showed  that  the  change  in  the  kidneys  which  results  in  atrophy  ia 
simply  the  extension  of  a  morbid  process  which  has  begun  in  tlic  small 
vessels  of  this  organ.     The  doctrine  of  arterio-sclerosis  was  thus  created. 


480  TEXT-BOOK  OF  MEDICINE 

What,  then,  is  arterio-sclerosis  ?  It  is  arteritis  of  the  arterioles,  and  especi- 
ally of  the  visceral  arterioles.  Endarteritis  results  in  fibrous  thickening  of 
the  tunica  intima,  in  constriction  of  the  arterioles,  and  in  fibrous  change  in 
its  walls. 

Atheroma  and  arterio-sclerosis,  which  are  so  unlike  at  first  sight,  result 
from  the  same  causes,  except  that  the  result  is  atheroma  in  the  large  arteries 
or  in  those  of  medium  size,  and  arterio-sclerosis  in  the  visceral  arterioles. 
Atheroma  of  the  large  arteries  is  said,  therefore,  to  be  the  result  of  arterio- 
sclerosis of  their  vasa  vasorum. 

The  characteristic  point  is  that  the  process  commences  in  the  small 
vessels,  but  as  it  does  not  remain  limited  to  them,  the  process  becomes 
extravascular,  and  extends  to  the  connective  tissue  and  the  elements  of  the 
organ,  which  are  replaced  by  newly-formed  fibrous  tissue.  The  change 
arises  in  the  arterioles,  and  extends  to  the  neighbouring  regions  in  the  form 
of  bands  and  islets  of  fibrous  tissue. 

Arterio-sclerosis,  when  once  present,  shows  no  Hmit.  According  to 
some  authors  (Martin,  Huchard,  Weber),  it  sums  up  the  pathogenesis  of 
nearly  all  the  chronic  affections  of  the  viscera. 

Certain  forms  of  nephritis,  formerly  considered  as  having  an  inter- 
stitial or  epitlielial  origin,  including  senile  nephritis,  which  has  been  looked 
on  as  epithelial  (Charcot  and  Gombault),  would  therefore  be  cases  of  renal 
sclerosis  of  vascular  origin. 

Arterio-sclerosis  of  the  coronary  arteries  would  embrace  the  whole  of 
cardiac  pathology.  The  heart  in  Bright' s  disease,  the  senile  heart,  the 
fatty  heart,  hypertrophic  fibrous  myocarditis,  and  myocarditis  associated 
with  valvular  lesions,  would  all  depend  on  arterio-sclerosis.  Valvular 
lesions  of  the  heart  would  depend  upon  the  primary  vascular  lesions,  and 
without  arterio-sclerosis  of  the  coronary  arteries  angina  pectoris  would  not 
exist. 

The  lesions  of  the  aorta  and  the  large  arteries  are  also  secondary  to 
arterio-sclerosis.  Atheroma  only  shows  itself  in  arteries  provided  with 
vasa  vasorum,  and  is  the  result  of  endarteritis  and  arterio-sclerosis  of  these 
vasa  vasorum.  The  proof  lies  in  the  fact  that  the  vasa  vasorum,  which 
correspond  to  the  atheromatous  patches,  are  always  affected  by  arteritis 
obliterans  (Martin). 

In  the  nerve  centres  arterio-sclerosis  plays  a  considerable  part,  so  that 
tabes,  general  paralysis,  many  syphilitic  lesions,  etc.,  may  have  their  origin 
in  arterio-sclerosis. 

The  genito-urinary  apparatus  is  also  under  the  ban  of  arterio-sclerosis, 
which  causes  fibrous  hypertrophy  of  the  prostate  and  the  bladder.  I  shall 
describe  later  the  lesions  of  the  kidneys. 

The  stomach  and  spleen  present  changes  due  to  arterio-sclerosis.     The 


DISEASES  OF  THE  VESSELS  481 

portal  vein,  too,  may  be  affected  by  phlebo-sclerosis  (Laennec's  atrophic 
cirrhosis). 

Such  are  the  chief  local  manifestations  of  arterio-sclerosis.  In  different 
cases  it  may  remain  localized  to  a  single  organ,  such  as  the  kidney,  heart,  or 
lung ;  it  may  attack  several  organs  at  once,  or  even  become  general  and  be  asso- 
ciated or  not  with  lesions  of  the  large  arteries,  and  especially  with  atheroma. 

These  views  of  arterio-sclerosis  are  of  much  interest,  but  it  must  be 
admitted  that  for  some  years  arterio-sclerosis  has  been  singularly  abused. 
It  has  become  all-invading,  and  has  been  held  to  explain  everything,  so 
that  when  any  difficulty  is  experienced  in  finding  a  pathogenic  or  chnical 
interpretation,  the  reply  is  :  '"'  It  is  arterio-sclerosis  !" 

Does  such  a  constant  relation  between  the  cause  and  effect  really  exist  ? 
Is  the  arterio-sclerosis  always  the  primary  lesion,  and  are  the  fibrous  lesions 
in  the  viscera  always  secondary  to  sclerosis  of  the  small  arteries  ?  When 
these  visceral  lesions  are  not  in  the  immediate  neighbourhood  of  the  dis- 
eased arteriole.,  the  partisans  of  this  doctrine  say  that  we  must  then  admit 
either  capillaritis  or  pericapillaritis  ;  but  then  we  have  reached  the  confines 
of  the  capillary  network  in  the  innermost  layers  of  the  tissues.  Why, 
then,  may  it  not  be  admitted  that  the  irritant  sclerogenous  substance, 
whether  bacillus  or  toxine  ;  whether  animal,  vegetable,  or  mineral ;  whether 
alcohol  or  lead,  may  be  able  to  act  upon  the  cells  of  the  connective 
tissue  and  of  the  organs  ?  The  desire  to  reduce  all  visceral  scleroses  to 
arterio-sclerosis  appears  to  me  exaggerated.  Reaction  is  taking  place  in 
this  matter.  Bard  and  Phihppe,  in  their  interesting  paper,  have  shown, 
as  regards  the  heart,  that  side  by  side  with  vascular  sclerous  hypertrophic 
myocarditis  there  is  room  for  interstitial  myocarditis,  in  which  the  arterio- 
sclerotic lesion  is  secondary.  In  general  paralysis,  according  to  Joffroy, 
encephalitis  is  much  more  probably  of  parenchymatous  than  of  vascular 
origin.  Some  authors,  confounding  the  lesions  and  its  effects,  find  it  a 
simple  matter  to  set  down  to  arterio-sclerosis  the  symptoms  of  "  Brightism," 
which  are  really  symptoms  of  toxicity.  The  result  is  the  confounding  of 
the  vascular  lesions  of  the  kidneys  with  the  multiple  effects  of  intoxication 
from  insufficiency  of  the  urinary  depuration. 

After  this  general  discussion,  let  us  pass  to  the  detailed  study  of  arteritis 
and  arterio-sclerosis.  Arteritis  may  develop  under  the  most  varied  con- 
ditions, and  may  have  almost  identical  results,  although  its  origin  is  very 
different.     It  is  therefore  necessary  to  divide  up  arteritis. 

Traumatic  Arteritis. 
These  cases  belong  chiefiy  to  the  domain  of  surgery.     Some,  however, 
are  of  interest  both  to  the  physician  and  the  surgeon,  such  as  tlioso  which 
develop  in  the  neighbourhood  of  superficial  or  of  deep  ulceration  of  the 


482  TEXT-BOOK  OF  MEDICINE 

skin,  or  of  a  viscus.  In  this  case  the  walls  of  the  artery  do  not  escape  the 
inflammatory  and  destructive  process  which  affects  the  surrounding  tissues, 
and,  accordingly,  two  eventualities  may  happen.  If  the  inflammatory 
process  predominates,  the  walls  of  the  artery  become  thickened  and  pro- 
liferate, the  cahbre  of  the  vessel  is  diminished,  the  blood  coagulates,  and  the 
artery  is  gradually  converted  into  an  impermeable  fibrous  cord,  which  may 
ultimately  be  destroyed,  without  untoward  consequences.  If,  on  the  other 
hand,  the  ulcerative  process  is  rapid  (ulcerative  or  suppurative  arteritis), 
the  walls  of  the  artery  are  destroyed  from  without  inwards,  before  coagula- 
tion of  the  blood  can  take  place,  lose  their  resistance,  and  finally  give  rise 
to  an  aneurysm.  This  sometimes  happens  in  the  interior  of  tubercular 
cavities  or  on  the  surface  of  gastric  ulcers.  If,  at  a  given  moment,  the  arterial 
tension  increases,  the  resistance  of  the  walls  is  insufficient,  the  aneurysm 
bursts,  and  fulminating  haemorrhage  occurs. 

The  arterial  lesions  which  occur  when  an  artery  is  obliterated  by  em- 
bolism are  also  related  to  traumatic  arteritis.  The  irritation  produced  by 
the  foreign  body,  whatever  may  be  its  point  of  departure  and  its  nature, 
leads  to  inflammation  of  the  tunica  intima  and  to  lesions  analogous  to  those 
which  we  shall  describe  later. 

Infective  Arteritis. 

Pathogenesis. — This  group  comprises  those  cases  which  supervene 
during  or  after  general  diseases.  They  have  been  verified  by  pathological 
anatomy  and  by  bacteriology,  and  their  existence  is  indisputable.  They 
are  most  often  seen  in  acute  diseases,  such  as  typhoid  fever,  etc.  (Taupin, 
Potain,  Vulpian,  Hayem) ;  diphtheria  (H.  Martin) ;  puerperal  conditions 
(Simpson) ;  scarlatina,  measles,  variola  (Brouardel) ;  malaria,  rheumatism 
(Lancereaux,  G-ueneau  de  Mussy),  etc.  Among  the  more  chronic  diseases  which 
may  cause  arteritis,  tuberculosis  and  syphihs  specially  deserve  mention. 

The  data  acquired  as  regards  the  evolution  of  the  tubercle  bacillus  show 
that  propagation  occurs  both  by  the  bloodvessels  and  by  the  lymphatics. 
If  it  is  arrested  in  an  arteriole,  a  colony  of  microbes  develops  at  this  point. 
The  irritation  thus  produced  in  the  walls  of  the  artery,  whatever  be  its  size, 
suffices  to  cause  specific  inflammation.  In  this  manner  the  starting-point 
of  most  tubercular  granulations  is  explained. 

Syphihtic  arteritis  will  be  studied  in  the  next  section. 

As  regards  infective  arteritis,  developing  in  the  course  of  the  maladies 
enumerated  above,  it  is  probable  that  the  arterial  lesion  is  directly  caused 
by  the  micro-organism  which  produces  the  infection,  unless  the  toxines 
secreted  by  it  can  be  also  incriminated.  These  cases  of  arteritis  would, 
therefore,  in  their  mechanism  resemble  another  class — namely,  the  toxic  class 
of  arteritis.      They  have,  however,  this  distinguishing  point— namely,  that 


DISEASES  OF  THE  VESSELS  483 

in  infective  arteritis  the  number  of  diseased  arteries  and  the  extent  of  the 
lesions  are  always  hmited,  while  toxic  arteritis  affects  a  large  number  of 
vessels,  and  involves  each  vessel  to  a  large  extent. 

Pathological  Anatomy. — The  following  lesions  are  found  in  infective 
arteritis  :  (1)  When  a  large  artery,  such  as  the  aorta,  is  affected,  the  inner 
wall  is  red,  rugose,  and  in  places  glazed,  while  other  parts  are  depressed  in  a 
cuplike  form,  and  resemble  the  pustule  of  variola  {vide  Aortitis),  and  the 
external  surface  shows  a  close  network  of  capillary  vessels  filled  with  blood. 
(2)  In  the  small  arteries  and  in  those  of  medium  size  the  lesions  are  not  visible 
to  the  naked  eye,  but  under  the  microscope  they  are  identical  with  those 
found  in  the  large  arteries.  They  comprise  an  increased  thickness  of  the 
tunica  intima  (endarteritis),  wliich  projects  into  the  lumen  of  the  vessel — 
sometimes  at  one  point  only  (parietal  arteritis,  Barie),  at  other  times 
around  the  whole  circumference  of  the  vessel.  When  the  artery  is  affected 
upon  one  side  only,  the  granulation  rarely  projects  sufficiently  to  ob- 
literate the  lumen,  which  is  simply  constricted.  If,  on  the  other  hand,  the 
arteritis  is  circumferential,  the  lumen  of  the  vessel  rapidly  disappears 
(obliterating  arteritis),  and  the  circulation  is  interrupted  in  the  whole  area 
suppHed  by  this  artery,  unless  the  collateral  circulation  supphes  the  defect. 
The  thickening  of  the  tunica  intima  depends  on  the  multiphcation  of  the 
anatomical  elements,  and  on  the  infiltration  of  leucocytes  between  these 
new-formed  elements. 

Endarteritis  may  exist  alone,  'but  as  a  rule  there  is  also  some  periarteritis. 
In  this  case  the  tunica  externa  is  thickened,  and  pushes  aside  the  structures 
in  contact  with  it.  In  this  case  also  the  inflammation  is  characterized  by 
the  appearance  of  embryonic  cells  between  the  connective  and  elastic 
bundles  of  the  tunica  externa.  All  the  elements  show  great  tendency  to 
undergo  fibrous  change. 

Symptoms. — The  symptoms  of  arteritis  in  acute  diseases  vary  according 
to  the  cahbre  of  the  vessel,  and  to  the  organs  which  it  supplies.  1.  If  the 
aorta  is  affected  (syphiUs,  variola,  puerperal  state,  and  malaria),  the  severe 
symptoms  of  acute  or  of  subacute  aortitis  will  appear.  2.  If  the  artery  is 
of  medium  size,  as  in  a  limb  (typhoid  fever),  the  patient  experiences  very 
acute  pain  along  the  artery,  or  at  the  extremity  of  the  Umb,  and  the  pain 
is  increased  by  pressure  and  movement.  At  the  same  time  the  pulse 
diminishes  or  disappears  completely,  and  the  limb  becomes  cold,  blue,  and 
insensitive.  A  hard  cord  which  rolls  under  the  finger  is  felt  along  tlie  course 
of  the  artery.  If  the  obliteration  is  complete  and  the  collateral  circulation 
is  not  re-established,  pustules  form,  livid  patches  appear,  and  the  limb  is 
affected  by  dry  or  moist  gangrene.  In  some  cases  the  results  are  not  always 
so  serious :  the  pulse  gradually  returns,  the  hard  cord  disappears,  and  the 
cyanosis  only  remains  in  the  form  of  violet-coloured  patches.     Walking 

31—2 


484  TEXT-BOOK  OF  MEDICINE 

may  cause  oedema,  lasting  several  months,  but  gangrene  is  averted,  and 
recovery,  although  slow,  is  the  usual  termination.  In  some  cases  arteritis 
makes  very  rapid  and  acute  progress,  as  we  shall  see  under  Typhoid  Fever. 

If  arteritis  affects  a  cerebral  artery  (typhoid  fever,  syphilis),  the  resulting 
troubles  depend  on  the  functions  of  the  area  supphed  by  the  diseased  vessel. 
As  the  arteries  of  the  motor  zone  are  most  often  affected,  the  symptoms 
are  nearly  always  very  grave,  and  include  hemiplegia,  aphasia,  contracture, 
etc.  In  the  case  of  syphilitic  arteritis,  however,  these  troubles  often  improve 
and  even  disappear  under  antisyphiHtic  treatment,  when  the  artery  recovers 
its  permeabihty,  as  in  a  case  of  syphilitic  arteritis  of  the  temporal  arteries 
pubhshed  by  Leudet.  For  further  detail  I  refer  to  the  section  on  Cerebral 
Syphilis. 

3.  If  the  diseased  arteries  are  of  small  calibre,  such  as  those  of  the  muscles 
or  of  the  viscera,  the  lesions  are  identical  with  those  already  described.  In 
some  cases  the  nutrition  of  the  invaded  tissues  is  severely  compromised. 
If  a  muscle  is  affected,  the  myositis  may  cause  softening,  and  end  in  rupture. 
If  the  arteritis  arises  in  the  heart,  for  example,  inflammation  of  arterial 
origin,  which  may  give  rise  to  all  the  lesions  and  chnical  signs  of  myocarditis, 
results.  As  a  general  rule,  these  inflammations  are  transient.  Lately, 
however,  cases  of  chronic  myocarditis  (Landouzy  and  Siredey),  encephahtis, 
myelitis  (Marie),  and  nephritis,  originating  in  infective  arteritis,  have 
been  published. 

Toxic  Arteritis— Atheroma— Arterio-Sclerosis. 

We  shall  include  in  this  group  arterial  lesions  consecutive  to  pathogenic 
agents,  to  their  toxines,  and  to  vegetable  or  mineral  poisons.  The  arterial 
lesions  in  alcohohsm  may  be  taken  as  our  type.  Still,  plumbism,  gout, 
rheumatism,  diabetes,  old  age,  and  the  infectious  diseases,  may  give  rise 
to  them.  In  some  cases  the  irritative  element  differs,  but  the  inflammatory 
processes  are  identical. 

They  may  be  reduced  to  two  chief  groups  : 

1.  As  in  the  preceding  case,  the  artery  may  be  affected  by  endoperi- 
arteritis,  which  diminishes  its  cahbre  and  changes  it  into  a  fibrous  tube. 
We  then  say  that  arterio-sclerosis  is  present  (Gull  and  Sutton). 

2.  The  tunica  intima  may  be  affected,  but  only  in  the  layers  subjacent 
to  the  endothehum.  At  this  level  yellowish  cupHke  patches  are  formed, 
having  the  dimensions  of  a  lentil  and  filled  by  a  fatty  pulp,  atheroma, 
which  flows  out  when  the  endothehal  covering  is  punctured.  If  the  fluid 
as  well  as  the  fatty  matter  is  reabsorbed,  the  calcareous  salts  only  remain, 
and  then  give  to  the  patch  a  rigid  consistency.  These  atheromatous  centres, 
which  may  exist  in  great  numbers  in  the  same  vessel,  may  finally  fuse,  and  give 
to  the  artery  a  cartilaginiform  or  ossiform  rigidity.      Accordingly,  the  name 


DISEASES  OF  THE  VESSELS  485 

of  ossification  of  the  arteries  has  been  given  to  this  disease,  although  it  is 
not  a  correct  term.  The  affected  vessel  loses  its  elasticity,  bursts  easily, 
and  allows  distension  (aneurysm),  while  the  irregularity  of  its  internal 
surface  favours  coagulation  of  the  blood  (tlirombosis). 

These  lesions,  which  are  sometimes  isolated,  sometimes  contiguous, 
occur  almost  exclusively  in  the  arteries  of  the  greater  circulation.  They 
are  usually  diffuse  and  always  run  a  very  slow  course.  When  the  whole 
arterial  system  is  invaded,  atheroma  cliiefly  affects  the  large  arteries, 
while  arterio-sclerosis  develops  by  preference  in  the  visceral  arterioles. 

Arterio-sclerosis  causes  changes  of  two  kinds  in  the  viscera  :  (1)  Peri- 
arterial inflammation  which  proceeds  by  foci,  in  the  centres  of  which  adiseased 
artery  is  always  found  (inflammatory  sclerosis)  ;  (2)  a  lesion  of  degenera- 
tion, in  which  foci  of  sclerosis  are  also  formed,  but  are  always  at  a  very  long 
distance  from  the  diseased  vessel  (dystrophic  sclerosis,  H.  Martin),  showing, 
therefore,  the  exact  opposite  of  what  occurs  in  the  preceding  case.  Some- 
times these  two  kinds  of  change  are  found  side  by  side  (mixed  sclerosis). 
Of  the  symptoms  of  atheroma  and  arterio-sclerosis,  some  are  due  to  the 
arterial  lesions  themselves,  while  others  depend  on  the  visceral  changes 
which  they  produce.  Among  the  former  (atheroma)  we  will  cite  the  tor- 
tuous course  and  rigid  character  of  the  arteries  and  the  increase  of  arterial 
tension,  which  is  shown  with  the  sphygmograph  by  a  sharp  line  of  ascent, 
followed  by  a  flat  top  and  a  wavy  line  of  descent ;  the  second  sound, 
wliich  is  accentuated,  and  has  a.  ringing  character;  and  the  frequency  of 
purpura  and  gangrene  of  the  extremities. 

Among  the  troubles  consecutive  to  the  visceral  changes  we  may  note 
cerebral  troubles,  such  as  vertigo,  loss  of  memory,  giddiness,  successive 
attacks  of  hemiplegia  and  aphasia,  and  faihng  intelligence,  which  may 
result  in  complete  dementia.  In  some  patients  the  heart  is  cliiefly  affected 
by  arterio-sclerosis,  palpitation,  hypertrophy  of  the  heart,  angina  pectoris, 
and  paroxysmal  dyspnoea  are  frequent.  In  other  patients  the  digestive 
functions  are  first  affected — loss  of  appetite  and  frequent  indigestion. 
Lastly,  in  a  fair  number  of  cases  renal  changes  open  the  scene  and  cause 
insufficiency  of  urinary  depuration,  and  the  numerous  symptoms  of 
Brightism,  which  must  be  carefully  elucidated  before  the  appearance  of 
the  grave  symptoms  of  confirmed  uraemia. 

The  treatment  of  atheroma  and  arterio-sclerosis  is  based  on  the  use  of 
iodides,  milk  diet,  and  remedies  which  will  lower  the  arterial  tension 
(Huchard). 


486  TEXT-BOOK  OF  MEDICINE 

IV.  SYPHILITIC  ARTERITIS— ARTERITIS  OBLITERANS— 

SYPHILITIC  GANGRENE— ARTERITIS  ECTASIANS 

—SYPHILITIC  ANEURYSM. 

In  the  course  of  syphilis  the  arterial  vessels  maybe  affected  alone,  without 
any  lesion  of  the  neighbouring  tissues.  These  cases  only  have  a  special 
clinical  history.  Sypliihtic  arteritis  of  the  brain,  spinal  cord,  aorta,  etc., 
is  dealt  with  under  syphiMs  of  these  organs.  I  shall  deal  at  present  only 
with  peripheral  arteritis,  and  in  particular  with  arteritis  of  the  limbs,  which 
forms  a  distinct  and  very  interesting  pathological  group. 

The  process  (either  in  the  arteries  of  the  Umbs  or  in  the  cerebro-meningeal 
ones)  may  result  in  two  different  kinds  of  lesions  :  on  the  one  hand,  more 
or  less  complete  obliteration  of  the  vessel ;  on  the  other  hand,  ectasia  of 
the  vessel  or  aneurysm. 

Arteritis  Obliterans — Gangrene. — I  do  not  know  of  a  more  typical 
case  than  that  presented  by  Leudet  (of  Rouen)  at  the  Blois  Congress  in 
1884. 

The  patient  -was  syphilitic,  and  suffered  from  painful  obliterating  arteritis  of  the 
anterior  frontal  branch  of  the  left  superficial  temporal  artery.  This  primary  arteritis 
obliterans,  limited  to  an  arterial  segment,  was  soon  followed  by  symmetrical  arteritis 
obliterans  of  the  right  side.  Leudet  was  able  to  follow  all  its  phases,  including  indura- 
tion, obliteration  of  the  artery,  diminution  and  cessation  of  the  pulse  ;  then,  under  the 
influence  of  antisyphilitic  treatment,  he  was  able  to  follow  the  re-establishment  of  the 
arterial  circulation,  return  of  the  pulse,  permeability  of  the  artery,  and  finally  cure. 

SyphiUtic  arteritis  obhterans  of  the  limbs  may  be  followed,  just  as 
atheromatous  arteritis,  by  mummification  of  the  extremities,  which  is  in 
every  way  comparable  to  ordinary  senile  gangrene.     Here  is  a  case  : 

An  old  woman  came  under  my  care  for  gangrene  of  the  right  leg  and  foot,  which 
had  come  on  suddenly  with  sharp  pain  two  months  before.  The  toes  were  blackish 
and  shrivelled  ;  the  dorsum  of  the  foot  was  li\id.  A  large  slough  had  invaded  the 
lower  part  of  the  limb.  The  pulse  was  absent  in  the  dorsahs  pedis  and  in  the  tibial 
arteries,  the  skin  was  cold  and  insensible,  and  the  picture  was,  in  a  word,  that  of  senile 
gangrene.  One  thing,  however,  struck  us  :  Over  the  forearm  and  abdomen  there  were 
irregular  pigmented  scars,  mth  polycyclical  outUnes,  and  on  the  left  upper  eyelid  a 
large  copper-coloured  papule,  with  scalloped  edges.  These  lesions  were  syphiUtic. 
I  at  once  concluded  tliat  the  gangrene  of  the  leg  was  due  to  syphiUtic  arteritis  obhterans. 
The  patient  was  given  injections  of  biniodide  of  mercury,  but  the  treatment  came  too 
late,  and  amputation  became  necessary.     The  patient  soon  succumbed. 

Examination  of  the  amputated  hmb  showed  that  the  gangrene  had  invaded  most  of 
the  posterior  muscles,  in  the  form  of  huge  lardaceous  infarcts  of  a  waxy-yellow  colour. 
The  femoral  artery  was  healthy  ;  the  branches  of  the  pophteal,  the  tibio-peroneal 
trunk,  and  the  posterior  and  anterior  tibial  arteries  were  obUterated  in  segments.  At 
these  spots  the  wall  of  the  artery  showed  a  ring-like  thickening,  and  the  lumen  was 
obhterated  by  adherent  thrombus.  Between  the  segments  the  lesions  were  absent  or 
very  slight.  Everywhere  else,  as  was  found  later  at  the  autopsy,  the  arteries  were 
healthy  and  free  from  atheroma.     Microscopical  examination  showed  that  this  process 


DISEASES  OF  THE  VESSELS  487 

originated  in  the  deep  part  of  the  subendothelial  layer  of  the  tunica  intima,  above  the 
internal  elastic  limiting  layer,  and  the  organization  of  a  thrombus  had  rapidly  com- 
pleted the  obhteration. 

Cases  of  this  kind  are  relatively  rare.  Aune,  however,  has  collected  seven, 
and  several  analogous  ones  have  been  pubhshed. 

Syphihtic  arteritis  attacks  the  lower  hmbs  (Charcot,  Fournier,  Podres, 
Hutcliinson)  as  often  as  the  upper  ones,  and  may.  be  bilateral,  symmetrical, 
or  multiple,  as  shown  by  Magrez's  case,  in  which  arteritis  obhterans  invaded 
in  succession  the  right  arm  and  the  legs,  with  gangrene  of  the  left  leg. 

The  onset  is  sometimes  progressive,  with  functional  troubles,  loss  of 
muscular  power,  and  intermittent  claudication  ;  at  other  times  sudden,  with 
very  sharp  pain.  Numbness,  formication,  coldness,  cyanosis,  and  oedema 
then  appear.  The  arterial  pulsations  disappear  in  the  affected  segment, 
and  if  the  artery  is  superficial  a  painful  cord  may  be  felt. 

The  slow  forms  may  be  arrested  by  treatment ;  the  permeabiUty  of  the 
vessel  becomes  re-established,  and  the  threatening  symptoms  disappear, 
although  a  fresh  attack  of  arteritis  may  show  itself  in  some  other  part.  In 
cases  of  sudden  onset  and  rapid  course  the  obhteration  results  in  dry  gan- 
grene. Accordingly,  when  a  patient  suffers  from  sharp  pain,  intermittent 
claudication,  chiUiness,  cyanosis,  and  gangrene  of  the  foot,  syphihtic  arteritis 
must  be  thought  of,  and  careful  search  made  for  other  stigmata  of  syphilis. 

From  the  anatomical  point  of  view  our  patient  showed  the  chief  characters 
of  syphihtic  arteritis.  We  see  cases  of  departmental  arteritis  affecting  a 
limited  area  of  a  limb.  In  this  region  the  lesions  do  not  show  the  same 
intensity  at  all  points  ;  one  segment  of  the  artery  is  respected,  while  another 
is  obliterated.  In  the  limbs,  as  in  the  brain,  arteritis  obliterans  is  chiefly 
segmental,  and  at  times  symmetrical  (Magrez's  case  affecting  the  lower  limbs, 
and  Leudet's  case  affecting  the  temporal  arteries).  When  these  anatomical 
characters  are  clear,  it  is  easy  to  distinguish  between  syphilitic  and  athero- 
matous lesions,  which  are  diffuse  and  general ;  but  there  are  exceptions,  and 
syphihtic  arteritis  may  be  also  more  or  less  general,  and  result  in  similar 
lesions  to  those  of  atheroma  (Cornil). 

The  histology  of  syphilitic  arteritis  obliterans  shows  nothing  specific. 
At  a  late  period  the  three  coats  of  the  artery  are  thickened  and  infiltrated, 
with  or  without  miliary  nodules,  resembUng  microscopic  gummata  (Joffroy). 
The  lesions  frequently  commence  with  endarteritis,  rarely  with  periarteritis. 
Obliteration  may  occur  as  the  result  of  two  processes.  Sometimes  we  find 
only  endarteritis  vegetans,  which  obliterates  the  artery  more  or  less  com- 
pletely, and  converts  it  into  a  fibrous  cord,  without  any  appreciable  throm- 
bus ;  at  otlier  times  (this  is  the  more  frequent)  there  is  thrombo-a^-teritis 
obliterans :  the  endothelium  desquamates,  or  becomes  necrosed,  and  the 
thrombus  contributes  very  largely  in  obhterating  the  vessel.     In  both  cases 


488  TEXT-BOOK  OF  MEDICINE 

the  arteritis  may  be  chronic  or  subacute.  It  appears  possible  to  differentiate 
it  from  ordinary  atheroma  by  the  greater  activity  and  the  more  rapid  course 
in  the  direction  of  obUteration,  as  well  as  by  the  lessened  tendency  to 
degenerative  lesions. 

Syphilitic  Aneurysm. — The  second  type  of  syphiHtic  arteritis  in  the 
limbs  results  in  dilatation  and  aneurysm.  The  dilatations  result  from  the 
same  process  of  embryonic  infiltration  of  the  coats  of  the  vessel ;  the  middle 
coat,  wliich  is  much  infiltrated,  has  lost  all  power  of  resistance,  and  yields 
at  one  or  at  several  points.  We  may  see  upon  some  vessels  buds  of  endarter- 
itis and  aneurysmal  dilatations.  Here,  as  in  the  brain,  these  dilatations 
may  be  cyhndrical  and  extensive,  or  circumscribed  and  aneurysmal. 
Aneurysms  sometimes  develop  in  several  arteries  (pophteal  and  innominate 
trunks,  Croft) ;  they  chiefly  affect  the  femoral,  popliteal,  subclavian,  brachial, 
and  radial  vessels.  I  have  seen  syphilitic  arteritis  of  the  left  radial  artery 
at  the  wrist,  which  had  resulted  in  the  formation  of  an  aneurysm. 

The  patient  had  been  previously  treated  for  a  large  serpiginous  ulcer  on  the  right 
arm.  I  saw  him  again  two  years  later  for  a  syphiUtic  cavity  in  the  right  lung.  Under 
mercury  and  iodide  of  potassium,  in  large  doses  for  a  long  period,  all  symptoms  were 
cured.  When  he  came  to  me  some  years  later  for  cerebral  troubles,  I  noticed  that  he 
wore  a  wrist-strap.  He  informed  me  that  for  some  weeks  past  faii'ly  firm  pressure  had 
been  employed  for  a  painful  aneurysm  of  the  left  radial  artery,  and  that  an  operation  had 
been  decided  upon,  as  no  benefit  accrued  from  the  compression.  I  asked  to  see  the 
aneurysm,  which  was  as  large  as  a  small  nut,  and  said  that  this  aneurysm  might  be 
the  result  of  syphiUs.  I  commenced  treatment  with  large  doses  of  mercury  and  iodides. 
The  aneurysm  gradually  diminished  in  size,  and  three  months  later  had  quite  dis- 
appeared. 

Treatment  is  very  efficacious  when  commenced  early,  before  the  lesions 
are  irremediable.  It  consists  in  giving  daily  an  injection  of  the  solution  of 
biniodide  of  mercury.  Iodide  of  potassium  may  be  given  in  addition  to  the 
mercurial  treatment. 

V.  ACUTE  AND  CHRONIC  AORTITIS. 

^Etiology. — Both  acute  and  clironic  aortitis  occur.  Primary  acute 
aortitis  does  not,  however,  exist.  "  In  the  immense  majority  of  cases  the 
lesions  of  acute  aortitis  develop  in  those  vessels  which  have  previously  been 
attacked  by  chronic  affections."  Accordingly,  these  different  varieties  of 
aortitis  should  be  described  in  the  same  chapter.  Consequently,  all  causes 
which  favour  the  development  of  atheroma,  including  old  age,  gout,  and 
alcohohsm,  find  their  place  in  the  aetiology  of  aortitis.  Syphilis  has  a  pre- 
eminent place  in  the  pathogenesis  of  aortitis  and  aortic  aneurysms.  Injury, 
blows,  and  contusions  may  be  held  guilty.  Infectious  diseases,  typhoid 
fever,  rheumatism,  tuberculosis,  variola,  scarlatina,  and  influenza  may  the 
more  excite  attacks  of  acute  aortitis  in  proportion  as  the  aorta  has  already 


DISEASES  OF  THE  VESSELS  489 

been  the  seat  of  chronic  lesions.  It  is  probable  that  bacteriological  researches 
will  finally  discover  the  pathogenic  agents  of  these  acute  attacks.  Cuzzatini 
has  found  the  pneumococcus  in  a  case  of  aortitis  set  down  to  cold. 

Pathological  Anatomy. — When  aortitis  is  frankly  acute  the  aorta  is 
dilated,  and  its  inner  surface  is  uneven.  The  lesion  commences  in  the  sub- 
endothelial  coat  of  the  tunica  intima  (Cornil  and  Ranvier).  The  tunica 
intima  shows  prominent  patches,  which  vary  in  size  from  a  pin's  head  to 
that  of  a  small  coin ;  they  have  been  named  gelatiniform  patches,  on  account 
of  their  transparent  and  gelatinous  appearance.  These  patches  are  formed 
of  spherical,  nucleated,  embryonic  cells,  and  some  branched,  flattened  cells, 
which  normally  are  found' in  the  hning  membrane.  The  patches  may  be  a 
hundred  times  as  thick  as  the  normal  membrane,  and  the  inflammatory 
process,  which  is  more  active  in  the  layers  bordering  on  the  endothelium 
when  the  aortitis  is  acute,  especially  affects  the  deep  layer  when  it  is  chronic. 
These  patches  are  sometimes  of  a  dark  brownish  colour. 

Small  fibrinous  clots  may  be  deposited  on  these  patches,  and  at  times 
become  the  origin  of  emboli.  The  middle  coat  is  but  httle  altered,  while  the 
external  coat  is  thickened  and  vascular.  In  some  cases  acute  aortitis  is 
ulcerative,  or  may  even  be  suppurative. 

The  lesions  of  acute  aortitis  may  spread  around  the  vessel,  and  cause 
pericarditis,  pleurisy,  lesions  of  the  cardiac  plexus,  and  consecutive  angina 
pectoris,  a  comphcation  which  plays  a  large  part  in  the  symptoms  of  aortitis. 

Chronic  aortitis,  Uke  chronic  -  arteritis,  which  is  frequently  associated 
^vith  it,  is  often  called  atheroma;  but  these  two  words,  arteritis  and 
atheroma,  have  not  the  same  signification,  for  the  word  atheroma,  which 
means  a  "  pulp,"  denotes  only  one  stage  of  chronic  arteritis.  Atheroma, 
"  this  vital  msting  "  (Peter)  and  chronic  arteritis  may  produce  such  changes 
in  the  artery  that  these  lesions  have  been  differently  called  deforming  and 
nodular  endarteritis,  or  arterial  atheromasia. 

The  lesions  of  chronic  aortitis  are  characteristic.  The  aorta  is  nodular 
and  dilated  ;  it  is  rigid  to  the  touch  and  hard  on  section  ;  on  its  inner  surface 
we  find  yellowish,  calcareous,  atheromatous  patches,  and  dilatations  of 
different  shapes.  The  inflammatory  process  in  chronic  aortitis  is  analo- 
gous at  the  onset  with  that  of  the  acute  disease.  The  lesion  begins  in  the 
subendothelial  layer  of  the  tunica  intima,  and  forms  patches  which  later 
undergo  fatty  and  calcareous  change— that  is  to  say,  atheroma. 

These  degenerations,  however,  are  not  always  the  result  of  an  influm- 
matory  process,  for  cases  occur  in  which  fatty  degeneration  of  the  arterial 
walls  is  the  primary  lesion  in  point  of  time  ;  this  lesion  may  affect  all 
three  coats,  and  may  in  its  turn  produce  slow  irritation  and  foci  of  chronic 
aortitis,  so  that  these  various  lesions  resemble  one  another,  or  are  complete 
in  themselves.     According  to  some  authors,  these  atheromatous  lesions, 


490  TEXT -BOOK  OF  MEDICINE 

which  are  apparently  primary,  are  the  result  of  arterio-sclerosis  of  the  vasa 
vasorum  (Martin). 

Whatever  be  their  origin,  the  lesions  of  chronic  aortitis  are  always 
accompanied  by  atheromatous  centres  and  calcareous  patches.  The  gela- 
tiniform  patches  of  the  tunica  intima,  by  their  fatty  change,  finally  form  an 
atheromatous  centre,  composed  of  fatty  detritus,  cholesterine,  and  crystals. 
The  fibrillary  groundwork  which  surrounds  these  foci  takes  on  a  chondroid 
appearance,  and  becomes  infiltrated  with  calcareous  granules.  If  the  wall  of 
the  vessel  is  intact  the  focus  projects  into  the  artery  as  an  atheromatous 
pustule,  but  if  the  endothelial  layer  bursts  the  contents  of  the  focus  are  carried 
away  by  the  blood-stream ;  the  blood  enters  the  focus,  and  the  blood-pressure 
at  this  point  may  cause  dilatation  and  aneurysm.  In  some  cases  atheroma 
prepares  the  way  for  spontaneous  rupture  of  the  aorta,  especially  of  its  intra- 
pericardial  portion.  The  blood  filters  between  the  atheromatous  patches, 
dissects  the  tunica  externa,  and  rupture  occurs  into  the  pericardium,  pleura, 
or  cellular  tissue.  In  chronic  aortitis  the  tunica  media  in  turn  undergoes 
change,  and  disappears  in  places,  as  the  result  of  fatty  degeneration  ;  it 
loses  its  resistance  and  elasticity,  while  the  tunica  externa  often  becomes 
fibrous,  so  that  the  whole  vessel  is  invaded ;  endarteritis,  mesarteritis,  and 
periarteritis  are  all  present  (Peter).  The  aortic  orifice  and  valves  often  par- 
ticipate in  the  process  of  aortitis.  In  some  cases  chronic  aortitis  is  associ- 
ated with  generalized  atheromasia. 

Description. — I  shall  first  deal  with  acute  aortitis,  or  at  least  with  acute 
attacks  which  supervene  in  the  course  of  a  chronic  process  that  is  often 
latent.  Acute  aortitis  behaves  differently,  according  ,to  the  case  ;  it  may 
pass  unnoticed,  just  as  acute  endocarditis  may  do,  or  it  may  be  accompanied 
by  a  feeHng  of  weight  and  oppression  in  the  precordial  and  epigastric  regions, 
or,  lastly,  it  may  give  rise  to  the  symptoms  of  angina  pectoris. 

Pain  and  dyspnoea  are  sometimes  the  chief  symptoms.  The  pain  is 
retrosternal,  stabbing,  continuous  or  paroxysmal,  and  radiates  to  the  arms, 
neck,  back,  intercostal  spaces,  larynx,  oesophagus  (dysphagia),  stomach 
(gastric  crises),  or  liver  (false  hepatic  coUc).  The  dyspnoea  is  also  continuous 
or  paroxysmal,  but  the  respiratory  rhythm  is  not  increased.  During  the 
attacks  of  pain  and  dyspnoea  we  see  pulsation  of  the  carotid  and  subclavian 
arteries,  and  the  patient  is  sometimes  seized  with  fits  of  cougliing,  and  brings 
up  bloody  expectoration.  On  auscultation,  fine  rales,  indicating  congestion 
and  oedema  of  the  lung,  are  found  over  a  somewhat  limited  area.  These 
attacks  of  congestion  are  not  solely  hmited  to  the  lungs  ;  they  affect  the  liver, 
which  becomes  enlarged  and  painful,  and  also  cause  intestinal  dilatation  and 
ballooning  of  the  belly  (Rendu).  Sometimes  acute  infective  aortitis  results 
in  the  formation  of  a  purulent  collection,  which  opens  into  the  vessel,  and 
presents  the  clinical  picture  of  pyaemic  endocarditis. 


DISEASES  OF  THE  VESSELS  491 

Let  us  now  consider  chronic  aortitis.  The  signs  of  chronic  aortitis  vary 
with  the  situation  of  the  lesion  ;  let  us  take  the  most  frequent  case — namely, 
that  of  atheroma  of  the  arch  of  the  aorta.  In  the  normal  state  the  transverse 
dullness  of  the  aortic  and  pulmonary  trunks  together  is  about  2  inches 
(Peter)  ;  in  chronic  aortitis  the  dullness  may  exceed  3  inches,  according  to 
the  dilatation  of  the  vessel. 

The  aorta  by  its  expansion  raises  the  subclavian  arteries,  so  that  we  can 
easily  feel  them  in  the  supraclavicular  hollows.  Auscultation  may  reveal 
differences  of  tone  or  blowing  murmurs  (Potain).  The  first  aortic  sound, 
which  in  the  normal  state  depends  on  the  sudden  tension  of  the  aorta,  may 
become  exaggerated,  harsh,  and  blowing  as  the  result  of  the  atheromatous 
roughness  of  the  vessel  wall.  The  second  sound,  which  in  the  normal  con- 
dition depends  on  the  closure  of  the  sigmoid  valves,  may  be  echoing  and 
metalhc  if  the  valves  have  lost  their  suppleness.  A  diastolic  murmur,  due 
to  concomitant  aortic  insufficiency,  may  also  be  heard.  The  pulse  is  hard, 
while  the  radial  artery,  which  often  participates  in  the  atheromasia,  is 
tortuous  and  indurated.  Atheroma  of  the  aorta,  hke  general  atheromasia, 
is  always  accompanied  by  hypertrophy  of  the  heart. 

The  chnical  picture  varies  according  as  chronic  aortitis  comprises  the 
whole  disease,  or  as  it  is  associated  with  a  lesion  of  the  aortic  orifice,  aortic 
aneurysm,  nephritis,  more  or  less  extensive  atheromasia,  or  local  arterio- 
sclerosis. 

In  short,  chronic  aortitis  alone  may  remain  silent  for  a  long  time,  and  is 
usually  revealed  by  attacks  of  acute  aortitis,  while  several  of  the  symptoms 
which  accompany  it  are  borrowed — viz.,  hypertrophy  of  the  heart,  aortic 
insufficiency,  angina  pectoris,  Bright's  disease,  etc. 

Aortic  aneurysm  and  chronic  aortitis  present  many  common  signs  and 
symptoms  ;  among  other  distinctive  signs  there  is  one  which  has  some  worth 
— namely,  that  chronic  aortitis  does  not  form  a  tumour  as  aneurysm  does, 
and  consequently  does  not  produce  symptoms  of  compression. 

Blood-letting  with  leeches  or  cupping,  blisters,  the  actual  cautery,  sub- 
cutaneous injections  of  morphia  and  antipyrin,  form  the  general  plan  of 
treatment.  Iodide  of  potassium  should  be  administered  in  large  and  con- 
tinuous doses  in  acute  and  chronic  aortitis. 

VI.  ANEURYSMS  OF  THE  THORACIC  AORTA. 

etiology. — Aneurysm  of  the  aorta  is  very  rare  before  the  age  of  thirty- 
five  years,  and  its  aetiology  is  closely  related  to  that  of  acute  and  clironio 
aortitis.  In  the  enumeration  of  its  causes  heredity  should  not  be  forgotten. 
Injuries  of  the  thoracic  region  and  heavy  manual  labour  have  an 
influence  on  aneurysm,  but  syphihs  is  tlie  chief  cause. 


492  TEXT-BOOK  OF  MEDICINE 

Pathological  Anatomy. — Aneurysm  of  the  thoracic  aorta  affects,  in 
order  of  frequency,  first,  the  ascending  aorta  ;  second,  the  convexity  of  the 
arch  ;  third,  the  descending  aorta.  The  aneurysm  varies  in  size  from  a  small 
nut  to  that  of  the  foetal  head,  and  its  shape  is  extremely  variable  ;  it  is  said 
to  be  sacciform  when  the  dilatation  is  limited  to  a  part  of  the  circumference, 
hke  a  sac  hanging  from  the  vessel ;  it  is  said  to  be  fusiform  when  the  dilata- 
tion is  equally  distributed  over  the  whole  circumference  of  the  invaded 
segment.  The  small  hemispherical  aneurysms  found  chiefly  at  the  origin  of 
the  aorta  are  called  cupuliform;  the  name  dissecting  is  given  to  the 
aneurysm  which  results  when  the  blood  infiltrates  between  the  internal  and 
middle  coats,  and  separates  them  to  a  certain  extent.  Two  or  three  aneurysms 
in  the  course  of  the  aorta  are  sometimes  found  in  the  same  patient. 

There  has  been  lengthy  discussion  upon  the  way  in  which  the  sac  forms, 
and,  according  to  the  part  assigned  to  the  different  coats  of  the  vessel,  the 
classification  of  aneurysms  into  mixed  internal,  mixed  external,  etc.,  has 
been  proposed,  but  the  question  should  be  simphfied.  When  an  artery  is 
affected  by  chronic  arteritis,  the  tunica  media  disappears,  and  the  sac  of  the 
aneurysm  is  formed  by  the  joined  internal  and  external  coats  ;  often,  indeed, 
the  walls  of  the  sac  are  formed  by  the  internal  coat  alone,  which  has  been 
modified  by  the  inflammation.  "  The  newly-formed  tissue  which,  wholly 
or  in  part,  constitutes  the  sac  is  made  up  of  flat  cells,  separated  by  a  fibrillary 
substance,  and  undergoes  fatty  change,  atheroma,  and  petrification  ;  we  may 
also  see  old  sacs  formed  of  an  inextensible  calcareous  shell "  (Cornil  and 
Ranvier). 

These  lesions  explain  the  formation  and  development  of  the  aneurysm ; 
the  tunica  media  disappears  as  the  result  of  endarteritis  and  periarteritis, 
and  the  resistance  of  the  vessel  becomes  insufficient,  so  that  the  artery  yields 
to  the  blood-pressure,  and  the  vulnerable  points  permit  distension.  The 
distension  of  the  vessel  does  not  necessarily  induce  thinning  of  its  walls,  for 
the  growth  of  the  morbid  tissue  continues  ;  at  some  points,  however,  thinning 
may  result  and  favour  the  rupture  of  the  sac. 

When  the  sac  is  opened,  blood-clots  and  laminated  fibrin  are  found. 
The  clots  are  soft  and  recent,  the  layers  of  fibrin  are  elastic  and  greyish  ;  the 
older  ones  are  found  nearer  the  walls  of  the  sac  and  are  resistant,  but  no 
trace  of  organization  is  seen. 

Aneurysm  of  the  aorta  is  not  always  associated  with  extensive  athero- 
masia  or  with  arterio- sclerosis  ;  indeed,  atheroma  may  be  only  present  in  the 
aorta  and  nowhere  else — that  is  to  say,  the  aorta  may  be  diseased  on  its  own 
account,  independently  of  any  other  arterial  lesion. 

The  heart,  which  some  authors  regard  as  being  always  hypertrophied  in 
cases  of  aortic  aneurysm,  often  preserves  its  normal  size,  as  I  have  several 
times  found. 


DISEASES  OF  THE  VESSELS  493 

The  neighbouring  tissues  and  organs  in  contact  with  the  aneurysm 
undergo  important  changes  ;  the  bones  show  excavations  :  this  is  not  the 
result  of  mechanical  wear  and  tear,  due,  as  was  first  supposed,  to  the  move- 
ments of  the  aneurysm,  but  is  the  result  of  an  irritative  process,  or  osteitis, 
which  brings  about  the  absorption.  In  other  cases  the  sac  is  bound  dowai 
to  the  neighbouring  organs,  and  spreads  the  inflammatory  process,  which 
leads  to  softening,  ulceration,  and  perforation  of  the  invaded  tissue  or  organ. 
The  fact  is  thus  explained  that  the  aneurysm  may  open  into  the  pleura, 
pericardium,  oesophagus,  trachea,  pulmonary  artery,  superior  vena  cava,  or 
right  auricle. 

The  communication  between  the  aortic  aneurysm  and  the  veins  gives  rise 
to  an  arterio-venous  aneurysm. 

Patients  suffering  from  aneurysm  of  the  aorta  are  frequently  tubercular 
— e.g.,  eighteen  times  in  forty-six  cases.  Various  interpretations  of  this 
secondary  phthisis  have  been  given  ;  it  has  been  supposed  that  the  disease  is 
brought  about  by  the  compression  of  the  pulmonary  artery,  and  it  has  been 
compared  to  the  tuberculosis  that  accompanies  constriction  of  this  vessel. 

In  one  of  my  patients  suffering  from  an  enormous  aneurysm  of  the  aorta, 
death  resulted  from  left  tuberculai  broncho-pneumonia,  which  had  developed 
consecutively  to  compression  of  the  bronchus  and  of  the  left  pulmonary 
artery  by  the  aneurysm. 

Symptoms. — Aneurysm  of  the  thoracic  aorta  is  sometimes  latent,  and 
the  person  affected  may  be  suddenly  carried  off  without  any  previous 
warning.  I  do  not  know  a  more  conclusive  case  than  one  published  by 
Roux  of  a  young  soldier,  twenty-two  years  of  age,  who  died  suddenly  from 
an  aneurysm  which  opened  into  the  pericardium.  As  a  rule,  events  do  not 
take  this  course,  and  the  aneurysm  shows  itself  by  certain  symptoms  and 
signs  ;  their  frequency  and  value  I  shall  now  discuss. 

1.  Pain.— Pain  may  be  the  first  symptom.  Its  situation  and  its  nature 
depend  on  the  nervous  network  affected  by  the  tumour,  so  that  we  see  spinal 
pain  and  intercostal  neuralgia  (lesions  of  the  spinal  nerves  at  their  point  of 
exit  from  the  vertebral  column),  pains  in  the  arms  or  in  the  hands,  and  cubital 
neuralgia  (lesions  of  the  brachial  plexus),  the  agonizing  pains  of  angina 
pectoris  (lesions  of  the  cardiac  plexus),  diaphragmatic  pain  and  phrenic 
neuralgia  (lesions  of  the  phrenic  nerve).  These  pains  may  be  continuous, 
intermittent,  or  paroxysmal,  and  many  persons  who  have  aneurysm  of  the 
aorta  think  that  they  are  suffering  from  simple  intercostal  neuralgia,  or  from 
angina  pectoris. 

2.  Dyspnoea. — The  respiratory  troubles  vary  much.  One  patient  may 
have  spasm  of  the  glottis,  with  attacks  of  suffocation  ;  another  has 
paralysis  of  the  posterior  crico-arvtonoid  muscles,  which  open  the  glottis  ; 
while  a  third  suffers  from  hiccough,  accompanied  by  angina  and  thoracic 


494  TEXT-BOOK  OF  MEDICINE 

constriction  (phrenic  nerve).  The  dyspnoea  is  sometimes  continuous,  or 
nearly  so,  being  excited  and  increased  by  the  least  efiort ;  inspiration  is 
painful,  and  accompanied  by  stridor  (compression  of  the  trachea  or  of  a  large 
bronchus).  Stridor,  whether  it  is  complete  or  incomplete,  is  a  symptom  of 
great  value  ;  when  the  patient  is  at  rest,  the  stridor  is  but  Httle  marked,  and 
only  a  slightly  prolonged  and  rough  inspiration  is  audible,  but,  as  the  result 
of  effort,  true  stridor  appears.  When  a  large  bronchus  is  compressed, 
auscultation  reveals  abolition  or  diminution  of  the  vesicular  murmur  in  the 
corresponding  lung.  Some  patients  have  fits  of  coughing  which  resemble 
whooping-cough. 

3.  Vocal  Troubles. — We  find,  according  to  the  case,  dysphonia  or 
bitonal  voice  (Jaccoud),  hoarseness  of  the  voice,  and  aphonia.  These  vocal 
troubles  may  be  intermittent  or  continuous,  and  depend  on  paralysis 
of  the  vocal  cords,  and  especially  of  the  left  cord,  as  may  be  readily  seen 
with  the  laryngoscope. 

4.  Dysphagia. — The  trouble  may  be  continuous  or  intermittent,  and 
depends  upon  many  causes  :  compression  of  the  oesophagus  by  the  aneurysm, 
paralysis  or  excitation  of  the  vagus  and  the  recurrent  nerve,  which  supply 
the  constrictors  of  the  oesophagus  and  pharynx. 

Physical  Signs. — On  examination  of  the  thorax  we  find  dullness  which 
is  in  direct  relation  to  the  size  of  the  tumour,  and  we  may  sometimes  discover 
bulging  in  the  aortic  region.  If  the  tumour  is  visible  externally,  it  shows 
pulsation,  so  that  we  might  say  there  are  two  hearts  in  the  chest  (Stokes). 
The  pulsation  of  the  tumour  may  be  single  or  double  ;  the  first  beat  is  due  to 
the  blood-wave  which  enters  the  aneurysm;  the  second  beat  has  been 
differently  interpreted  :  it  may  be  due  to  the  return  of  the  blood- wave  into 
the  sac,  or  to  the  reflux  of  blood  from  the  collateral  arteries.  Perhaps  the 
two  beats  only  represent  the  distension  of  the  aneurysmal  tumour  at  two 
different  periods  (Franck).  The  beats  which  occur  later  than  the  cardiac 
systole  are  expansile,  and  are  sometimes  accompanied  by  thrill. 

Auscultation  over  the  sac  reveals  splashing  and  blowing  sounds,  which 
may  be  single  or  double,  and  audible  in  the  anterior  thoracic  region,  and 
sometimes  in  the  interscapular  region.  The  first  splashing  sound  is  due  to 
the  shock  of  the  blood-wave  upon  the  walls  of  the  aneurysm,  while  the  second 
is  due  to  the  closure  of  the  sigmoid  valves.  The  first  blowing  sound  is  due 
to  the  roughening  of  the  aorta  from  atheroma,  or  its  compression  by  the 
aneurysm ;  the  second  sound  {souffle  de  retour)  is  due  to  the  return  of  the 
blood-wave  into  the  sac,  or  to  the  aortic  insufficiency  wliich  sometimes 
accompanies  aneurysm. 

The  radial  pulse  presents  peculiar  characters,  the  fines  of  ascent  and 
descent  being  practically  of  the  same  length,  because  the  jerky  movement  of 
the  arterial  pulse  is  converted  into  an  almost  continuous  movement  by 


DISEASES  OF  THE  VESSELS  495 

the  presence  of  an  extensible  sac  in  the  course  of  the  arterial  tree  (Marey). 
If  the  aneurysm  is  proximal  to  the  origin  of  the  large  arteries,  the  radial  pulse  is 
isochronous  on  both  sides ;  if  the  aneurysm  is  situated  between  the  left  sub- 
clavian artery  and  the  innominate  trunk,  the  left  radial  pulse  is  delayed. 

This  retardation  of  the  pulse  depends  chiefly  upon  the  extensibility  of 
the  walls  of  the  aneurysm ;  the  blood-wave  is  weakened  and  delayed.  If, 
however,  the  sac  of  the  aneurysm  is  but  httle  extensible,  and  covered  with 
stratified  or  calcified  clots,  it  loses  its  extensible  properties,  and  then  the 
conditions  change.  The  signs  given  by  the  expansile  pulsations  in  the 
tumour,  the  double  beats,  the  splashing  and  blowing  sounds,  and  the 
characters  of  the  pulse,  all  depend  on  the  degree  of  extensibihty  in  the  walls 
of  the  aneurysm. 

In  some  cases  total  suppression  of  the  radial  pulse  has  been  noted.  It 
may  depend  on  obHteration  of  the  subclavian  artery  by  clots  in  the  sac,  or 
on  a  patch  of  atheroma  that  has  developed  at  the  orifice  of  the  collaterals 
of  the  aorta,  in  which  case  the  pulsation  of  the  subclavian  artery  can  no 
longer  be  felt ;  the  suppression  of  the  radial  pulse  may  also  depend  on 
arterial  obhteration,  caused  by  an  embolus  detached  from  the  fibrinous  clots 
in  the  aneurysm,  in  which  case  the  symptoms  appear  suddenly ;  it  may,  lastly, 
depend  upon  constriction  of  the  artery  from  endarteritis  obliterans,  in  which 
case  the  symptoms  of  obHteration  are  much  more  gradual. 

Compression  of  a  venous  trunk  (vena  cava  or  innominate  vein)  may  cause 
oedema  and  collateral  venous  circulation,  as  described  under  Tumour  of  the 
Mediastinum.  When  the  circulation  in  the  superior  vena  cava  is  inter- 
rupted, the  head,  upper  limbs,  and  trunk — that  is,  the  regions  drained  by  the 
superior  caval  system — are  cyanotic,  oedematous,  and  show  a  network  of 
dilated  veins,  while  the  abdomen  and  lower  limbs  are  of  normal  colour. 

Condition  of  the  Pupil. — The  presence  of  a  tumour  may  cause  in- 
equahty  of  the  pupils,  the  one  being  smaller  or  larger  than  the  other  ;  if  the 
sympathetic  nerve  is  destroyed  by  the  aneurysm,  the  pupil  on  the  corre- 
sponding side  is  contracted  (myosis),  because  the  paralysis  of  the  dilator 
fibres  permits  the  free  action  of  the  constrictor  fibres  which  arise  from  the 
common  oculo- motor  nerve. 

If  the  sympathetic  nerv6  is  irritated  but  not  destroyed  by  the  aneurysm, 
the  pupil  on  the  corresponding  side  may  be  dilated  (mydriasis)  from  over- 
action  of  the  dilator  fibres.  In  any  case  the  light  reflex  is  not  abolished. 
Inequality  of  the  pupils  is  an  important  sign  of  aneurysm,  and  may  help  to 
distinguish  aneurysm  from  aortitis  in  which  a  tumour  is  absent. 

InequaUty,  however,  does  not  always  indicate  the  presence  of  a  tumour  ; 
it  may  be  found,  according  to  Babinski,  in  syphilitic  persons  who  have 
neither  aneurysm  nor  mediastinal  tumour.  They  may  have  mydriasis  or 
myosis,  but  the  important  point  is  that  the  light  reflex  is  lost  (Robertson's 


496  TEXT-BOOK  OF  MEDICINE 

sign).     The  inequality  of  the  pupils  is  due  to  syphilis  of  the  nervous  system; 
and  is  associated  with  lymphocytosis  in  the  cerebro- spinal  fluid. 

Inequality  of  the  pupils  in  an  aortic  case  may  therefore  have  no  direct 
relation  to  aortitis  or  aneurysm,  but  may  be  a  functional  effect  of  syphilis  if 
the  patient  has  that  disease.  Babinsld  has  pubhshed  cases  in  support  of 
his  opinion ;  Vaquez,  Widal,  and  Lemierre  have  confirmed  his  view,  and  I 
have  seen  the  following  case  at  the  Hotel- Dieu  : 

A  man,  tliirty-six  years  of  age,  who  had  had  a  severe  attack  of  angina  pectoris, 
was  admitted  under  my  care.  He  had  been  picked  up  moribund  and  brought  to  the 
hospital.  Some  hours  elapsed  before  he  could  give  us  exact  information.  He  gave 
a  clear  history  of  angina  pectoris  ;  for  months  past  he  had  had  similar  attacks.  His 
heart  was  hypertrophied,  and  a  to-and-fro  murmur  was  heard  in  the  second»right  space. 
The  attacks  of  angina  pointed  to  suprasigmoid  aortitis.  Eight  pupil  much  dilated. 
If  we  had  been  unable  to  push  investigations  farther,  we  might  have  stopped  at  aortic 
enlargement. 

The  hght  reflex,  however,  was  also  absent.  Syphilis  of  the  nervous  system  was 
showTi  by  lymphocytosis  of  the  cerebro-spinal  fluid.  He  had  had  syphiUs  twenty  years 
before.  The  inequality  of  the  pupils  was  therefore  dependent  upon  syphilis,  and  it 
was  possible  to  exclude  a  tumour.  The  autopsy  showed  the  accuracy  of  this  diagnosis : 
aortitis,  no  enlargement,  no  tumour  of  the  aorta  ;  the  lesion  in  the  nervous  system 
was  posterior  spinal  meningitis. 

Inequality  of  the  pupils  in  disease  of  the  thoracic  aorta  may  depend  on 
two  different  causes  :  it  may  be  due  to  interference  with  the  sympathetic 
nerve  by  an  aneurysm,  or  it  may  depend  on  a  specific  lesion  of  the  nervous 
system  coexisting  or  not  with  syphihtic  aortitis ;  in  the  latter  case  we  find 
Argyll-Robertson's  sign  and  lymphocytosis. 

Inequahty  of  the  pupil  in  lesions  of  the  aorta  does  not  therefore  of 
necessity  imply  the  existence  of  an  aneurysm. 

Topographical  Diagnosis. — The  existence  of  an  aortic  aneurysm  will  be 
recognized  by  the  signs  and  symptoms  just  enumerated.  Its  exact  position 
must  also  be  diagnosed  as  accurately  as  possible,  because  it  appears  to  me 
that  its  gravity  depends  more  upon  the  situation  than  upon  the  size. 

It  is  generally  beUeved  that  the  largest  aneurysms  are  the  most  for- 
midable ;  there  is  some  truth  in  this  assertion,  but  it  is  far  from  being  the 
rule.  Some  aneurysms  of  small  size  are  more  formidable  than  large 
aneurysms.  An  aneurysm  which  grows  towards  the  exterior  may  exist  for 
many  years,  in  spite  of  its  great  size,  before  compromising  the  patient's  Hfe, 
while  small  aneurysms,  in  relation  with  a  bronchus  or  the  trachea,  may 
produce  rapidly  fatal  haemorrhage  in  patients  who  have  been  almost  ignorant 
of  the  lesion.  Careful  study  of  symptoms  will  help  us  to  locahze  the  exact 
situation  of  the  aneurysm. 

Aneurysms  which  develop  in  the  convex  portion  of  the  arch  and  those 
of  the  anterior  portion  may  reach  a  very  large  size,  without  causing  ulceration 
and  perforation  of  the  trachea,  with  which  they  are  in  no  immediate  relation. 


DISEASES  OF  THE  VESSELS 


497 


These  aneurysms  grow  forwards  and  upwards  towards  the  sternum  and 
ribs,  which  become  eroded  by  rarefying  osteitis.  They  show  themselves  by 
dulhiess,  blowing  murmurs,  and  expansile  pulsation :  signs  most  marked 
over  the  tumour  ;  while  their  intensity  is  in  relation  with  the  prominence  of 
the  aneurysm,  and  the  more  or  less  complete  disappearance  of  the  chest-wall. 
Rupture  into  the  trachea  is  not  to  be  feared — at  least,  as  long  as  the  tumour 
does  not  affect  the  whole  cahbre  of  the  artery,  including  its  posterior  wall, 
and  does  not  cause  ulcerative  mischief  in  the  direction  of  the  trachea. 

On  the  other  hand,  these  mishaps  are  relatively  frequent  when  the 
aneurysm  is  close  to  the  loop  of  the  left  recurrent  nerve.  This  variety 
merits  special  recognition  ;  I  have  called  it  aneurysm  of  the  recurrent 
type. 

In  this  region  the  aorta  beyond  the  bifurcation  of  the  pulmonary  artery 
is  placed  in  front  and  a  little  to  the  left  of  the  trachea,  and  proceeds  towards 


Fig.  20. — Aneurysm  of  the  Aorta,  Recurrent  Type. 

A,  Section  of  the  aneurysm  of  the  aorta ;  b,  bronchus;  r,  recurrent  nerve ;  ce,  oesoph- 
agus ;  t,  trachea ;  I,  larynx ;  p,  pneumogastric  nerve ;  c,  common  carotid 
artery. 

the  loft  bronchus,  around  which  it  passes  from  before  backwards,  and  from 
right  to  left.  At  this  point  the  aorta  is  in  immediate  relation  with  the  lower 
part  of  the  trachea  and  the  origin  of  the  left  bronchus  ;  it  is  contiguous  to  the 
air-passages  on  its  concave  side  and  its  anterior  segment.  Accordingly,  from 
the  point  of  view  of  prognosis,  aneurysms  are  here  formidable,  even  when 
they  are  of  small  dimensions,  because  experience  proves  that  opening  of 
the  aneurysm  into  the  trachea  or  into  the  bronchi,  with  most  terrible 
liyL'morrhages,  occurs  most  often  in  this  region  (Ordonneau). 

How  can  the  situation  of  these  aneurysms  be  recognized  ?  Dysphagia, 
a3sophagism  (spasms  of  the  oesophagus),  pharyngism  (spasms  of  the 
pharynx),  and  fits  of  suffocation  and  of  strangulation  (spasms  of  the 
glottis),  vocal  troubles  (want  of  synergy  of  the  vocal  cords),  and  attacks 
of  precordial  pain,  are  among  the  symptoms  which  help  us  in  the  topo- 
graphical diagnosis  of  aortic  aneurysm  of  the  recurrent  type. 

'62 


498 


TEXT-BOOK  OF  MEDICINE 


These  symptoms  are  nearly  all  due  to  the  close  relation  of  the  loop  of 
the  left  recurrent  nerve,  which  serves  as  a  guide  to  the  troubles  it 
occasions. 

The  importance  of  this  variety  of  aneurysm  wiU  justify  tiie  following 
details  : 

The  two  recurrent  or  laryngeal  nerves  which  arise  from  the  vagus  and  from  the 
internal  branch  of  the  spinal  accessory  have  different  relations.  The  recurrent  nerve 
on  the  right  side  arises  at  the  level  of  the  subclavian  artery,  which  it  embraces,  forming 
a  curve  with  its  concavity  upwards.  It  has  no  thoracic  portion,  and  therefore  usually 
escapes  in  tumours  of  the  mediastinum  and  in  aortic  aneurysms.  The  left  re- 
current nerve,  on  the  contrary,  has  a  thoracic  portion,  that  corresponds  to  the  first 
two  dorsal  vertebrae.  It  arises  to  the  left  of  the  fibrous  cord,  that  represents  the 
obliterated  ductus  arteriosus,  turns  round  the  lower  and  posterior  portion  of  the  arch 
of  the  aorta,  which  it  embraces,  forming  a  curve  with  its  concavity  upwards,  and  is 
therefore  exposed  to  pressure  from  mediastinal  tumours  and  aortic  aneurysms. 


Fig.  21. — Recuekent  Nerves  :  Posterior  View. 

A,  Arch  of  the  aorta  ;  ce,  oesophagus  ;  c,  common  carotid  artery  ;  I,  larynx  ;  t,  trachea  ; 
h,  b,  bronchi ;  j3,  p,  pneumogastric  nerves ;  r,  r,  recurrent  nerves,  one  of  wliich  (the 
left)  coasts  the  arch  of  the  aorta,  and  ascends  along  the  oesophagus  and  the 
trachea  towards  the  larynx ;  the  other,  in  a  hke  manner,  coasts  the  innominate 
trunk  on  the  right  side. 


The  recurrent  nerves  give  off  the  following  branches  (Hirschfeld) : 

1.  Cardiac  branches,  which  arise  from  the  loop  of  origin  of  the  recurrent  nerves, 
and  pass  either  directly  to  the  cardiac  plexus  or  by  their  union  to  the  cardiac  branches 
of  the  great  sympathetic  and  vagus. 

2.  (Esophageal  branches,  which  arise  from  the  left  recurrent  nerve,  and  are  dis' 
tributed  to  the  coats  of  the  upper  portion  of  the  oesophagus.  The  lower  portions  of 
this  tube  receive  their  nerves  directly  from  the  vagus. 

3.  Pharyngeal  branches,  to  the  inferior  constrictor  of  the  pharynx. 

4.  Tracheal  branches,  which  arise  in  part  from  the  right  recurrent  nerve. 

6.  After  the  recurrent  nerves  have  passed  through  the  inferior  constrictor  of  the 
pharynx,  their  terminal  branches  supply  all  the  muscles  of  the  larynx,  except  the  crico- 
thyroid muscles,  which  are  innervated  by  the  external  laryngeal  branch  of  the  superior 
laryngeal  nerve. 

The  recurrent  nerves  send  motor  iibres  to  the  laiynx,  but  furnish  mixed  fibres  to 
the  oesophagus,  pharynx,  and  trachea.  These  different  organs,  further,  receive  a  direct 
and  indirect  innervation  from  the  spinal  accessory  and  vagus  nerves.     The  indirect 


DISEASES  OF  THE  VESSELS  499 

innervation  is  supplied  through  the  intermediary  tract  of  the  recurrent  nerves  ;  the 
direct  innervation  is  supplied  by  branches  arising  directly  from  the  spinal  accessory 
and  vagus. 

The  researches  carried  out  by  French  physiologists  have  established  the  following 
conclusions  (CI.  Bernard,  Chauveau),  as  regards  the  respective  part  played  by  the  spinal 
accessory  and  vagus  in  the  compUcated  movements  of  these  organs  : 

The  vagus  is  the  motor  nerve  of  the  oesophagus,  either  by  its  direct  branches  or  by 
the  intermediary  of  the  recurrent  nerve.  The  vagus  and  spinal  accessory  in  part 
supply  the  larynx.  The  inferior  constrictor  receives  fibres  from  the  vagus  through 
the  recurrent  nerve,  and  the  upper  part  of  the  superior  constrictor  receives  a  direct 
branch  from  the  spinal  accessory. 

Among  the  muscles  of  the  larynx  the  larger  number,  including  the  constrictors 
of  the  glottis  and  the  vocal  muscles,  properly  speaking,  are  innervated  from  the  spinal 
accessory  through  the  recurrent  nerve.  The  other  muscles  arc  innervated  by  the 
pneumogastric,  and  include  the  crico-arytenoid  muscles,  which  make  the  vocal  cords 
tense,  and  receive  their  nerve  supply  directly  from  the  vagus  by  the  exterior  laryngeal 
nerve ;  and  the  posterior  thyro-arytenoid  muscles,  which  dilate  the  glottis,  and  are 
consequently  respiratory  muscles,  suppUed  by  the  vagus  tlirough  the  recurrent 
nerves. 

It  is  now  easy  to  understand  the  production  of  the  symptoms  present  in  aortic 
aneurysm  of  the  recurrent  type. 

1.  The  attacks  of  dysphagia  and  the  spasms  of  the  oesophagus  and  of  the  pharynx 
are  exjjlained  by  excitation  of  the  recurrent  nerve,  some  branches  of  which  pass 
to  the  upper  part  of  the  oesophagus  and  to  the  inferior  constrictor  of  the  pharynx. 
They  are  accorchngly  symptoms  of  excitation,  and  not  of  paralysis,  for  dysphagia  due 
to  paralysis  of  a  recurrent  nerve  would  be  incomplete,  and  would  produce  continuous 
embarrassment.  There  would  not  be  paroxysmal  attacks  of  pain,  which  are  proper 
to  muscular  spasms. 

2.  The  attacks  of  suffocation  and  strangulation,  as  well  as  the  vocal  troubles,  are 
also  explained  by  excitation  of  the  recurrent  nerve.  For  a  long  while  these  troubles, 
due  to  dyspnoea,  were  not  clearly  understood.  The  authorities,  Avho  considered  them 
due  to  lesions  of  the  recurrent  nerve,  were  near  the  truth,  though  they  were  wrong  in 
referring  them  to  paralysis  of  the  nerve  and  to  consequent  relaxation  of  the  vocal 
cords.  Krishaber,  in  1866,  in  a  paper  "  On  the  Occasion  for  Tracheotomy  in 
Aneurysms  of  the  Aortic  Arch,"  was  the  first  to  give  the  true  interpretation  of  this 
dyspnoea.  This  monograph,  in  which  the  author  shows  himself  to  be  equally  expert 
as  an  experimenter  and  as  a  clinician,  deserves  to  be  quoted  in  extenso. 

The  attacks  of  suffocation  that  supervene  in  persons  suffering  from  aneurysm  of 
the  aorta,  are  not  due  to  paralysis  of  the  recurrent  nerve,  as  had  been  supposed.  The 
nerve,  instead  of  being  paralyzed,  is  stimulated  by  its  close  relation  to  the  aneurysmal 
sac.  The  muscles  of  the  larynx  are  in  a  state  of  contraction  as  a  result  of  this  stimulus, 
instead  of  being  relaxed.  The  glottis  is  in  consequence  narrowed  spasmodically,  and 
the  embarrassment  in  breatliing  is  due  to  this  naiTowing.  This  statement  has  been 
confirmed  by  experiments  and  Vjy  laryngoscopic  examination. 

Section  of  one  recurrent  nerve  in  an  adult  animal  produces  relaxation  of  the  corre- 
sponding vocal  cord,  with  dysphonia,  but  the  respiration  is  in  no  way  affected.  In 
a  similar  manner,  paralysis  of  one  recurrent  nerve  in  man  produces  relaxation  and 
immobility  of  the  corresponding  vocal  cord,  but  suffocation  does  not  follow.  Paralysis 
of  the  recurrent  nerve  is  sometimes  seen  in  aortic  aneurysm,  and  Potain  has  iiublishod 
a  case  in  which  paralysis  of  the  vocal  cord,  recognized  with  the  laryngoscope,  confirmed 
the  diagnosis  of  an  aneurysm  of  the  aorta. 

When,  on  the  contrary,  the  recurrent  nerves  of  the  animal  are  stimulated,  tlio 
intrinsic  muscles  of  the  larynx  enter  into  action,  and  as  the  constrictor  muscles  act 

32—2 


500  TEXT-BOOK  OF  MEDICINE 

chiefly  upon  the  single  dilator  muscle,  the  glottis  becomes  constricted,  and  the  animal 
is  suffocated. 

A  similar  phenomenon  occurs  in  man.  How,  then,  can  stimulation  of  one  recurrent 
nerve  affect  both  vocal  cords  at  once,  and  produce  spasms  of  the  glottis  ?  How  can 
unilateral  excitation  produce  a  bilateral  effect  ?  Paralysis  of  one  recurrent  nerve 
causes  paralysis  of  the  corresponding  vocal  cord.  Why,  then,  does  excitation  of 
a  single  nerve,  such  as  occurs  in  aortic  aneurysm,  or  in  any  other  mediastinal  tumour, 
produce  spasm  of  both  lips  of  the  glottis  and  attacks  of  suffocation  ?  Krishaber  has 
given  us  an  explanation  of  this  interesting  fact  by  studying  the  role  of  the  arytenoid 
muscle. 

This  muscle,  which  is  single  and  inserted  on  the  two  edges  of  the  thyroid  cartilages, 
always  has  the  effect  of  bringing  its  two  insertions  together  when  it  contracts.  It  is 
the  only  muscle  in  the  economy  which  exerts  its  action  simultaneously  on  both  sides 
of  a  symmetrical  organ.  Accordingly,  excitation  of  one  of  the  recurrent  nerves  deter- 
mines, on  the  one  hand,  constriction  of  the  interhgamentous  glottis  by  the  action  of 
the  lateral  crico-arytenoid  muscles  and  of  the  thyro-arytenoid  muscle  on  the  corre- 
sponding side,  and,  on  the  other  hand,  the  complete  occlusion  of  the  respiratory  glottis 
by  the  bilateral  action  of  the  arytenoid  muscle.  Respiratory  and  vocal  troubles  result 
from  this  action. 

These  experimental  results  have  been  verified  with  the  laryngoscope  in  a  patient 
during  an  attack  of  suffocation  caused  by  an  aortic  aneurysm.  The  whole  left  cord 
(side  on  which  the  recurrent  nerve  was  stimulated)  was  drawn  over  to  the  middle  line. 
The  right  vocal  cord  remained  in  its  normal  position,  as  regards  its  anterior  two-thirds, 
but  the  space  between  the  arytenoid  cartilages — that  is  to  say,  the  respiratory  glottis — 
was  completely  closed.  Extreme  embarrassment  of  respiration  resulted  from  this 
spasm  of  the  glottis,  and  the  voice  was  altered  in  character.  The  alteration  of  the  voice 
was  due  to  the  tetanization  of  one  vocal  cord,  to  the  forced  approximation  of  the 
arytenoid  cartilages,  and  to  the  respiratory  distress.  In  another  case  the  left  vocal 
cord  was  paretic,  while  the  voice  was  hoarse  and  bitonal.  During  the  attacks  of  suffoca- 
tion, however,  the  laryngoscope  showed  that  the  two  cords  were  in  a  condition  of 
spasm,  and  almost  completely  obliterated  the  glottis.  The  spasm  affected  both  vocal 
cords,  although  the  left  nerve  (as  was  verified  at  the  autopsy)  was  alone  affected  by  the 
aneurysm. 

This  research  explains  the  attacks  of  suffocation,  strangulation,  dysphonia,  aphonia, 
pharyngism,  and  oesophagism  which  often  accompany  aneurysm  of  the  recurrent  type. 
These  symptoms  may  appear  alone,  in  succession,  or  in  combination.  It  is  difficult 
to  explain  why  the  presence  of  a  tumour  in  the  region  of  the  recurrent  nerve  produces 
at  one  time  paralysis  and  at  another  time  excitation.  It  would  seem,  theoretically, 
that  the  nerve  would  be  excited  at  first,  while  its  fibres  are  still  intact,  and  paralyzed 
later,  when  the  fibres  are  in  part  destroyed  by  the  pressure  of  the  tumour.  Nothing  of 
the  kind,  however,  occurs.  In  some  cases  the  paralytic  stage  is  not  preceded  by  a 
phase  of  excitation,  and  in  other  cases  almost  complete  destruction  of  the  recurrent 
nerve  has  been  found  post  mortem,  although  the  patient  has  shown  no  recurrent  symp- 
toms. It  is  also  difficult  to  say  why  the  symptoms  of  excitation,  suffocation,  and 
strangulation  come  on  in  the  form  of  intermittent  attacks,  wlien  the  determining  cause 
is  in  continuous  action.  Such  an  occurrence  is  fairly  common  in  troubles  of  the  nervous 
system,  which  frequently  assume  an  intermittent  form,  although  the  provoking  cause 
is  continuous. 

However  this  may  be,  the  symptoms  allow  the  localization  of  an  aneurysm  in  the 
neighbourhood  of  the  left  recurrent  nerve — that  is  to  say,  in  the  region  where 
aneurysm  is  most  grave,  because  it  so  often  opens  into  the  trachea  and  the  bronchi. 
The  aneurysm  may  not  be  as  large  as  an  egg  or  a  nut,  but  it  is  very  serious  when  situated 
in  this  region. 


DISEASES  OF  THE  VESSELS 


501 


Termination. — Aortic  aneurysm  takes  several  years  to  develop  ;  recovery 
is  unfortunately  the  exception,  and  death  occurs  in  various  ways.  In  about 
half  the  cases  death  supervenes  without  rupture  of  the  aneurysm  :  the 
patient  dies  from  pneumonia,  for  suppurative  pneumonia  is  frequent  in 
aortic  aneurysm,  from  pulmonary  phthisis ;  from  asphyxia,  consecutive  to 
compression  of  the  trachea  and  bronchi ;  from  complications  caused  by 
compression  of  the  pulmonary  vessels  or  of  the  vena  cava ;  or  sometimes 
from  attacks  of  angina  pectoris,  as  in  two  cases  which  I  have  recently  seen. 

When  death  results  from  rupture,  the  opening  involves,  in  order  of 
frequency,  the  trachea,  the  bronchi,  the  pleura,  the  pericardium,  the  lungs, 
the  oesophagus,  and,  very  rarely,  the  skin.* 

When  an  aortic  aneurysm  opens  into  the  trachea  or  a  bronchus,  the  result- 
ing haemoptysis  is  sometimes  so  severe  and  sudden  that  death  occurs  in  a 
few  minutes.  I  have  seen  sudden  death  on  two  occasions.  In  other  cases, 
however,  the  aortic  aneurysm,  whatever  the  point  of  rupture,  may  cause  a 
series  of  small  haemorrhages,  that  lasts  for  days  and  weeks  before  inducing 
death.  In  a  certain  number  of  cases  the  patient,  for  several  days  and  on 
several  occasions,  brings  up  bloody  sputum,  which  is  the  prelude  of  fatal 
haemoptysis. 

Rupture  into  the  pleura  is  fairly  frequent ;  the  blood  may  filter  slowly 
into  the  pleura  producing  a  pleural  haematoma,  the  origin  of  which  is 
sometimes  misunderstood.  Thoracentesis  is  performed  once  or  twice,  and 
when  the  patient  dies,  we  are  surprised  to  find  post  mortem  an  effusion  of 
blood  into  the  pleura  consecutive  to  the  opening  of  an  aortic  aneurysm. 

Rupture  into  the  pericardium  is  not  rare,  as  Godart  has  collected 
forty-seven  cases. 

*  The  relative  frequency  of  these  perforations  is  as  follows  (Ball  and  Charcot, 
"  Dictionnaire  des  Sciences  Medicales,"  tome  v.,  p.  546) : 

Right  auricle 
Pericardium 


Pulmonary  artery 

Pleura  -;    .  , 
(right 

Anterior  mediastinuiii 

Left  lung 

Trachea 

[left 
Bronchi  J  right 

(both 
Gilsophagus 
Duodenum 
Peritoneum 
SuVjperitoneal  tissue 
Cellular  tissue  of  the  anterior  thoracic  wall 
Rupture  externally     . . 
Death  without  rupturu 


1 

8 
2 

11 
8 
8 
6 
3 
3 
1 
3 
3 
1 
2 
5 
2 
4 

54 


502  TEXT-BOOK  OF  MEDICINE 

Rupture  of  the  aneurysm  through  the  skin  takes  place  under  different 
conditions  ;  the  perforation  may  occur  externally,  or  may  be  subcutaneous 
and  cause  wide  effusion  of  blood. 

Diagnosis. — Aneurysm  of  the  thoracic  aorta  and  chronic  aortitis,  with 
atheroma  and  general  dilatation  of  the  aorta,  have  many  symptoms  in 
common :  pain,  dyspnoea,  attacks  of  angina  pectoris  are  seen  in  both  cases, 
as  well  as  rupture  of  the  aorta  and  consecutive  heemorrhage.  An  aneurysm, 
however,  forms  a  prominent  tumour,  which  gives  rise  to  distinctive  signs ; 
the  tumour  alters  the  character  of  the  radial  pulse,  gives  the  sensation  of 
two  hearts  beating  in  the  chest,  and  determines  compression  of  the  trachea 
with  stridor ;  compression  of  the  veins  with  oedema  and  varicose  dilatations ; 
and  compression  of  the  recurrent  nerve  with  the  symptoms  already  described. 
Tumours  of  the  mediastinum  also  cause  pressure  symptoms,  but  they 
do  not  present  a  double  impulse  beat,  the  murmurs  of  aneurysm,  or  the 
inequality  and  want  of  synchronism  in  the  two  pulses. 

It  is  also  necessary  to  make  the  diagnosis  from  arterio-venous  aneurysm, 
for  the  aorta  may  communicate  with  the  superior  vena  cava,  the  auricles, 
the  pulmonary  artery,  and  the  right  ventricle ;  but  diagnosis  is  sometimes  very 
difficult,  for  the  symptoms  are,  as  a  rule,  simply  an  exaggeration  of  those 
already  produced  by  compression  of  a  venous  trunk — i.e.,  oedema,  cyanosis, 
collateral  circulation,  and  tendency  to  coma.  On  auscultation  a  continuous 
blowing  murmur,  with  systohc  reduplication,  may  be  heard. 

Lastly,  the  diagnosis  between  aneurysm  of  the  aorta  and  that  of  the 
innominate  artery  must  be  made.  In  the  latter  case  the  distinctive  signs 
are  as  follows  :  Prominence  of  the  right  clavicle  ;  bulgi'ng  and  dullness  in  the 
right  clavicular  region  ;  pulsation  and  murmurs  in  this  region ;  compression 
of  the  veins  on  the  right  side,  with  stasis  in  the  right  jugular  vein,  cervical  and 
tracheal  pains,  which  are  more  marked  on  the  right  side. 

Treatment. — The  treatment  of  aneurysm  of  the  aorta  is  general  and 
local.  Local  treatment  of  the  sac  by  electro-puncture  has  given  good  results, 
and  this  means,  which  is  still  on  trial,  has  appeared  to  be  of  some  efficacy.  A 
definite  opinion  as  to  injections  of  gelatine  caimot  yet  be  given  (Lancereaux). 
Mercurial  treatment  will  be  considered  under  Syphihtic  Aneurysms. 

VII.  SYPHILIS  OF  THE  AORTA— SYPHILITIC  AORTIC 
ANEURYSMS. 

At  the  Hotel-Dieu*  I  have  devoted  three  lectures  to  this  important 
question ;  they  will  serve  as  my  material  for  this  section. 

Discussion. — Syphihtic  infection  may  cause  numerous  lesions,  including 
subacute  and  chronic  aortitis,  atheromatous  and  gummatous  degeneration, 

*  "  Syphilis  de  I'Aorte,"  Clinique  Medicale  de  V Hotel-Dieu,  4"^^  5^%  et  6™^  le§ons, 
1897. 


DISEASES  OF  THE  VESSELS  503 

lesions  of  the  aortic  orifice  and  sigmoid  valves,  large  aneurysms,  sacciform 
aneurysm  of  the  recurrent  t}^e,  small  aneurysms  which  may  be  multiple  and 
cupuhform,  coronaritis  obhterans,  and  coronaritis  with  miliary  aneurysms. 

Aortic  syphihs  does  not  always  show  itself  by  diffuse  lesions  ;  in  many 
cases  the  lesions  are  locahzed  to  a  segment  of  the  vessel,  forming  a  kind  of 
segmentary  aortitis,  which  is  somewhat  analogous  to  syphihtic  segmentary 
arteritis.  Distinct  cUnical  types  result,  and  show  a  special  group  of  signs 
and  symptoms.  It  is  therefore  not  enough  to  describe  as  a  whole  the  syphi- 
htic changes  in  the  thoracic  aorta ;  it  is  necessary,  as  far  as  possible,  to  divide 
them  into  certain  forms,  and  I  shall  make  an  effort  to  do  so  in  this  section. 

It  must,  however,  be  understood  that  the  aortic  lesions  which  we  are 
about  to  study,  are  syphihtic  in  nature,  and  no  doubts  must  be  left  in  the 
mind  as  to  this  fact. 

The  recognition  of  syphihtic  arteriopathies  is  of  recent  date.  Not  long 
ago  savants  doubted  the  action  of  syphihs  upon  the  arteries,  and  authorities 
are  still  found  whose  opinions  differ  from  those  which  I  shall  now  state  as  to 
the  action  of  syphihs  on  the  aorta.  That  syphihs  may  attack  the  arteries, 
just  as  many  infectious  diseases  do,  need  cause  no  surprise,  and  it  is  clear 
that  syphihtic  arteritis  must  enter  into  the  hst  of  infectious  diseases  of  the 
arteries.  The  proof  is,  however,  wanting,  both  as  regards  the  pathogenic 
agent  of  syphihs,  which  we  do  not  know,*  and  also  as  regards  the  character  of 
the  arterial  lesions  which  often  have  no  special  nature  ;  but,  on  the  other 
hand,  we  find  conclusive  proofs  and  arguments  in  the  efl&cacy  of  specific 
treatment,  and  also  in  other  considerations. 

When  a  patient  suffering  from  tertiary  lesions  is  at  the  same  time  affected  by 
syphihtic  arteritis,  whether  it  be  obUterating  or  dilating,  in  parts  which  are  accessible 
to  the  sight  (hmbs  and  face),  and  when  under  specific  treatment  he  recovers  from  the 
tertiary  lesions  and  from  the  arteritis,  it  is  evident  that  the  arteritis  in  question  was 
of  a  syphihtic  nature. 

When  an  individual  who  is  still  young,  and  has  no  other  cause  for  arteritis  or  for 
atheroma,  contracts  syphihs,  and  in  the  early  months  of  his  infection  is  affected  by 
cerebral  arteritis,  which  sometimes  results  in  obliteration  of  the  artery,  with  all  its 
consequences,  or  at  other  times  in  aneurysm,  with  rupture  (see  section  on  Cerebral 
SyphiUs),  a  direct  relation  between  the  syphilis  and  the  lesion  of  the  artery  cannot  be 
denied. 

Now,  syphihs,  which  has  a  marked  predilection  for  the  cerebral  arteries,  and  also 
injures  the  peripheral  arteries — i.e.,  the  temporal,  radial,  pophteal,  femoral,  or  in- 
nominate trunks — has  no  reason  for  sparing  the  aorta,  and,  in  fact,  it  does  not  do  so. 
When  aortitis,  with  aneurysm,  occurs  in  a  young  man  about  six  years  after  syphihtic 
infection,  and  no  other  causes  capable  of  explaining  the  aortitis  can  be  found,  it  is 
rational  to  consider  the  lesion  of  the  aorta  as  due  to  syphihs  (case  of  Kalindero  and 
Babes).  When  an  individual  is  seized  four,  six,  or  ten  years  after  infection  with  agonizing 
pains,  due  to  aortitis,  which  is  cured  by  specific  treatment,  it  is  natural  to  consider 
both  the  angina  pectoris  and  the  lesion  of  tlio  aorta  as  due  to  syphilis  (cases  of  Hallopeau, 

*  Cf.  p.  477,  where  mention  is  made  of  the  spirochaeta. — ^Tkans. 


504  TEXT-BOOK  OF  MEDICINE 

Rumpf,  Vicenzo  Vitone,  and.  personal  case).  When  obliterating  arteritis  of  the  Syhian 
artery  occurs  in  a  syphilitic  patient,  and  yields  to  specific  treatment,  it  is  rational  to 
attribute  this  cerebral  arteritis  to  syphihs,  and  if  this  individual  some  years  later  suffers 
from  aortitis  with  aneurysm,  it  is  also  natural  to  attribute  the  aortic  lesion  to  syphilis 
(personal  case).  When  aortitis,  with  its  train  of  symptoms,  appears  in  an  individual 
suffering  from  pustulo-crustaceous  syphilides,  it  is  very  difficult  not  to  doubt  that 
there  are  two  tertiary  manifestations,  which  occur  simultaneously  or  in  succession, 
affecting  the  skin  on  the  one  hand  and  the  aorta  on  the  other  (personal  cases).  When 
syphilitic  perforation  of  the  roof  of  the  j^alate  is  seen  in  a  woman  suffering  from  aortic 
aneurysm,  it  is  only  right  to  admit  that  in  such  a  patient  the  tertiary  manifestations 
of  syphilis  have  attacked  successively  the  aorta  and  the  roof  of  the  palate  (Jaccoud's 
case).  When  aneurysm  of  the  aorta  supervenes  in  a  syphilitic  patient  who  has  lesions 
of  the  parietal  bone,  liver,  and  testis,  it  may  be  affirmed  that  the  aortic  lesion  is  also 
of  syphilitic  origin  (Buehle's  case). 

These  arguments  appear  to  me  to  be  decisive.  The  aorta  is  not  immune  to  syphihs. 
It  may  be  added  that  these  effects  are  generally  tardy.  In  this  respect  there  is  some 
difference  between  syphihs  of  the  cerebral  arteries  and  syjjhilis  of  the  aorta.  In  short, 
while  syphihs  may  affect  the  arteries  of  the  brain  at  a  very  early  stage — even  five  or 
six  weeks  after  infection — I  do  not  think  that  such  an  early  onset  has  ever  been  seen 
as  regards  the  aorta,  ^\^len  I  recall,  one  by  one,  my  cases  of  syiihilitic  lesions  of  the 
aorta,  I  find  that  these  lesions  have  appeared  only  at  a  very  advanced  stage.  In  three  of 
my  patients  at  the  Hotel-Dieu,  syphilis  of  the  aorta  supervened  from  fourteen  to  twenty 
years  after  the  chancre  ;  in  two  of  my  patients  at  the  Necker  Hospital,  the  aorta  was 
infected  only  at  an  advanced  period ;  in  one  patient  at  the  Saint-Antoine  Hospital 
the  first  signs  of  aortic  aneurysm  appeared  eighteen  years  after  infection ;  in  one 
of  Duguet's  patients  the  aortic  lesions  supervened  twenty  years  after  infection. 
Mauriac  considers  that  aortic  lesions  appear,  as  a  rule,  about  twelve  years  after  the 
chancre,  and  I  place  among  the  earliest  the  case  of  KaUndero,  in  which  syphiUtic 
aneurysm  of  the  aorta  came  on  seven  years  after,  and  the  cases  of  Rumpf  and 
Vicenzo  Vitone,  in  which  syphilitic  aortitis  supervened  four  years  and  six  years  after 
infection.  These  facts  are  of  importance,  and  serve  to  emphasize  the  fact  that,  if 
cerebral  arteritis  is  to  be  feared  during  the  first  year  of  infect^on,  there  is  no  fear  of 
aortitis  for  many  years. 

Division. — We  are  now  clear  as  to  the  existence  and  the  time  of  appear- 
ance of  syphilitic  lesions  of  the  aorta  ;  let  us  discuss  in  detail  each  of  these 
lesions  and  their  localizations.  From  the  pathological  point  of  view  they 
differ  but  little  from  the  lesions  of  common  aortitis  :  atheroma  is  found  in  its 
different  forms  and  stages  ;  the  same  deformities  of  the  vessels  and  the  same 
tendency  to  dilatation  and  to  aneurysm  are  seen.  There  is  notliing,  either 
in  the  anatomical  or  in  the  histological  picture,  that  can  serve  to  difEer- 
entiate  the  lesions  of  chronic  syphihtic  aortitis  from  those  of  aortitis  due  to 
other  causes.  An  interesting  point,  however,  is  that  the  aorta  is  sometimes 
the  seat  of  true  gummata,  which  may  give  rise  to  small  cupulif orm  aneurysms, 
regarded  by  some  authors  as  characteristic  of  syphihs. 

These  various  lesions,  including  thickening,  induration,  atheroma,  gum- 
mata, dilatation,  aneurysms,  etc.,  are  sometimes  diffuse  and  indefinitely  dis- 
tributed over  the  thoracic  aorta ;  at  other  times  they  are  localized  to  a  clearly 
defined  region,  and  present  the  following  anatomical  and  clinical  types : 


DISEASES  OF  THE  VESSELS  505 

1.  Suprasigmoid  syphilitic  aortitis. 

2.  Sypliilis  of  the  aortic  orifice  with  incompetence. 

3.  Large  aneurysms  of  the  aorta. 

4.  Aneurysm  of  the  recurrent  type. 

5.  Small  multiple  cupuhform  aneurysms. 

6.  Obhterating    coronaritis    and    miliary    aneurysms    of    the 

coronary  arteries. 
This  classification  is  far  from  being  final,  and  does  not  include  diffuse 
aortitis  of  the  thoracic  trunk,  but  it  is  perfectly  applicable  to  a  fairly  large 
number  of  cases  in  which  the  aortitis  is  locahzed  to  a  circumscribed  region  of 
the  aorta. 

1.  Suprasigmoid  Syphilitic  Aortitis. 

In  this  type  the  lesion  is  confined  to  the  first  portion  of  the  ascending 
aorta,  thus  forming  a  kind  of  segmentary  aortitis,  that  may  be  called  supra- 
sigmoid. 

In  this  form  we  find  pain  and  angina  (angor  pectoris).  •  The  pain,  which 
may  be  slight  or  violent,  transient,  continuous  or  paroxysmal  and  acute, 
with  suffocation  and  a  sense  of  constriction  in  the  chest,  radiates  hke  the 
pain  of  angina  pectoris,  and  has  its  maximum  in  the  sternal  or  in  the  pre- 
cordial region,  which  is  painful  on  pressure. 

In  a  patient  with  these  symptoms  the  attention  is  at  once  called  to  the 
aorta.  On  percussion,  no  enlargement  of  the  vessel  can  be  made  out ;  on 
auscultation,  no  murmur  is  heard.  Under  such  circumstances,  and  in  tlie 
absence  of  any  appreciable  lesion,  every  possible  supposition  is  considered, 
including  neuralgia  of  the  cardiac  plexus,  smoker's  heart,  hysteria,  cardialgia 
of  tabes — in  short,  all  the  causes  that  are  capable  of  producing  cardiac 
neuralgia ;  while  sufficient  consideration  is  not  paid  to  syphilis,  because  it 
may  date  back  ten,  twelve,  or  fifteen  years,  and,  it  may  be  added,  because 
this  suprasigmoid  aortitis  has  not  yet  been  sufficiently  recognized.  For  my 
part,  I  consider  it  one  of  the  most  frequent  manifestations  of  aortic  syphilis. 
The  situation  and  nature  of  the  pains  which  it  excites  are  sufficient  to  attract 
attention  and  lead  to  the  diagnosis. 

These  pains  should  cause  no  surprise,  and  no  elaborate  theories  are 
necessary  to  explain  them.  Let  us  not  forget  that  syphiUtic  arteritis  is 
sometimes  extremely  painful.  One  of  Leudet's  patients  had  very  severe 
pain  in  the  temporal  arteries,  which  were  affected  by  syphilitic  arteritis  ;  one 
of  my  patients  suffered  much  pain  in  the  radial  artery,  which  was  the  seat  of 
a  syphilitic  aneurysm  ;  persons  suffering  from  syphiUs  of  the  cerebral  arteries 
(basilar  and  Sylvian  arteries)  have  at  times  fearful  headache  due  to  the 
arteritis.  The  same  remark  appUes  to  syphiUtic  aortitis.  Why  should  it 
not  be  extremely  painful  when  the  aorta  adjoins  the  nerves  of  the  cardiac 


506  TEXT-BOOK  OF  MEDICINE 

plexus,  whicli  is  always  ready  to  produce  the  syndrome  of  angina  pectoris  ? 
Tlie  agonizing  sternal  or  retrosternal  pain  wliich  radiates  to  the  neck  and 
left  arm  may  be  the  result  of  syphilitic  aortitis,  especially  when  the  supra- 
sigmoid  segment  is  affected. 

The  following  cases  prove  the  truth  of  this  view  : 

About  fifteen  years  ago  Potain  and  myself  saw  a  woman,  still  young,  with 
angina  pectoris.  The  pains  had  been  coming  on  for  some  weeks  past,  and  had  finally 
become  very  severe.  They  were  continuous,  yet  broken  by  agonizing  paroxysms,  Uke 
those  of  angina  pectoris.  The  aortic  orifice  was  healthy ;  the  aorta  showed  no  dilata- 
tion. She  was  too  young  for  atheroma ;  tobacco,  hysteria,  and  tabes,  were  out  of  the 
question.  Treatment  proved  unsuccessful,  though  an  ice-bag  gave  some  rehef.  A 
tertiary  ulcer  appeared  on  the  right  thigh.  Specific  treatment  was  at  once  employed  ; 
the  ulcer  was  soon  cured,  and  the  pains  of  angina  pectoris  completely  disappeared.  I 
ask,  WTiat  could  this  case  be,  except  an  attack  of  syphilitic  aortitis  which  had  left  the 
aortic  orifice  intact  ? 

Some  years  ago,  with  Duplay  and  Ramond,  I  saw  a  gentleman  suffering  from 
serpiginous  ulceration,  which  had  destroyed  part  of  the  right  thigh.  He  was  finally 
cured.  Five  years  later,  very  sharp  j^ain  in  the  cardio-aortic  region.  Auscultation 
revealed  no  lesion  o£  the  aortic  orifice.  I  thought  of  suprasigmoid  aortitis.  Remember- 
ing the  serpiginous  ulceration,  I  prescribed  specific  treatment,  which  he  did  not  take. 
Some  months  later  Ramond  was  called  out  to  see  him.  He  was  suffering  from  most 
terrible  precordial  pain,  and  died  in  a  few  hours. 

Hallopeau  has  published  a  very  interesting  memoir  on  this  subject, 
in  which  he  describes  syphilitic  angina  pectoris  : 

A  man  of  thirty-six  years  of  age,  ten  years  before  had  had  benign  syphiUs,  which 
was  properly  treated.  He  was  taken  ill  one  night  with  acute  precordial  pain,  radiating 
to  the  left  shoulder.  During  the  next  few  days  the  pain  recurred  several  times  in  the 
twenty-four  hours,  and  radiated  as  far  as  the  left  elbow  and  the  end  of  the  last  three 
fingers.  The  symptoms  of  angina  pectoris  disappeared  completely  under  treatment 
with  mercury  and  iodide. 

In  the  monograph  to  which  I  have  just  alluded,  Hallopeau  has  collected 
the  three  following  cases  : 

The  first,  reported  by  Rumpf,  concerns  a  man,  twenty-nine  years  of  age,  who,  six 
years  before,  had  had  chancre,  followed  by  secondary  symptoms,  when  he  felt  violent 
pain  in  the  precordial  region,  radiating  into  the  back  and  the  left  arm.  The  pain  came 
back  in  the  form  of  attacks,  and  was  accompanied  by  a  feehng  of  thoracic  constriction 
and  palpitations.  The  attacks  at  first  were  some  days  apart ;  later  they  occurred  daily. 
Auscultation  revealed  no  abnormal  sign  at  the  aortic  orifice,  proving  that  the  supra- 
sigmoid aortitis  had  not  encroached  upon  it.  The  age  of  the  patient  excluded  atheroma, 
and  syphilis  could  alone  be  held  guilty.  Treatment  confirmed  the  diagnosis,  and 
recovery  finally  occurred. 

The  other  two  cases  are  given  by  Vicenzo  Vitone.  One  of  his  patients,  thirty-four 
years  of  age,  was,  four  years  after  infection,  taken  ill  with  headache  and  vertigo,  and 
later  with  crises  of  angina,  suffocation,  and  precordial  pain,  which  radiated  to  the  left 
arm.  These  attacks  occurred  several  times  a  day.  On  auscultation  no  lesion  of  the 
aortic  orifice  was  found,  doubtless  because  the  aortitis  was  confined  to  the  suprasigmoid 
segment.  The  condition  was  due  to  syphilis,  because  subcutaneous  injections  of  mer- 
cury arrested  the  attacks. 


DISEASES  OF  THE  VESSELS  507 

The  other  patient  suffered  from  attacks  of  angina  pectoris,  which  recurred  several 
times  a  day,  although  on  auscultation  it  was  impossible  to  discover  the  slightest  lesion 
ol  the  aorta  or  of  the  heart.  In  this  case  too  the  angina  pectoris,  which  certainly 
depended  on  suprasigmoid  aortitis,  was  cured  by  subcutaneous  injections  of  calomel. 

These  cases  prove  that  syphiUtic  aortitis  may  be  extremely  painful,  and, 
just  as  arteritis  in  cerebral  syphilis  shows  its  presence  by  headache,  so 
aortitis  shows  its  presence  by  the  symptoms  of  angina  pectoris,  from  the 
most  mild  to  the  most  severe  forms.  As  long  as  the  lesion  remains  hmited 
to  the  suprasigmoid  segment  of  the  aorta,  the  valves  are  not  invaded,  and 
the  orifice  remains  healthy ;  the  symptoms  of  angina  pectoris  are  the  only 
evidence  of  the  lesion,  but  they  are  quite  sufficient  to  indicate  the  diagnosis. 

I  cannot  lay  too  great  stress  on  suprasigmoid  aortitis,  which  is  a  favourite 
locahzation  of  sypliihs  of  the  aorta.  In  a  patient  suffering  from  angina 
pectoris  without  atheroma,  lesions  of  the  aortic  orifice,  or  dilatation  of  the 
aorta,  we  are  too  often  incUned  to  diagnose  neuralgia  due  to  tobacco, 
hysteria,  or  arthritis,  and  to  mistake  the  true  nature  of  the  disease  ;  we  accuse 
the  patient  of  smoking  or  of  drinking  too  much,  cut  off  his  tobacco,  tea,  and 
alcohol,  and  then  consider  our  treatment  sufficient.  We  are  wrong.  We  are 
not  sufficiently  familiar  with  the  idea  that  aortitis  may  arise  ten,  twelve, 
or  fifteen  years  after  infection,  at  a  time  when  the  patient  himself  no  longer 
thinks  of  it,  and  we  do  not  remember  that  aortitis,  when  it  is  confined  to  the 
suprasigmoid  segment,  may  excite  no  other  symptoms  than  those  of  angina 
pectoris.  It  is  the  more  important  not  to  make  a  mistake,  because  syphilitic 
aortitis,  when  taken  in  time,  is  curable ;  if  it  is  left  to  itself,  it  may  lead  to 
invasion  of  the  sigmoid  valves  and  coronary  arteries,  dilatation  of  the  aorta, 
formation  of  cupuliform  aneurysms,  or  rupture  of  the  vessel. 

2.  Syphilis  of  the  Aortic  Orifice — Aortic  Incompetence 
due  to  Syphilis. 

After  having  described  suprasigmoid  aortitis,  let  us  consider  the  changes 
caused  by  its  extension  to  the  aortic  orifice  and  the  sigmoid  valves.  To 
give  an  idea  of  this  process  I  have  only  to  sketch  the  history  of  one  of 
my  patients  at  the  Hotel-Dieu  : 

A  strong  policeman,  who  was  forty-five  years  of  age,  had  for  some  time  experienced 
such  acute  cardiac  pain  that  he  was  unable  to  work.  He  could  not  wear  his  tunic 
buttoned,  because  the  least  pressure  over  the  sternum  was  unbearable.  Moreover, 
crises  of  angina  pectoris,  with  all  their  train  of  symptoms,  appeared  on  the  least  move- 
ment, sometimes  even  without  any  apparent  cause. 

For  some  time  life  had  been  intolerable.  He  could  not  clean  his  room,  and  could 
only  walk  very  slowly  from  one  tree  to  another,  as  policemen  are  wont  to  do  on  their 
beat,  without  being  seized  with  angina  and  suffocation,  which  pulled  him  up  short. 
Percussion  of  the  sterno-costal  region  caused  fairly  sharp  pain.  Auscultation  showed 
that  the  angina  pectoris  was  associated  witii  aortitis  and  aortic  incompetence. 

Having  made  the  first  step  in  the  diagnosis,  it  was  necessary  to  find  the  cause  of 


508  TEXT-BOOK  OF  MEDICINE 

the  aortic  lesion  and  of  the  angina.  He  was  not  suffering  from  arterio -sclerosis,  in  the 
true  sense  of  the  word,  and  had  no  renal  disease,  for  he  had  no  albuminuria  and  no 
symijtoms  of  Bright's  disease.  He  was  an  aortic  case,  with  incompetence  of  the  orifice 
and  hypertroi)hy  of  the  heart. 

The  aortic  incompetence  was  consecutive  to  a  lesion  of  the  aorta,  and  not  to  one  of 
the  heart.  The  sigmoid  valves  had  been  invaded  from  the  side  of  the  endarterium, 
and  not  of  the  endocardium.  This  distinction  was  established  by  the  fact  that  aortic 
insufficiency,  consecutive  to  lesions  of  the  endocardium,  and  most  commonly  seen  in 
rheumatic  cases,  is  rarely  painful,  and  may  pursue  its  course  for  a  long  while  without 
causing  symptoms  of  angina  pectoris.  On  the  other  hand,  aortic  insufficiency  consecutive 
to  lesions  of  the  aorta  is  preceded  or  accompanied  by  symptoms  of  angina. 

It  was  not  sufficient,  however,  to  diagnose  aortitis  and  aortic  insufficiency  ;  it  was 
also  necessary  to  know  what  was  the  cause  of  these  lesions.  He  was  free  from  any 
infectious  disease  which  might  cause  aortitis,  but  seventeen  years  before  he  had  had 
a  chancre,  followed  by  enlargement  of  the  inguinal  glands,  mucous  patches  in  the 
mouth,  etc.  I  was  justified,  therefore,  in  making  a  diagnosis  of  syphilitic  aortitis 
with  valvular  incompetence.  The  treatment  confirmed  the  diagnosis.  I  gave  fifteen 
injections  (oily  solution  of  biniodide  of  mercury),  and  later  a  fresh  series  of  twelve 
injections.  The  improvement  was  so  marked  that  six  weeks  after  admission  he  returned 
to  duty.  He  came  back  every  year  for  treatment  with  mercury,  and  the  acute  symj)- 
toms  never  reappeared. 

This  case  is  a  typical  one  of  aortic  insufficiency,  associated  with  syphilitic  aortitis. 
The  lesion  of  the  orifice  was  not  improved  by  the  treatment;  the  diastolic  murmur 
did  not  diminish,  because  the  lesion  of  the  orifice  was  irremediable  ;  but,  at  any  rate, 
the  treatment  was  very  effective,  as  regards  the  symptoms  of  pain  and  dyspna?a,  so 
that  we  may  hope  that  the  lesion  will  not  be  fatally  progressive,  and  that  it  may  be 
arrested. 

For  seven  years  I  heard  nothing  of  him,  but  in  September,  1905,  he  came  to  the 
Hotel-Dieu,  when  I  inquired  as  to  his  health. 

"  Sir,"  said  he,  "  for  seven  years  I  have  had  no  jsain.  I  do  my  own  work,  and  also 
do  day-work  for  others.  My  health  is  gi-and,  and  there  is  not  a  better  worker  for 
miles  round.  I  dig  all  day,  and  in  summer  I  do  harvesting  from  four  in  the  morning 
till  eight  at  night." 

Such  was  his  statement.  Seven  years  ago  he  had  been  under  treatment  for  such 
severe  angina  that  death  appeared  imminent.  Fortunately,  the  angina  was  due  to 
syphihs,  and  injections  of  biniodide  of  mercury  worked  a  wonderful  cure.  The  valvular 
lesion  will  always  remain  as  marked  as  it  was  seven  years  ago,  but  we  may  say  that  it 
has  become  harmless.  He  has  gone  back  to  Ardeche  to  work.  Perhaps  I  shall  find 
him  still  in  good  health  in  yea.rs  to  come. 

3.  Syphilitic  Aneurysms  of  the  Aorta. 

My  opinion  is  that  aneurysms  of  the  aorta  are  in  most  cases  of  syphiUtic 
origin.  I  recognize  more  than  ever  that  syphihs  has  a  marked  predilection 
for  the  aorta.  Too  much  importance  cannot  be  given  to  early  diagnosis. 
All  treatment  depends  upon  it. 

Syphihtic  aortitis  may  result  in  dilatation  of  the  vessel  and  in  aneurysms 
of  every  size.  They  may  assume  considerable  proportions,  as  in  a  man 
suffering  from  aneurysm  of  the  arch. 

The  first  warnings  were  of  two  years'  duration.  He  felt  acute  pain  in  the  left 
cervical  region  and  the  left  arm,  without  any  symptom  of  angina  pectoris.     He  had 


DISEASES  OF  THE  VESSELS  509 

so  little  distr&ss  that  he  could,  without  the  least  breathlessness,  ascend  several  stories, 
while  carrying  heavy  weights.  The  pains  which  he  experienced  were  not  like  those 
seen  in  cases  of  aortitis  of  the  preceding  type.  It  must  be  added  that  the  localization 
of  the  lesion  was  quite  different ;  and  while,  in  the  other  patients,  the  suprasigmoid 
aortitis  reacted  on  the  branches  of  the  cardiac  plexus  in  the  form  of  angina  pectoris, 
here  the  aneurysm  of  the  terminal  portion  of  the  arch  left  the  cardiac  plexus  intact,  but 
affected  the  branches  of  the  brachial  plexus. 

\Mien  this  cer\'ico- brachial  neuralgia  appeared,  he  consulted  Fournier,  who 
diagnosed  syphilitic  aneurysm  of  the  aorta.  He  had  had  a  chancre,  followed  by 
secondary  symptoms.  In  1884  he  was  treated  for  syphilitic  endarteritis  obliterans  of 
the  left  Sylvian  artery  at  the  Saint-Antoine  Hospital.  At  this  time,  after  violent 
headache,  right  hemiplegia  with  aphasia,  appeared.  I  saw  the  patient  some  days 
later,  and  at  once  prescribed  mercurial  inunctions  and  iodide  of  potassium.  The 
aphasia  and  hemiplegia  tinally  ended  in  complete  recovery. 

Ten  years  later  he  suffered  from  aortitis  of  the  same  nature,  which  ended  in  aneurysm. 
These  details  were  known  to  Fournier,  who  at  once  recognized  the  mark  of  syphilis, 
which,  ten  years  apart,  affected  the  Sylvian  artery  and  the  aorta.  The  proof  that  the 
aortitis  was  really  syphihtic  is  that  mercury  and  iodide  of  potassium,  prescribed  by 
Fournier,  cured  the  cervico-brachial  neuralgia,  which  no  other  treatment  had  been 
able  to  assuage.  The  aneurysm  underwent  no  change,  for  it  was  the  result  of  two 
lesions  which  do  not  retrocede,  but  the  extreme  pain  caused  by  the  aneurysm  yielded 
to  the  specific  treatment.  He  came  to  see  me  for  the  neuralgia,  which  had  again  become 
intolerable.   Under  the  influence  of  specific  remedies  the  pains  and  insomnia  disappeared. 

A  patient,  thirty-six  years  of  age,  was  admitted  into  the  Saint-Antoine  Hospital 
for  an  enormous  syphiUtic  aneurysm  of  the  aorta.  At  the  age  of  fifteen  he  had  con- 
tracted syphilis,  which  was  followed  later  by  tertiary  ulcerations,  Avith  indelible  scars 
and  painful  exostoses.  Sixteen  years  after  the  chancre,  paias  appeared  in  the  right 
shoulder,  and  were  more  intense  at  night.  Later  they  spread  over  the  whole  arm  and 
right  side  of  the  chest.  Six  months  later,  oedema  of  the  chest-wall  on  the  right  side  and 
venous  dilatation.  Millard,  finding  pulsation  to  the  right  of  the  sternum,  diagnosed  a 
syphilitic  aneurysm  of  the  aorta,  and  prescribed  Gibert's  syrup,  A^ith  iodide  of  potassium. 
The  redema  and  the  collateral  circulation  disappeared,  but  the  severe  pains  soon 
returned,  and  the  patient  was  taken  into  my  ward.  At  the  right  of  the  sternum,  in  place 
of  the  upper  ribs,  wliich  had  disappeared,  I  found  a  large  aneurysm.  The  pains  in  the  arm 
and  shoulder  were  so  sharp  that  the  patient  could  get  no  rest.  It  was  clear  that  he  had 
suffered  from  a  series  of  syphilitic  troubles,  ending  in  aneurysm  of  the  aorta.  I 
ordered  mercurial  inunction  and  iodide  of  potassium.  The  pains  diminished,  the  nights 
became  better,  but  no  evident  change  in  the  aneurysm  could  be  seen.  He  died  sud- 
denly from  fulminating  haemoptysis. 

The  autopsy  revealed  enormous  dilatation  of  the  ascending  aorta  and  of  the  arcli, 
the  walls  of  which  were  thickened.  The  sac  was  studded  with  small  secondary 
aneurysms  ;  some  were  hollowed  out  like  a  cup,  while  others  projected  in  the  form  of 
nodes,  due  to  the  stratified  layers  of  fil)rin  which  filled  the  cup  and  were  raised  above 
the  wall  of  the  artery.  Indeed,  the  sac  contained  a  crop  of  small  aneurysms,  due  to 
circumscribed  gummata,  as  has  been  described  by  LetuUe,  Kalindero,  and  Babes. 

These  tumours  may  occur  at  any  point  of  the  thoracic  aorta.  The  lesions 
found  post  mortem  show  sliglit  difTerciices.  In  some  cases  the  process  is 
disseminated  over  the  aorta,  whicli  is  dilated,  thickened,  and  studded  with 
atheromatous  patches  at  different  spots  ;  in  other  cases  the  aortitis  is  limited 
to  a  segment  upon  which  the  aneurysm  develops  later,  and  the  vessel  is 
almost  normal  in  the  rest  of  its  extent. 


510 


TEXT-BOOK  OP  MEDICINE 


4.  Aneurysm  of  the  Aorta  of  the  Recurrent  Type. 

Let  us  noAv  consider  the  lesion  which  I  have  named  aneurysm  of  the 
recurrent  type.  I  have  employed  this  name  because  the  aneurysm  develops 
in  the  region  of  the  aorta  contiguous  to  the  loop  of  the  left  recurrent  nerve, 
and  because  its  most  prominent  symptoms  depend  upon  the  close  relation 
of  this  nerve. 

The  anatomical,  clinical,  and  experimental  details  of  this  variety  of 
aortic  aneurysm  have  been  described  in  the  preceding  chapter,  to  which  I 
refer  the  reader. 

Dysphagia,  attacks  of  pharyngism,  oesophagism,  suffocation  and  strangu- 
lation, and  vocal  troubles,  locahze  the  aneurysm  in  the  neighbourhood  of  the 
recurrent  nerve.     This  situation  is  especially  serious,  because  rupture  into 


Fig.  22. — Aneueysm  of  Rectjreent  Type. 
i.  Larynx  ;  p,  p',  vagus  nerve ;  A,  aorta  ;  r,  r',  recurrent  nerves. 


the  trachea  and  bronchi  most  frequently  occurs  here.  The  aneurysm  may 
not  be  larger  than  a  nut,  but  it  is  very  serious  when  situated  in  this  region, 
as  the  following  cases  prove. 

The  first  of  these  cases  is  taken  from  Ordonneau's  thesis. 

A  man,  fifty-eight  years  of  age,  came  into  the  H6tel-Dieu  at  Nantes  for  violent 
pain  in  the  neck  and  upper  part  of  the  chest.  His  respiration  was  embarrassed,  and 
inspiration  was  characteristic  of  spasm  of  the  glottis.  The  voice  was  hoarse  ;  swallow- 
ing was  painful.  As  he  felt  better,  he  left  the  hospital,  but  returned  soon  after  in  a 
much  worse  state.  He  was  cyanosed,  the  aphonia  was  complete,  the  dysphagia  was 
more  severe,  and  the  attacks  of  oppression  were  terrible.  As  he  was  syphihtic,  we 
thought  of  laryngeal  syphihs,  with  consecutive  oedema.  Tracheotomy  was  performed. 
He  succumbed  during  the  night. 

At  the  autopsy  the  larynx  was  found  free  from  disease.      At  the  lower  part  of 


DISEASES  OF  THE  VESSELS  511 

the  trachea,  on  its  left  side,  there  was  an  aneurysm  of  the  arch  of  the  aorta,  no 
larger  than  a  nut.  The  aneurysm  was  adherent  to  the  trachea,  and  was  skirted 
laterally  by  the  left  recvirrent  nerve.  The  portion  of  the  trachea  which  was  not  in 
contact  with  the  aneurysm  showed  on  its  inner  surface  an  ulcer  a  few  milhmetres  in 
diameter.  At  this  point  the  aneurysmal  sac  was  partly  formed  by  the  trachea,  and  was 
so  thin  that  it  would  certainly  have  opened  into  the  air-passage  in  a  short  time. 

This  case  is  an  exact  reproduction  of  the  statements  made  above.  The  syphiUtic 
aneurysm  was  of  small  dimension,  and  did  not  compress  the  trachea  or  the  cesophagus. 
The  dyspncea  and  dysphagia,  therefore,  were  not  produced  by  pressure  on  these  tubes. 
Its  existence  was  revealed  by  aphonia,  dysphagia,  spasms  of  the  glottis,  and  asphyxia, 
due  to  the  close  relation  of  the  recurrent  nerve.  Even  if  the  patient  had  survived  these 
complications,  he  was  threatened  by  fatal  haemorrhage,  for  the  aneurysm  was  on  the 
point  of  bursting  into  the  trachea. 

Savard  has  published  a  similar  case  : 

A  soldier,  forty-four  years  of  age,  who  had  contracted  syphihs,  was  many  years 
after  taken  ill  with  vocal  troubles  and  dyspnoea.  Later  the  aphonia  became  complete, 
and  the  difficulty  in  breathing  was  compUcated  by  terrible  attacks  of  suffocation  and 
8ucking-in.  As  auscultation  of  the  chest,  the  heart,  and  the  aorta,  gave  negative 
results,  the  possibihty  of  syphihs  affecting  the  bronchial  glands  was  thought  of,  and 
iodide  of  potassium  prescribed.  The  situation,  however,  continued  to  grow  serious, 
and  on  the  second  day  after  admission  he  died  from  haemoptysis  in  less  than  a  minute. 
The  autopsy  revealed  an  aneurysm  of  the  size  of  a  nut,  forming  a  diverticulum,  attached 
to  the  aorta.  The  aneurysm,  which  was  adherent  to  the  left  bronchus  and  to  the  trachea, 
compressed  the  left  recurrent  nerve.  After  the  trachea  and  bronchi  had  been  opened, 
Savard  found  at  the  origin  of  the  left  bronchus  a  perforation,  establishing  com- 
munication between  the  bronchus  and  the  aneuiysm.  The  haemoptysis  had  taken 
place  through  this  oi^ening.  This  case>  which  is  absolutely  typical,  proves  the  gravity 
of  aneurysms,  even  of  small  size,  when  they  are  near  the  loop  of  the  recurrent  nerve. 
It  further  proves  that  these  aneurysms  may  reveal  themselves  by  none  of  the  usual 
signs,  and  may  only  betray  their  presence  by  the  signs  special  to  aneurysms  of  the 
recurrent  type. 

When  the  aneurysm  develops  in  this  region,  it  almost  completely  escapes 
our  methods  of  investigation,  especially  if  it  is  of  small  size  ;  it  causes  no 
expansile  pulsation,  no  double  impulse,  no  dullness,  and  no  murmurs  ;  its 
presence  is  not  always  shown  by  pain.  In  some  cases  nothing  can  be  seen, 
heard,  or  felt,  but  yet  we  can  arrive  at  the  diagnosis  of  the  aneurysm  by  the 
symptoms  I  have  indicated. 

Kalindero  and  Babes  have  well  brought  out  the  role  of  gummatous 
aortitis  and  circumscribed  gumma  in  the  pathogenesis  of  syphihtic  aneurysm 
of  the  aorta.  Among  their  cases  there  is  one  wliich  absolutely  conforms  to 
the  recurrent  type. 

A  physician,  twenty-nine  years  of  age,  had  contracted  sypliilis  seven  years  previously. 
Treatment  had  for  a  long  time  kept  him  free  from  any  manifestations  of  sypliiUs, 
when,  six  years  after  the  infection,  he  was  taken  ill  with  dyspliouia,  cough,  ami  severe 
dyspnrpa.  Tlio  physicians  at  Bucharest,  after  laryngoscopic  examination,  wore  of 
opinion  tliat  tlic  tradu-a  and  recurrent  nerve  were  being  compressed  l)y  asiiuill  aneurysm 
or  by  enlarged  glands,     lu  a  few  months  the  laryngeal  symptoms  disappeared,  the 


512  TEXT-BOOK  OF  MEDICINE 

attacks  of  suffocation  were  averted,  he  resumed  his  work,  and  his  liealth  appeared 
perfect.  One  day,  without  any  warning,  he  died  from  fulminating  haemoptysis  in  a 
few  minutes.  Before  his  death,  however,  he  had  still  the  time  and  the  astonishing 
presence  of  mind  to  -svrite  a  few  lines  to  Babes,  begging  him  to  make  a  post  mortem 
and  preserve  the  specimen. 

The  autopsy  demonstrated  the  existence  of  patches  of  syphiUtic  aortitis  and  of  a 
sacciform  aneurysm  as  large  as  a  nut,  which  had  developed  in  the  concavity  of  the  arch 
of  the  aorta.  The  aneurysm  rested  on  the  left  bronchus,  and  pushed  the  lower  end  of 
the  trachea  sUghtly  to  the  right  side.  The  aneurysm  had  opened  into  the  left  bronchus 
by  a  perforation  5  milhmetres  in  diameter. 

It  is  easy  to  reconstruct  the  different  stages  in  this  case.  We  have  a  young  man 
who  contracts  syphihs.  Seven  years  later  syphilitic  aortitis  supervenes,  and  is  chiefly 
locahzed  to  the  aortic  segment  which  is  in  relation  with  the  loop  of  the  left  recurrent 
nerve.  At  this  point  an  aneurysm  of  small  size  develops,  and  shows  its  presence  by 
symptoms  due  to  the  proximity  of  the  recurrent  nerve — Aaz.,  dyspnoea,  spasm  of  the 
glottis,  and  vocal  trouble.  After  this  warning  everything  becomes  normal,  but  the 
aneurysm  pursues  its  insidious  course,  without  pain,  pulsation,  or  any  visible  signs. 
One  day  rupture  occurs,  and  is  accompanied  by  fulminating  hsemoptysis. 

I  have  seen  a  similar  case,  which  shows  how  aneurysm  of  the  recurrent 
type  behaves. 

I  saw,  with  Dr.  Woelcker,  a  gentleman,  fifty  years  of  age,  who  for  some  months  had 
experienced  suffocation,  with  vocal  troubles  and  difficulty  in  swallowing.  Swallowing 
was  painful  and  almost  impossible  during  the  attacks,  while  the  aphonia  was  complete, 
and  the  suffocation  so  marked  that  the  patient  repeatedly  thought  that  he  was  dying. 
Between  the  attacks  the  voice  remained  hoarse,  deglutition  was  difficult,  and  the 
breathing  was  far  from  being  normal.  Examination  of  the  cardio-aortic  region  yielded 
negative  results.  As  the  patient  was  syphilitic,  I  thought  of  some  mecUastinal  lesion, 
and  aneurysm  of  the  recurrent  type  came  into  my  mind.  I  told  his  family  of  the 
possibility  of  fulminating  haemoptysis.  In  order  to  gain  further  informatioD,  however, 
I  asked  for  a  laryngoscopic  examination  by  Dr.  Bonnier. 

When  Woelcker  and  Bonnier  arrived  at  the  house  to  examine  the  patient,  the 
servants  told  them  that  he  had  just  died  of  fulminating  haemoptysis.  This  catastrophe 
verified  the  diagnosis,  and  I  have  not  the  shghtest  doubt  that  this  patient,  hke  those 
of  KaUndero  and  Savard,  died  from  rupture  of  the  aneurysm  into  the  left  bronchus  or 
the  trachea. 

Such  cases  prove  that  aneurysm  of  the  recurrent  type  has  its  special 
symptoms  :  dysphonia,  aphonia,  and  attacks  of  sufEocation,  of  strangulation, 
of  pharyngism,  or  of  oesophagism,  with  or  without  precordial  pain,  are 
therefore  found  more  or  less  in  every  case.  These  symptoms  may  occur  in 
succession  or  in  combination.  They  appear  in  the  form  of  attacks,  and 
though  they  may  last  only  a  short  while  as  a  kind  of  warning  (Kahndero's 
case),  they  are  none  the  less  of  the  highest  importance.  They  allow  us  to 
locaUze  the  aortic  aneurysm  in  the  neighbourhood  of  the  recurrent  nerve — 
that  is  to  say,  in  a  region  which  is  especially  serious,  and  in  wliich  opening  of 
the  aneurysm  into  the  trachea  or  into  the  bronchi  most  usually  occurs.  It 
would  therefore  be  wrong  to  consider  that  the  largest  aneurysms  are  the 
most  formidable.  An  aneurysm  which  develops  towards  the  exterior,  and 
sometimes  reaches  considerable  size,  as  in  the  case  described  above,  may  last 


DISEASES  OF  THE  VESSELS  513 

for  several  years,  in  spite  of  its  size,  before  compromising  the  patient's  life ; 
while  small  aneurysms  which  are  in  relation  with  the  bronchus  or  with  the 
trachea  may  cause  fulminating  haemoptysis  in  persons  who  scarcely  suspect 
the  existence  of  an  aortic  lesion.  By  careful  study  of  the  symptoms,  which  I 
have  tried  to  put  clearly,  and  by  laryngoscopic  examination,  we  can  as  accu- 
rately as  possible  define  the  topography  of  aortic  aneurysm  of  the  recurrent 
type. 

5.  Cupuliform  Aneurysms— ^Gummata  of  the  Aorta. 

Let  us  now  consider  syphilitic  aortitis  with  circumscribed  gummata, 
which  result  in  multiple  cupuliform  aneurysms,  varying  in  size  from  a  pea 
to  a  nut.  Several  of  these  small  aneurysms  may  be  counted  at  intervals  in 
the  course  of  the  thoracic  aorta  ;  we  might,  indeed,  speak  of  an  eruption  of 
small  aneurysms.  These  aneurysms  sometimes  develop  upon  an  aorta 
which  is  neither  deformed  nor  dilated  ;  at  other  times  they  are  set  on  the 
waUs  of  a  large  aneurysmal  dilatation.  According  to  several  authors,  these 
small  aneurysms  are  absolutely  special  to  syphilis.  The  subjoined  cases 
will  give  an  exact  idea  of  this  variety. 

On  November  9,  1892,  a  man,  forty-three  years  of  age,  was  admitted  for  precordial 
pains,  with  angina  and  suffocation,  which  used  to  come  on  suddenly  after  a  walk,  or 
after  some  rather  sudden  movement,  or,  indeed,  -vnthout  apparent  cause.  On  several 
occasions  the  crisis  had  been  so  violent  that  the  patient  thought  he  was  dying.  The 
l)ain  started  in  the  i)recordial  region,  and.  radiated  into  the  left  arm  and  hand.  The 
duration  was  variable.  The  first  crisis  'had  been  short,  but  the  later  ones  came  on  in 
rapid  succession,  and  then  lasted  several  hours,  practically  without  any  respite.  The 
I)atient  did  not  dare  to  walk  or  to  go  upstairs  :  he  dreaded  lying  do\\Ti,  because  he  was 
afraid  of  a  reappearance  of  the  crisis. 

He  evidently  had  angina  pectoris,  and  it  behoved  us  to  search  for  the  cause.  When 
he  uncovered  for  examination,  we  noticed  above  the  left  clavicle  a  large  and  absolutely 
characteristic  pustolo-crustaceous  syphihde,  and  learnt  that  he  had  been  syphilitic 
for  ten  years.  Percussion  and  auscultation  of  the  cardio-aortic  region  gave  negative 
results.  The  aorta  was  not  increased  in  size,  and  the  aortic  orifice  was  absolutely 
healthy.  The  patient  had  neither  lead-poisoning,  gout,  diabetes,  tabes,  nor  hysteria, 
and  was  not  a  smoker.  As  tertiary  syphilis  was  in  full  activity,  it  was  permissible  to 
diagnose  syphiUtic  aortitis. 

On  the  evening  of  admission  he  refused  to  he  down,  so  much  did  ho  dread 
a  crisis.  He  was  seized  with  a  terrible  attack  of  angina  pectoris.  He  was  undressed 
and  put  to  bed,  but  he  had  scarcely  lain  down,  when  he  jumped  up  in  agony,  said  that 
he  was  dying,  and  passed  away  in  a  few  moments.  At  the  autopsy  my  first  care  was 
to  examine  the  aorta.  It  was  not  dilated,  but  on  the  surface  we  saw  four  small 
aneurysms,  at  intervals,  from  below  upwards.  The  first  aneurysm  was  of  the  size  of  a 
large  pea,  and  situated  at  the  level  of  the  right  auricle.  The  second  aneurysm,  of  the 
same  size,  was  4  centimetres  above  the  })receding  one,  in  front  and  to  the  right  of  the 
aorta.  The  third  aneurysm,  of  the  size  of  an  almond,  formed  a  prominence,  aljout 
a  centimetre  higher  up,  at  the  junction  of  the  ascending  and  horizontal  portions  of  the 
aorta.  A  fourth  aneurysm,  of  the  size  of  a  cherry,  wiis  situated  on  the  anterior  part 
of  the  aorta,  at  the  origin  of  tlio  innominate  trunk.  The  aorta  was  opened,  and  the 
integrity  of  the  aortic  orifice  and  sigmoid  valves  was  proved.     The  vessel  was  thickcuod 

33 


514  TEXT-BOOK  OF  MEDICINE 

and  studded  with  patches  of  gummatous  and  atheromatous  aortitis.  The  first  and 
third  of  these  aneurysms  were  excavated  in  the  form  of  a  thin  transparent  cup,  which 
would  soon  have  ruptured.  The  second  and  fourth  aneurysms  formed  a  hard  prominent 
projection,  composed  of  fibrinous  clots,  adherent  to  the  wall.  On  histological  examina- 
tion of  the  thirmest  portion  of  the  aneurysm,  the  tunica  media  had  almost  disappeared. 
The  coronary  arteries  were  incised  and  carefully  examined.  Their  walls  showed  arteritis 
at  different  points,  but  their  orifice  was  absolutely  free,  and  the  lumen  was  not  ob- 
literated. 

He  had  been  attacked  by  acute  syphiUtic  aortitis,  which  had  rapidly  caused  multiple 
aneurj^sms.  The  aortic  orifice  and  the  sigmoid  valves  had  been  spared,  and  death  had 
supervened  in  an  attack  of  angina  pectoris,  consecutive  to  aortitis.  Let  us  remark,  in 
passing,  that  death  was  not  attributable  to  cardiac  ischemia,  consecutive  to  obhtera- 
tion  of  the  coronary  arteries,  for  the  heart  was  not  ischemic,  and  the  coronary  arteries 
were  permeable  at  every  point. 

A  man,  fifty-eight  years  of  age,  was  admitted  for  agonizing  dyspnoea,  which  had 
begun  about  two  years  previously,  and  had  soon  been  followed  by  precordial  pain, 
radiating  into  the  left  arm.  Although  the  pain  and  the  dyspnoea  were  present  together, 
the  latter  was  the  chief  trouble.  On  auscultation  of  the  heart,  I  found  a  diastohc  murmur 
of  aortic  insufficiency,  and  a  systolic  one  of  mitral  insufficiency.  I  therefore  made  the 
following  diagnosis  :  Angina  pectoris,  consecutive  to  aortitis  which  had  encroached 
on  the  aortic  orifice,  \\'ith  aortic  and  mitral  incompetence.  We  had  still  to  discover 
the  cause  of  this  aortitis,  and  as,  after  revie'vnng  the  probable  causes,  I  could  only  find 
one — syphiUs,  which  the  patient  had  had  nine  years  before — it  appeared  to  me 
natural  to  put  the  aortitis  down  to  syphihtic  infection.  I  prescribed  mercurial  in- 
unctions and  iodide  of  potassium.  A  few  days  later  the  patient  was  seized  with  a  terrible 
attack  of  dyspnoea  and  pain,  which  during  the  preceding  days  had  recurred  at  closer 
and  closer  intervals,  and  he  succumbed  in  a  few  minutes. 

At  the  autopsy  our  attention  was  first  directed  to  the  aorta.  It  was  dilated  with 
patches  of  chronic  aortitis.  We  counted  seven  small  aneurysms  at  intervals,  from 
below  upwards.  The  first  aneurysm  w^as  as  large  as  a  plum-stone,  and  situated  in  front 
and  to  the  right  of  the  aorta,  on  a  level  with  the  apex  of  the  right  auricle.  The  second 
aneurysm,  of  the  same  size,  was  situated  above  the  preceding  one.  The  third  aneurysm 
was  smaller,  and  situated  higher  up.  The  fourth  was  situated  on  the  anterior  part  of 
the  aorta,  near  the  innominate  trunk.  The  fifth  aneurysm  occupied  the  anterior  part 
of  the  aorta,  near  the  left  carotid.  The  sixth  was  situated  close  to  the  left  subcla\"ian 
artery.  The  size  of  each  of  these  last  three  aneurysms  was  equal  to  a  cherry-stone. 
Lastly,  a  seventh  aneurysm,  of  the  size  of  a  walnut,  occupied  the  ascending  and  lateral 
portion  of  the  aorta. 

Some  of  these  aneurysms  were  cupuliform ;  others  were  covered  by  fibrinous  clots, 
wliich  projected,  fike  nodes,  into  the  lumen  of  the  vessel.  Histological  examination 
of  the  more  affected  parts  revealed  complete  disappearance  of  the  tunica  media.  The 
coronary  arteries  were  carefully  examined,  but  were  not  obliterated  either  at  their 
orifice  or  in  their  course.  We  found  only  some  atheromatous  patches  1  centimetre 
from  the  orifice  of  the  i:iosterior  coronary.  The  heart  muscle  was  much  hypertrophied, 
especiall_y  in  the  left  ventricle.  Bands  of  fibrous  tissue  were  found  on  histological 
examination. 

These  two  cases  are  very  instructive.  They  prove  that  aortic  syphiUs 
may  take  the  form  of  circumscribed  gummata,  with  or  without  other  lesions 
of  the  vessel.  In  these  cases,  as  in  most  syphihtic  lesions  of  the  ascending 
aorta,  the  angina  pectoris  was  so  severe  that  both  our  patients  died  from  it. 
They  died,  although  there  was  no  inflammation  of  the  coronary  arteries, 


DISEASES  OF  THE  VESSELS  515 

proving  that  obliteration  of  the  coronary  arteries  is  far  from  being  the 
only  cause  of  fatal  angina  pectoris. 

The  multiplicity  of  syphihtic  aneurysms  was  shown  by  Jaccoud  in 
1886  in  his  clinical  lectures  at  the  Pitie,  where  he  quotes  several  well-known 
cases. 

These  include :  the  case  published  by  VcaUin,  of  a  man  forty-fiv'e  years  of  age,  who 
was  syphihtic,  and  died  suddenly  from  haemorrhage  into  the  pericardium.  At  the 
post  mortem  four  aneurysms  were  found  on  the  thoracic  aorta. — The  case  of  Orlebard, 
of  a  syphihtic  j^atient,.  twenty-nine  years  of  age,  at  whose  autopsy  three  anemysms  of 
the  thoracic  aorta  were  found,  the  first  being  situated  above  the  posterior  sigmoid, 
the  second  a  httle  higher,  and  the  third  below  the  origin  of  the  innominate  trunk.— 
Malecot's  case  of  a  man,  fifty-eight  years  of  age,  who  was  both  alcohoUc  and  syphihtic  ; 
post  mortem  three  aortic  aneurysms  were  found :  one  at  the  origin  of  the  aorta,  the 
second  on  the  arch,  and  the  third  just  above  the  diajDhragm. 

Nalty's  case  (Verdie's  thesis)  deals  with  a  man  who  had  had  sj^phihs  five  years 
before.  One  day  he  noticed  a  beating  at  the  root  of  the  neck.  Six  months  later  a 
pulsating  tumour  appeared  in  the  same  region,  below  and  a  httle  to  the  right  of  the  sterno- 
clavicular articulation.  This  tumour  was  an  aneurysm.  As  the  patient  had  tertiary 
ulcers  on  the  thigh  and  knee,  it  was  reasonable  to  ascribe  the  aneurysm  to  syphihs, 
and  treatment  was  presci'ibed.  After  transient  improvement  the  situation  tjocame 
worse,  and  the  patient  died.  At  the  autopsy  two  aneurysms  were  found — one  at  the 
level  of  the  innominate  artery,  the  other  in  the  aorta.  The  latter  compressed  the 
trachea  behind,  and  in  front  projected  into  the  sterno-cIa\'icuIar  region.  Besides 
these  two  large  aneurysms  there  were  upon  the  aorta  several  small  aneurysms, 
characterized,  says  the  author,  by  erosions  of  the  walls  of  the  vessel  and  gummatous 
I^rojections.  Further,  numerous  guramata,  varying  in  size  from  a  pin's  head  to  a  cherry- 
stone, were  scattered  over  the  surface  of  the  heart  and  the  endocardium. 

Jonas  has  reported  the  case  of  a  man,  thirty-three  years  of  age,  who  had  had  syphilis 
for  nineteen  years,  and  three  months  before  was  attacked  by  cardiac  and  aortic  troubles. 
He  died,  and  at  the  autopsy  enlargement  of  the  whole  ascenchng  part  of  the  aorta  was 
found.  Its  surface  was  irregular  and  partly  calcified,  and  4  centimetres  above  the 
aortic  orifice  eight  or  nine  aneurysms,  var^'ing  in  size  from  a  pea  to  that  of  a  filbert, 
were  counted. 

In  syphilitic  aortitis,  which  has  been  carefully  studied  by  I^rault  and 
LetuUe,  the  whole  of  the  arterial  wall  is  infiltrated  at  a  circumscribed  spot 
by  embryonic  lesions.  "  Round  cells,  united  at  different  spots  into  confluent 
nodules,  have  a  suspicious  appearance.  We  are  generally  right  at  some 
period  or  other,  if  not  in  recognizing,  at  least  in  suspecting,  the  formation  of 
miliary  gummata." 

Kalindero  and  Babes  are  still  more  explicit  on  the  presence  of  syphilitic 
gummata  in  the  aorta.  According  to  these  authors,  the  multiple  small 
aneurysms  are  due  to  gummata  of  the  walls  of  the  aorta.  These  authors  say 
that,  in  addition  to  aneurysm  of  the  aorta  due  to  sclerous  aortitis,  we  see 
small  circumscribed  aneurysms,  due  to  the  development  of  syphilitic  gum- 
mata in  the  walls  of  the  vessel. 

Sy|)liilitic  Icsiotis  of  the  aorta  arc,  lii<e  every  form  of  aortitis,  liable  to 
secondary  infection.      Kalindero  and  Babes  have  bruught  liiis  point  out 

33—2 


516  TEXT-BOOK  OF  MEDICINE 

clearly.  They  found  that  microbes  invade  the  inflamed  vessel.  I  quote  the 
result  of  their  researches  :  "  The  most  internal  layer  of  the  tunica  intima  is 
a  little  more  easily  stained  and  more  uniform  than  in  the  normal  state,  and 
contains  a  sheet  of  microbes  in  the  form  of  diplococci,  or  short,  very  straight 
bacilli,  which  stain  well  with  anihne  dyes,  or,  better  still,  with  hsematoxyhn. 
Nests  or  larger  nodules  containing  these  microbes  are  found  at  difEerent- 
places." 

0.  Syphilitic  Coronaritis. 

Syphihs  of  the  coronary,  just  as  of  other  arteries,  shows  two  chief  forms  : 
we  may  find  obhteration  or  dilatation  "with  aneurysm. 

Letulle  has  recorded  a  case  of  obliterating  syphihtic  coronaritis. 

A  woman,  thirty-nine  years  of  age,  who  was  syphilitic,  -wath  right  hemiplegia  and 
aphasia,  died  from  cerebral  softening,  following  obliterating  endarteritis  of  the  left 
Sylvian  artery.  Syj^hilitic  lesions  were  found  in  several  of  the  organs.  Letulle 
found  the  right  heart  seamed  with  fibrous  bands,  and  atrophied  in  its  whole  lower  half. 
On  section,  most  of  the  coronary  arterioles  in  the  right  myocardium  were  affected  by 
obliterating  endarteritis. 

Balzer  has  pubUshed  a  case  of  syphihtic  mihary  aneurysms  of  the 
coronary  arteries. 

The  patient  was  a  man,  fifty  years  of  age,  who  showed  a  tertiary  syphilitic  ulcer, 
wliich  had  destroyed  the  septum  and  subseptum  of  the  nose  and  part  of  the  upper  lip. 
He  died  of  phthisis,  and  the  autopsy  revealed  the  following  lesions  :  The  anterior 
coronary  artery  was  the  seat  of  about  thirty  miliary  aneurysms,  placed  in  a  row  on  the 
anterior  surface  of  the  ventricle,  over  the  aortic  and  pulmonary  infundibula.  These 
aneurysms  were  as  large  as  a  pin's  head,  and  involved  the  arterioles  of  the  pericardium. 
After  being  detached  from  the  wall  of  the  heart  and  stained  with  picro-carmine,  they 
showed  every  known  type,  being  sacciform,  fusiform,  and  dissecting.  The  rupture  of 
one  of  these  aneurysms  set  up  fatal  hsemorrhagic  isericarditis. 

Haushalter,  at  the  post-mortem  examination  of  a  syphilitic  patient  who  died 
suddenly  while  eating  a  meal,  found  coronaritis  obKterans,  characterized  histologically 
by  masses  developed  in  the  tunica  vascularis.  Ihe  masses  exactly  resembled  gum- 
matous lesions  in  appearance. 

Treatment. — Mercury  is  the  sovereign  remedy  for  syphilitic  aortitis  ;  it 
may  be  given  in  conjunction  with  iodides.  I  prefer  oily  or  watery  injections 
of  biniodide  of  mercury.  An  injection  containing  ^  grain  of  biniodide  is 
given  daily  for  a  fortnight.  The  treatment  is  stopped  for  a  time  and  then 
repeated.  Iodide  of  j)otassium  may  be  prescribed  during  the  intervals  when 
mercury  is  not  being  given. 

Under  the  influence  of  this  treatment  (which  is  described  in  the 
Appendix),  we  often  witness  the  disappearance  of  the  acute  pains  of  sypliihtic 
aortitis,  and  of  the  headache  due  to  cerebral  arteritis  ;  we  can  also  master 
cervico-brachial  or  intercostal  neuralgia,  which  sometimes  accompanies  the 
growth  of  aneurysm.  The  dyspnoea,  vocal  troubles,  dysphagia,  spasms  of 
the  glottis,  and  attacks  of  oppression,  resulting  from  an  aneurysm  in  the 


DISEASES  OF  THE  VESSELS  517 

neighbourhood  of  the  recurrent  nerve,  may  disappear,  or,  at  any  rate, 
become  less  severe. 

The  efficacy  of  the  treatment  is  proved  by  the  cases  which  I  have  quoted. 
My  patient  at  the  Hotel-Dieu,  in  whom  angina  pectoris  was  most  severe,  was 
completely  reheved  by  the  treatment,  and  was  able  to  resume  his  duties  as  a 
policeman.  My  other  patient,  in  whom  the  aneurysm  formed  a  large 
thoracic  tumour,  and  who  had  intractable  cervico-brachial  neuralgia,  was 
completely  freed  from  his  pain  by  the  treatment  which  Fournier  had  already 
prescribed  at  the  Saint-Louis  Hospital,  and  which  I  continued  at  the  Hotel- 
Dieu.  The  patient  whom  I  saw  with  Potain  had  syphihtic  angina  pectoris, 
in  which  treatment  had  failed  ;  he  was  completely  reheved  by  mercury  and 
iodides.  The  patients  of  Hallopeau,  Rumpf ,  and  Vicenzo  Vitone  also  suffered 
from  syphihtic  angina  pectoris,  and  were  cured  by  mercurial  preparations, 
given  either  by  the  mouth  or  by  injections.  The  patient  whom  I  had  at 
the  Saint-Antoine  Hospital,  and  in  whom  Millard  had  already  diagnosed 
sypliihtic  aneurysm  of  the  aorta,  lost  liis  dyspnoea,  brachial  neuralgia,  and 
oedema  under  treatment  with  mercury  and  iodides.  In  one  of  Jaccoud's 
patients  treatment  brought  about  an  improvement,  which  lasted  two  years, 
"  and  would  perhaps  have  been  final  if  it  had  not  been  abandoned  too  soon." 

In  Nalty's  patient  the  treatment  produced  a  very  notable  diminution  in 
the  dyspnoea  and  cough,  and  for  some  time  the  pulsations  of  the  aneurysms 
were  less  intense,  and  the  tumour  seemed  to  diminish  in  size.  In  short, 
dyspnoea,  cough,  and  especially  pain,  improve  or  disappear  under  the 
influence  of  early  treatment. 

When  such  a  result  has  been  obtained,  we  ought  not  to  remain  satisfied. 
Syphihs  is  naturally  obstinate,  and  does  not  yield  easily  ;  let  us  beware, 
therefore,  of  considering  as  a  cure  what  is  most  often  a  momentary  improve- 
ment. Treatment  may  have  mastered  the  pains  or  other  symptoms  which 
accompany  aortitis  at  its  onset,  as  well  as  at  a  more  advanced  period,  but  this 
is  not  sufficient.  Even  when  these  symptoms  do  not  reappear,  and,  much 
more  so  if  they  do,  let  us  begin  treatment  again  for  a  second  or  a  third  time, 
the  duration  of  such  treatment  being  from  fifteen  to  eighteen  days  on  an 
average,  and  the  periods  that  divide  the  treatment  being  some  weeks,  or  at 
most  some  months. 

If  we  are  thoroughly  imbued  with  these  principles,  and  have  the  oppor- 
tunity of  attacking  syphihtic  aortitis  at  its  onset,  we  can  obtain  therapeutic 
successes  ;  we  can  judge  of  this  by  the  results  I  have  just  given.  If, 
however,  the  aortic  lesions  are  already  old,  and  an  aneurysm  has  already 
appeared,  are  we  to  abstain  from  all  specific  treatment  ?  Sucli  is  not  my 
opinion,  and  although  we  cannot  count  here  on  success,  we  hav(^  at  any  rate 
the  satisfaction  of  being  able  to  im{)rove  the  patient's  condition,  to  avert 
imminent  danger,  and  to  arrest  the  invasion  of  the  lesions. 


518  TEXT-BOOK  OF  MEDICINE 

VIII.  DIAGNOSIS  BETWEEN  ANEURYSM  AND  NERVOUS 
PULSATION  OF  THE  ABDOMINAL  AORTA. 

Aneurysm  is  far  less  common  in  the  abdominal  than  in  the  thoracic  aorta. 
Lebert,  in  69  cases  of  aortic  aneurysm,  found — Ascending  aorta,  24  ;  arch,  27  ; 
descending  aorta,  9  ;  abdominal  aorta,  9.  The  enlargement  in  most  cases  is 
near  the  coehac  axis  ;  the  structure  is  similar  to  that  of  the  thoracic  aneurysm. 
The  only  special  point  is  the  frequency  of  rupture  into  the  subperitoneal 
tissue,  and,  as  a  result,  a  diffuse  aneurysm. 

The  abdominal  tumour  has  practically  the  same  causation  as  the  thoracic 
aneurysm,  but  its  locaUzation  gives  rise  to  certain  special  symptoms.  The 
pains  may  simulate  those  of  lumbar  neuralgia  ;  they  may  be  acute  and 
paroxysmal.  Some  patients  cannot  He  down  in  bed,  and  are  compelled  to 
assume  a  sitting  posture.  The  pains  may  be  due  to  pressure  on  the  nerve 
trunks,  or  to  erosion  of  the  vertebral  bodies.  The  weakness  of  the  legs  and 
the  pain  make  walking  difficult.  The  aneurysm  is  shown  on  palpation  by  a 
tumour,  and  by  pulsation  more  readily  felt  in  thin  persons.  When  we  press 
the  abdominal  wall  back,  we  can  feel  a  pulsating  tumour  in  the  subumbilical 
region,  either  in  the  median  line  or  to  one  side,  usually  the  left.  A  diastolic 
murmur  is  audible  on  auscultation.  The  femoral  pulse  is  later  than  the 
radial  pulse.  Rupture  usually  takes  place  into  the  retroperitoneal  tissue. 
Arterio-venous  aneurysm  is  extremely  rare.  Aneurysm  of  the  abdominal 
aorta  has  given  rise  to  numerous  errors  in  diagnosis  ;  aneurysm  may  some- 
what resemble  the  epigastric  pulsation  found  in  aortic  insufl&ciency,  the 
transmitted  pulsation  seen  in  adherent  pericardium,  and  the  pulsation  of  the 
aorta  transmitted  by  tumours  of  the  pancreas,  the  stomach,  or  the  small 
omentum.  Abdominal  aortitis  may  also  show  some  resemblance  to 
aneurysm.  The  usual  mistake,  however,  Ues  in  confusing  aneurysm  of  the 
abdominal  aorta  with  the  so-called  nervous  pulsation  of  the  vessel.  "  Violent 
pulsation  along  the  course  of  the  abdominal  aorta  is  found  in  some  subjects, 
while  material  lesions  are  absent."  I  have  frequently  seen  this  nervous 
pulsation  in  persons  who  were  afraid  that  they  had  an  aneurysm,  and  have 
pointed  out  this  fact  to  my  class  at  the  Hotel-Dieu. 

Nervous  pulsation  of  the  aorta  is  usually  seen  in  hypochondriacal, 
neurasthenic,  or  hysterical  persons,  in  cases  of  flatulent  dysjDepsia,  and  in 
anaemic  women  during  menstruation  or  pregnancy.  The  sufferer  usually 
discovers  the  pulsation,  and  comes  to  the  physician,  who  recognizes,  on 
inspection  and  palpation,  the  pulsation  in  question.  On  depressing  the 
abdominal  wall  the  hand  feels  a  violent  pulsation,  which  is  most  marked 
when  the  patient  is  lying  down.  On  auscultation  a  shock  seems  to  lift  the 
head,  and  pressure  on  the  vessel  with  the  stethoscope  produces  a  systolic 
murmur  ;  no  pain  is  felt. 


DISEASES  OF  THE  VESSELS  519 

The  pulsation  is  periodic ;  it  may  last  for  months,  appearing  and  disap- 
pearing suddenly.  The  condition  is  not  serious,  though  the  sufferer  grows 
alarmed  from  the  violent  pulsation,  loses  sleep,  and  becomes  neurasthenic. 
Correct  diagnosis  is  therefore  important.  "  Laennec  and  Bayle  both  admit 
making  an  error  ;  the  former,  profiting  by  his  error,  has  left  us  an  interesting 
description  of  this  phenomenon." 

In  my  own  cases  the  following  diagnostic  points  have  given  me  help  ; 
the  beats  are  just  as  forcible  in  aneurysm  as  in  nervous  pulsation,  but  in  the 
former  case  we  fuid  a  tumour. 

Aneurysm  is  frequently  accompanied  by  lumbo-abdominal  neuralgia  ; 
similar  pain  is  not  seen  in  nervous  pulsation.  Aneurysm  runs  a  slow  and 
progressive  course ;  the  symptoms  appear  gradually,  and  the  pulsation  does 
not  at  once  reach  its  maximum  ;  nervous  pulsation,  on  the  other  hand,  may 
appear  from  one  day  to  the  next,  cease,  and  reappear  periodically. 

Nervous  pulsation,  though  important,  has  been  scarcely  noticed  in  the 
text-books,  but  it  was  known  to  Hippocrates,  who  states  that  the  son  of 
Eratolos  had  marked  pulsation  after  an  attack  of  dysentery.  The  symptom 
was  well  known  to  Bailleu,  Morgagni,  and  Lancisi.  Its  pathogenesis  is  still 
a  question  of  theory.  The  important  point  is  correct  diagnosis  and  proper 
treatment. 

Two  women  under  my  care  at  the  Hotel-Dieu  for  nervous  pulsation  of 
the  aorta  were  afflicted  with  flatulent  dyspepsia  and  dilatation  of  the 
stomach.  I  prescribed  lime-waterbefore  and  after  meals,  and  a  cold  douche 
every  morning.  Rapid  improvement  followed,  and  the  patients  left  the 
hospital  freed  from  all  symptoms.  Valerian,  bromides,  and  hydrotherapy 
are  indicated  when  the  nervous  condition  appears  to  dominate  the  situation. 


IX.  CARDIO-AORTIC  LESIONS  IN  TABES— TABETIC  ANGINA 

PECTORIS. 

Discussion. — Patients  suffering  from  tabes  may  show  lesions  of  the  heart 
and  aorta.  This  fact,  which  now  appears  commonplace,  was  unknown 
twenty  years  ago.  Vulpian,  in  1879,  was  the  first  to  note  the  coexistence 
of  cardio-aortic  lesions  and  locomotor  ataxy. 

A  pationt,  who  for  six  ycar.s  had  sufTerod  \vilh  lightning  pains  in  tho  lower  limbs, 
also  had  aortio  insufiicicncy  and  stenosis.  Jie  died,  and,  on  the  one  hand,  the  sj)inal 
lesions  of  tabes,  and,  on  the  other  liand,  aortic  mischief,  were  found.  Tho  sigmoid  valves, 
which  were  thickened  and  shrivelled  up,  had  caused  insuflficiency  and  constriction  of 
the  orifice.  In  another  of  Vulpian's  cases,  a  woman,  fifty-ono  years  of  ago,  sufTered 
from  tabes,  accompanied  by  a  double  lesion  of  the  aortic  orifice,  with  dilatation  of  the 
aorta  and  symptoms  «)f  angina  pectoris.  She  died,  and  at  tho  autopsy  the  medullary 
Ie8ion.s  of  taltes  and  aortic  insufhcieney  were  found.  The  aorta  was  very  dilated  and 
incru.'jted,  especially  at  the  arch,  with  numerous  patches  of  atheroma. 


520  TEXT-BOOK  OF  MEDICINE 

This  coexistence  of  tabetic  and  cardio-aortic  lesions  had  not  escaped 
Vulpian.  "  I  cannot  state,"  says  he,  "  that  the  relation  of  cause  and  effect 
exists,  but  I  feel  that  I  must  call  your  attention  to  this  coexistence,  and 
Charcot,  at  the  Salpetriere,  has  many  times  in  my  presence  insisted  on 
the  frequency  of  aortic  lesions  in  ataxic  patients." 

Charcot  and  Bouchard  published  in  186G  an  analogous  case. 

Their  patient,  who  was  subject  to  severe  attacks  of  dyspnoea,  was  affected  with  the 
lightning  pains  of  tabes,  as  well  as  an  aortic  lesion  with  a  to-and-fro  murmur.  He  died, 
and  at  the  autopsy  tabes  and  cardio-aortic  lesions  were  found.  Heart  much  hyper- 
trophied ;  aorta  dilated  and  incrusted  with  atheroma ;  sigmoid  valves  shrivelled  up, 
incompetent,  and  studded  on  their  free  edge  with  small  warty  vegetations. 

In  1890  Grasset,  who  had  collected  twenty-four  cases,  including  two 
personal  ones,  discussed  the  pathogenesis  of  cardio-vascular  troubles  in 
tabes,  and  implicated  the  reaction  of  the  lightning  pains  upon  the 
heart. 

Letulle  has  published  two  cases  of  aortic  lesions  in  tabes,  and  puts  them 
down  to  general  arterio-sclerosis,  which  produces  both  morbid  conditions. 
In  1881  Jaubert  collected  twelve  fresh  cases.  True,  in  1883,  brought  for- 
ward six  other  cases,  and  Teissier,  in  1884,  described  among  atrophic 
lesions  perforation  of  the  sigmoid  valves,  and  compared  it  to  perforating 
ulcer  of  the  foot.  Raymond,  in  the  Dictionnaire  des  Sciences  Medicales, 
thus  sums  up  the  question :  "  The  most  probable  hypothesis  regards 
the  aortic  and  mitral  lesions  of  tabetics  as  an  accidental  compHcation 
induced  by  early  senility,  or  developed  as  the  result  of  such  causes  as 
rheumatism,  alcohol,  and  syphilis,  which  commonly  intervene  in  such 
cases." 

Syphilis  occupies  the  chief  place  in  the  pathogenesis  of  cardio-aortic  lesions 
in  tabes.  We  know  how  skilfully  Fournier  sought  to  prove  that  tabes  is  a 
syphilitic  or  a  parasyphiHtic  lesion.  By  the  same  reasoning  it  was  very 
natural  to  suppose  that  syphilis  produces  simultaneously  the  medullary  and 
aortic  lesions  of  tabes.  Bouveret  had  already  published  the  case  of  a 
syphihtic  patient,  who  was  attacked  at  the  same  time  by  aortic  constriction 
and  early  tabes  ;  antisyphiUtic  treatment  determined  rapid  improvement. 
Schultze,  in  1892,  saw  two  cases  of  aortic  insufficiency  in  syphilitic  patients 
with  tabes,  and  did  not  hesitate  to  set  down  the  tabes  and  the  aortic  lesion 
to  the  account  of  syphilis.  The  same  opinion  has  been  expressed  by 
Marie. 

It  is  certain  that  we  possess  a  large  number  of  cases  in  which  aortic  and 
mitral  lesions  have  appeared  in  the  course  of  confirmed  tabes.  They  may  be 
distinct  or  associated  ;  aortic  lesions,  however,  are  three  times  as  frequent  as 
mitral  ones.  Nordmann  notes  twenty  mitral  as  against  fifty-one  aortic 
lesions.     As  regards  my  personal  experience,  I  have  several  times  seen  aortic, 


DISEASES  OF  THE  VESSELS  521 

but  never  mitral,  lesions.     Rendu  has  stated  the  same  opinion.     Nordmann's 
statistics  are  as  follows  : 

(Aortic  insufficiency,  38. 
Aortic  stenosis,  7. 
Aortic  insufficiency  and  stenosis,  6. 
Aneurysms  of  the  arch  of  the  aorta,  4. 

T    nn  J!      -1     1  I    •         •     i  1    J  •     f  Mitral  insufficiency,  10. 

In  20  cases  of  mitral  lesions  m  tabetic       ,,.,     ,    ,         .        • 
.  -    Mitral  stenosis,  4. 

^  [  Insufficiency  and  stenosis,  6. 

The  present  view  is  that  the  aortic  lesions  are,  like  tabes  itself,  of  syphi- 
litic origin.  I  do  not  profess  to  decide  the  question  of  pathogenesis,  and 
shall  content  myself  with  the  following  statement : 

If  syphihs  is  indeed  the  cause  of  tabes  and  of  aortic  lesions  at  one  and 
the  same  time,  why  do  the  aortic  lesions  never  appear  after  tabes  ?  Why 
does  not  syphihs  cause  in  some  cases  tabes,  and,  later,  aortic  lesions,  and  in 
other  cases  aortic  lesions,  and,  later,  tabes  ?  I  ask,  further,  why  do  not 
people  with  syphiHtic  aortitis  (and  they  are  numerous)  become  tabetic  ? 
There  is  in  every  case  an  anomaly  which  clashes  with  my  opinion.  Further, 
if  sypliilis  really  induce,  at  one  and  the  same  time,  tabes  and  aortitis,  why 
does  syphihs  in  a  tabetic  patient  reserve  all  its  blows  for  the  aorta,  and  why 
does  it  spare  the  other  vessels-,  notably  the  cerebral  arteries,  which  are  so 
often  affected  in  syphihs  ?  Tliis  is  another  unexplained  anomaly.  Lastly, 
if  the  aortic  lesions  of  tabetic  patients  are  syphiUtic,  why  are  they  usually  so 
indolent,  while  syphihtic  aortitis,  like  angina  pectoris,  is  nearly  always 
painful  ?  I  give  these  ideas,  and  although  they  may  not  be  of  such  a 
character  as  to  solve  the  present  question,  they  at  least  throw  some  doubt 
on  the  interpretation  of  the  aortic  lesions  given  by  the  most  reliable  authors. 
They  tend  to  take  from  syphilis  the  preponderant  role  which  has  been  given 
to  it,  and  if  this  role  is  true  in  tabes,  the  question  of  cardio-aortic  lesions 
in  tabetic  patients  appears  to  me  of  small  import. 

Symptoms. — The  clinical  course  of  the  cardio-aortic  manifestations  in 
tabes  present  some  peculiarities,  and  the  most  prominent  fact  is  that  they 
are  often  unknown  to  the  sufferers.  I  cannot  do  better  than  compare  them 
from  this  point  of  view  with  the  joint  troubles  in  tabes,  which,  in  spite  of 
the  marked  disorganization  of  the  joint,  are  usually  painless,  so  that  patients 
can  perform  every  movement  without  feeling  the  least  pain.  This  relation 
between  the  articular  and  cardio-aortic  lesions  is  a  novel  argument  in  favour 
of  the  theory  which  tends  to  consider  these  lesions  as  trophic  troubles. 
Grasset  had  clearly  seen  that  the  aortic  lesions  of  ataxic  patients  do  not  show 
themselves  by  the  usual  symptoms ;  they  must  be  looked  for,  or  they  will 
often  pass  unnoticed.  Jaubert,  Rendu,  Albespy,  and  Nordmann  note  the 
singular  tolerance  of  cardio-aortic  lesions  in  tabes.     I  have  proved  the  truth 


522  TEXT-BOOK  OF  MEDICINE 

of  this  assertion,  and  I  have  several  times  found,  to  my  surprise,  marked  aortic 
lesions  after  a  long  and  careful  examination  of  a  tal3etic  patient,  who  in  the 
course  of  his  interrogatory  had  in  no  way  drawn  my  attention  to  his  aorta. 
These  lesions  are  not,  however,  always  latent.  One  patient  has  palpitation, 
another  pain  and  dyspnoea,  but  these  symptoms  are  rarely  alarming  or  end  in 
syncope  and  the  agonizing  pains  of  angina  pectoris.  The  cardio-aortic 
lesions  are  well  borne  by  the  patient,  and  scarcely  seem  to  make  the  prognosis 
of  tabes  worse.     Tabetic  patients  rarely  die  from  heart  trouble. 

Some  tabetics  show  true  attacks  of  angina  pectoris  without  aortic 
lesions.  A  tabetic  patient  who  formed  the  subject  of  one  of  my  chnical 
lectures*  had  violent  angina  pectoris,  without  appreciable  lesions  of  the 
aorta.  I  thought  that  this  was  a  case  of  neuralgia  of  the  cardiac  plexus, 
comparable  to  those  visceral  crises  which  are  constantly  met  with  in  tabes. 

This  idea  of  angina  pectoris,  which  is  independent  of  lesions  of  the  aorta 
and  coronary  arteries,  and  supervenes  as  a  visceral  crisis  of  tabes,  appears 
to  me  estabhshed  by  undoubted  proofs,  and  is  admitted  by  several  writers. 
These  crises  would  appear  to  be  related,  says  Leyden,  to  neuralgia  of  the 
cardiac  nerve,  or  neuralgia  cordis,  according  to  Romberg's  expression. 
Leyden  quotes  the  following  cases  in  support  of  liis  opinion  : 

A  man,  thirty- eight  years  of  age,  who  suffered  from  locomotor  ataxia,  had  for  three 
or  four  weeks  attacks  which  began  with  violent  pain  in  the  region  of  the  heart,  and 
lasted  about  half  an  hour.  During  the  attack  the  heart  beat  as  though  it  would  burst, 
but  auscultation  revealed  no  lesions.  The  heart  sounds  were  pure,  the  aortic  orifice 
was  healthy,  the  rachal  artery  was  normal,  and  there  was  no  trace  of  arterio-sclerosis. 
Another  of  Leyden's  cases  is  that  of  a  tabetic  who  suffered  at  first  with  larjTigeal,  and 
later  with  cardiac  crises,  characterized  by  terrible  angina,  with  pain  radiating  into  the 
left  arm.  During  the  attacks  the  patient  thought  that  he  was  going  to  die.  Leyden 
takes  care  to  remark  that  on  auscultation  he  found  neither  murmurs  nor  abnormal 
sounds,  which  shows  that  this  case  was  one  of  visceralgia  in  the  true  sense  of  the  word. 

Berbes  had  reported  an  analogous  case  in  a  man,  fifty-one  years  of  age, 
suffering  from  tabes,  who  was  taken  ill  with  typical  angina  pectoris. 

The  cardiac  crises  were  preceded  by  laryngeal  crises.  In  this  case,  too,  it  was  a 
question  of  visceralgic  angina  pectoris,  for  no  lesions  of  the  heart  and  aorta  were  found 
on  auscultation. 

Landouzy  has  published  a  similar  case. 

A  woman,  thirty-nine  years  of  age,  who  was  a  proved  case  of  tabes,  but  not  of  syphilis, 
suffered  from  frequent  gastric  crises.  She  was  at  times  seized  with  attacks  of  angina 
pectoris,  accompanied  by  palpitation,  precordial  distress,  and  dyspnoea,  and  a  tearing 
sensation,  which  started  in  the  sternum  and  radiated  into  the  left  arm.  This  case  was 
also  one  of  visceralgia,  for  the  patient  showed  neither  signs  nor  symptoms  of  aortic 
lesions. 

Groedel  has  reported  the  case  of  a  man,  forty-one  years  of  age,  who,  in  the  course  of 


*  Dieulafoy,  1897.     "  Angine  de  Poitrine  tabetique,"  7'"''  le^on  {Clinique  Medicate 
de  V Hotel -Dieu). 


DISEASES  OF  THE  VESSELS  523 

tabes,  was  seized  with  violent  attacks  of  angina  pectoris.  He  was  awakened  one  night 
with  a  feehng  of  angina  and  precordial  pain.  During  the  attack  his  face  was  pale  and 
covered  viith  sweat,  and  his  pulse  was  small  and  rapid.  Although  these  attacks  were 
repeated  several  times  during  the  year,  it  was  impossible  to  discover  any  aortic  lesion 
on  auscultation. 

Debove  has  discussed  tabetic  angina  pectoris  in  detail. 

In  one  patient  the  attack  of  angina  pectoris  was  always  preceded  by  girdle  pains. 
The  pain  appeared  in  the  precordial  region,  at  the  level  of  the  third  rib,  radiated 
to  the  left  arm  as  far  as  the  end  of  the  little  finger,  and  was  so  acute  that  it  seemed  to 
the  patient  as  though  "  everything  stopped  still  inside  him."  After  this  first  attack 
he  was  advised  to  give  up  tobacco.  Although  he  did  not  smoke  during  this  period, 
the  attacks  did  not  cease.  Auscultation  revealed  no  lesion  of  the  heart  or  of  the  aorta. 
Debove  accordingly  considered  these  attacks  "  as  a  visceral  crisis,  analogous  to  those 
which  may  affect  other  organs  in  tabes  ;  in  fact,  as  the  visceral  crisis,  which  is  angina 
pectoris."  Further,  the  patient  in  question  suffered  later  from  crises  affecting  the 
anus,  testis,  and  urethra. 

I  am  of  the  same  opinion  as  Debove  and  Leyden,  and,  in  opposition  to 
Huchard,  I  allow  the  existence  of  a  cardio-aortic  visceralgia,  which  may  be 
fatal ;  it  is  a  neuralgia  cordis,  independent  of  aortic  lesions  and  coronaritis. 
Tabes,  which  is  essentially  a  painful  disease,  excites  violent  crises  in  the 
lower  limbs,  the  thorax,  the  face,  and  the  stomach,  in  which  case  the  crises 
resemble  the  pains  of  an  ulcer  ;  in  the  kidney,  where  they  simulate  renal 
colic  ;  in  the  rectum,  the  testis,  the  urethra,  and  the  larynx.  Why,  then, 
should  we  deny  to  the  nerves  of  the  cardiac  plexus  what  is  so  readily  con- 
ceded to  the  nerves  of  other  region^  and  organs  ? 

It  is  the  more  rational  to  admit  visceralgic  angina  pectoris  in  tabetic 
patients,  as  the  same  patient  often  has  visceral  crises  in  other  organs  ;  thus 
my  patient  had  had  gastric,  urethral,  and  rectal  crises  when  he  was  seized 
with  angina  pectoris.  In  Debove' s  case  the  crises  of  angina  pectoris  were 
preceded  by  girdle  pains,  and  were  followed  by  rectal,  testicular,  and  urethral 
crises  ;  Landouzy's  patient  suffered  from  gastric  crises  when  angina  pectoris 
supervened ;  one  of  Leyden's  patients  had  terrible  laryngeal  crises  before 
angina  pectoris  appeared.  Cardio-aortic  visceralgia  is,  therefore,  neither  a 
strange  nor  isolated  fact  in  the  history  of  tabes  ;  it  belongs  to  the  group  of 
other  visceralgias,  and  may  precede,  follow,  or  alternate  with  them. 

If,  however,  it  is  reasonable  from  clinical  proof  to  admit  tabetic  angina 
pectoris  apart  from  any  lesion  of  the  aorta  and  coronary  arteries,  have  we 
also  undoubted  anatomical  proofs  ?  We  have  such  proofs,  as  is  shown  by 
the  following  case,  which  Vulpian  published  in  the  Revue  de  Medecine  in  1885  : 

A  man,  thirty-thrco  years  of  age,  was  taken  ill  -with  the  first  symptoms  of  tabes  at 
llie  ago  of  twenty-nine,  and  from  the  first  liad  gastric  crises.  In  the  course  of  tabes 
lie  (ixpcrienced  complete  attacks  of  angina  jxrtoris,  which  Vulpian  described  minutely. 
Vulpian  excluded  hysteria,  of  which  he  found  no  stigmata.  He,  therefore,  admitted 
in  this  oaso  the  existence  of  tabetic  angina  jiectoris,  independent  of  any  cardio-aortio 
lesion,  an  examination  of  the  heart  and  aorta  had  proved  the  integrity  of  these  organs. 


524  TEXT-BOOK  OF  MEDICINE 

The  patient  died  of  phthisis,  and  the  diagnosis  was  confirmed.  The  spinal  cord  showed 
the  classical  lesions  of  tabes,  but  the  heart  and  aorta  were  absolutely  healthy.  Cardiac 
neuralgia  in  tabes  is,  therefore,  an  accomplished  fact. 

Histological  researches  have  also  confirmed  this  opinion  ;  peripheral 
neuritis  explains  the  neuralgic  pains,  the  real  cause  of  which  has  till  now 
passed  unnoticed.  Oppenheim  found  degeneration  and  atrophy  of  the 
pneumogastric  nerve  in  a  case  of  tabes,  accompanied  by  gastric  crises  and 
by  angina  pectoris,  witli  pain  radiating  into  the  left  arm.  Grocco  and 
Fusari  found  changes  in  the  cardiac  plexus,  in  the  vagus,  and  the  laryngeal 
nerves,  and  in  the  abdominal  sympathetic  and  the  coehac  plexus,  in  a  patient 
who  had  had  attacks  of  angina  pectoris,  with  gastric  and  laryngeal  crises. 
Pitres  and  Vaillard  admit,  as  regards  the  case  in  question,  that  the  visceralgic 
crises  of  tabetic  patients,  including  those  of  angina  pectoris,  may  be  due  to 
neuritis  of  the  corresponding  visceral  nerves. 

We  may,  therefore,  say  that  tabetic  patients  may  be  affected  by  cardio- 
aortic  neuralgia,  which  reproduces  the  syndrome  of  angina  pectoris,  just  as 
they  are  affected  by  visceralgic  crises  of  the  stomach  (gastric  crises),  kidneys 
(renal  crises),  urethra  (urethral  crises),  bladder  (vesical  crises),  testis  (testic- 
ular crises),  and  rectum  (ano-rectal  crises).  All  these  crises  form  part  of 
the  painful  symptom-complex  of  tabes,  and  are  made  up  of  acute  hghtning 
pains  in  the  organ  and  limbs. 

To  sum  up  :  A  tabetic  patient  may  show,  on  the  one  hand,  aortic  lesions 
with  or  without  angina  pectoris,  and,  on  the  other  hand,  angina  pectoris 
without  aortic  lesions.  In  the  former  case  the  aorta  is  atheromatous  and 
dilated,  while  the  aortic  orifice  is  damaged,  and,  a  temarkable  fact,  these 
aortic  lesions,  which  in  other  cases,  as,  for  example,  in  syphilis,  are  so  painful, 
are  usually  slight  and  painless  in  tabes.  Hence  an  apparent  paradox  results — 
viz.,  that  the  tabetic  patients  who  have  terrible  attacks  of  angina  pectoris  are 
generally  those  who  have  not  aortic  lesions.  They  are  affected  by  neuralgia 
or  neuritis  of  the  cardiac  plexus. 

The  treatment  of  angina  pectoris  in  tabes  must  now  claim  our  attention. 
Mercury  and  iodide  should  never  be  omitted  if  the  patient  is  syphiUtic,  for 
it  is  not  impossible  that  he  may  have  suprasigmoid  aortitis.  Further, 
there  is  a  series  of  therapeutic  measures  which  I  recommend  as  regards  local 
treatment — the  application  of  the  cautery  point  to  the  thoracic  region,  or, 
better  still,  an  issue  which  is  allowed  to  suppurate  ;  this  issue,  which  is  an 
old  therapeutic  measure,  and  has  been  too  much  neglected  in  our  time,  gives 
excellent  results.  I  also  recommend  an  ice-bag  day  and  night  over  the  heart. 
To  avoid  the  weight  of  the  ice-bag  we  should  suspend  it  from  a  hook,  and  to 
avoid  erythema  we  must  protect  the  skin  of  the  precordial  region  with  lint 
or  oiled  silk.  Injections  of  morphin  or  heroin  may  be  given  in  doses  of 
i  grain ;  aspirin,  and  antipyrin,  are  of  much  service. 


DISEASES  OF  THE  VESSELS  525 

With  these  various  therapeutic  measures  we  may  also  employ  suspension, 
as  in  my  case,  for  it  has  a  beneficial  effect  upon  the  pains  of  tabes ;  prudence 
and  moderation  must,  however,  be  observed,  for  a  crisis  of  angina  pectoris 
arising  during  suspension  would  have  dire  results. 


X.  ANGINA  PECTORIS. 

Description. — The  cardiac  neuralgia  w^hich  is  called  angina  pectoris 
(Heberden)  is  a  painful  affection  that  supervenes  in  the  forms  of  attacks. 
The  patient  is  suddenly  seized  ^^^tll  an  attack,  which  may  come  on  without 
appreciable  cause,  or  as  the  result  of  emotion,  fatigue,  shght  exercise,  or  a 
somewhat  hearty  meal.  In  the  region  of  his  heart,  along  the  left  border 
of  the  sternum,  he  feels  a  stabbing  pain,  which  radiates  to  the  neck,  the 
epigastrium,  or  the  thorax.  As  a  rule,  the  pain  affects  the  left  arm,  the 
hand,  and  the  last  two  fingers  (area  of  the  ulnar  nerve),  while  the  skin  of  the 
hand  becomes  pale.  When  the  attack  is  violent,  the  pain  is  accompanied  by 
an  appalling  sensation  of  constriction  and  dyspnoea,  and  the  patient,  who  is 
bathed  in  a  cold  sweat,  feels  as  though  gripped  in  a  vice,  or  squeezed  by  an 
enormous  weight.  Suffocation  and  syncope  appear  imminent,  and  the  un- 
fortunate sufferer,  who  can  neither  speak  nor  move,  remains  quite  con- 
scious, and  experi3nces  the  inexphcable  feeling  of  impending  death.  "  It  is 
as  though  there  were  a  momentary  cessation  of  life  "  (Eisner).  The  attack 
lasts  some  seconds  or  some  minutes,  and  then  disappears,  leaving  the  follow- 
ing traces  :  Jiurabness  of  the  left  arm,  swelhng  of  the  testis  (Laennec),  urgent 
desire  to  urinate,  eructation  of  gas,  vomiting,  and  marked  lassitude. 

The  attack,  however,  is  not  always  of  the  classical  form  just  described. 
The  pain  which  starts  from  the  heart,  radiates  in  the  most  diverse  manner  ; 
it  may  not  be  hmited  to  the  left  side,  but  may  invade  the  arm  and  hand  on 
both  sides,  spread  up  the  neck  as  far  as  the  articulation  of  the  jaw,  descend 
towards  the  epigastrium,  and  surround  the  trunk  like  a  girdle,  or  pass  down 
into  the  groin  as  far  as  the  testis.  The  pain  may  follow  an  inverse  course, 
starting  in  the  hand  and  rapidly  travelling  up  towards  the  chest  like  an 
aura.  This  fact  led  Trousseau  to  suppose  that  angina  pectoris  is  sometimes  a 
manifestation  of  epilepsy — that  is,  an  epileptiform  neuralgia. 

During  the  attack,  and  in  spite  of  the  imminence  of  suffocation,  ausculta- 
tion reveals  no  abnormal  sounds  ;  the  heart  beats  arc  normal  or  slow  ;  they 
may  be  irregular,  if  the  angina  is  associated  with  cardio-aortic  k\sious  ;  in 
some  cases  they  are  hurried. 

In  some  patients  the  symptoms  are  of  a  different  character,  and  the 
attack  of  pain  is  sometimes  replaced  by  attacks  of  dyspnoea,  with  or  without 
palpitation.      The  dyspnoea  is  at  times  so  marked  that  the  painful  clement 


526  TEXT-BOOK  OF  MEDICINE 

is  of  secondary  moment.     This  agonizing  and  paroxysmal  dyspnoea  some- 
what recalls  the  severe  dyspnoea  of  uraemia. 

In  many  cases  angina  pectoris  is  not  acute  ;  the  patient  constantly  ex- 
periences for  weeks  or  months  continuous  or  intermittent  pain  in  the  left 
arm,  with  a  feeling  of  discomfort  and  oppression  in  the  precordial  region. 
This  chronic  condition  is  sometimes  interrupted  by  acute  attacks.  Loss  of 
appetite,  saUvation,  constipation,  and  ballooning  of  the  belly  are  common 
during  the  attacks. 

^Etiology.- — Angina  pectoris  and  its  varieties  may  be  the  result  of  many 
causes.  In  some  cases  it  is  a  neuralgia  which  is  independent  of  any  appreci- 
able lesions,  though  sometimes  complicated  by  neuritis  ;  it  is  most  often 
associated  with  lesions  of  the  aorta  and  coronary  arteries.  In  order  to 
simjDlify  the  cjuestion  of  pathogenesis,  I  would  thus  state  the  case  : 

In  the  first  variety  angina  pectoris  is  the  result  of  some  lesion  of  the  aorta 
and  coronary  arteries.  The  coronaritis  usually  affects  both  coronary 
arteries.  The  lesions  of  atheroma,  endarteritis,  and  arterio-sclerosis  of  the 
coronary  arteries  produce  stenosis,  and  may  end  in  obUteration.  Ischemia 
of  the  heart,  symptoms  of  angina  j)ectoris,  and  sudden  death  may  be  the 
result.  All  cases  of  aortitis,  whether  acute  or  chronic,  infective,  syphihtic, 
gouty,  or  atheromatous,  favour  tliis  variety. 

Angina  pectoris  resulting  from  aortic  lesions  without  affection  of  the 
coronary  arteries  belongs  to  the  second  variety.  Under  Syphihtic  Aortitis  I 
have  given  the  report  of  two  patients  who  died  from  angina  pectoris  ;  the 
autopsy  demonstrated  the  presence  of  aortic  lesions,  and  the  complete  per- 
meability of  the  coronary  arteries.  This  proves  that -ischemia  of  the  heart, 
consecutive  to  coronaritis  obhterans,  is  not  indispensable  to  a  fatal  attack  of 
angina  pectoris,  although  some  authors  hold  a  different  opinion. 

Cases  of  angina  pectoris  without  aortic  lesions  and  coronaritis  are  placed 
in  the  third  variety,  and  comprise  neuralgia  and  neuritis  of  the  cardiac 
plexus,  which  are  similar  to  the  neuralgias  of  the  facial,  sciatic,  and  other 
nerves. 

Tumours  of  the  mediastinum  which  are  close  to  the  cardiac  plexus  may 
excite  the  neuralgia  or  the  neuritis  which  provokes  angina  pectoris.  In 
these  cases  inflammation  or  neuritis  of  the  cardiac  plexus,  with  or  without 
participation  of  the  phrenic  nerve,  has  been  found  at  the  autopsy  (Lan- 
cereaux,  Peter). 

In  the  form  of  neuralgia  angina  pectoris  is  associated  with  epilepsy, 
hysteria,  cerebro-cardiac  neuropathy  (Krishaber),  diabetes  (Vergely),  and 
Brightism  (personal  case)  ;  it  is  also  caused  by  the  abuse  of  tobacco  (Beau), 
tea,  or  coffee.  The  gouty  diathesis  may  show  itself  by  angina  pectoris,  just 
as  it  does  by  migraine  or  by  attacks  of  asthma.  Rheumatism  may  also  lead 
to  cardiac  neuralgia ;  angina  pectoris  sometimes  appears  during  an  attack 


DISEASES  OF  THE  VESSELS  527 

of  acute  rheumatism,  while  at  other  times  it  is  essentially  rheumatic,  thouf^h 
the  patient  has  not  yet  suffered  from  articular  rheumatism  (Viguier). 

In  the  preceding  chapter  I  have  quoted,  among  others,  Vulijian's  remark- 
able case  of  a  tabetic  who  suffered  from  angina  pectoris  :  post  mortem 
Vulpian  found  no  trace  of  any  aortic  lesion ;  the  case  was  one  of  cardiac 
visceralgia.  Tabetic  patients  have  crises  of  cardiac  neuralgia,  just  as  they 
have  neuralgic  crises,  affecting  the  stomach,  rectum,  urethra,  etc. 

According  to  some  authors,  every  true  angina  pectoris  is  due  to  con- 
striction of  the  coronary  arteries  and  consecutive  ischemia  of  the  heart, 
while  the  other  varieties  are  false  angina  pectoris. 

These  authors,  therefore,  would  make  two  great  classes  of  angina  pectoris. 
In  the  one  they  would  place  angina  pectoris  with  lesions  of  the  coronary 
arteries — that  is,  the  true  and  fatal  form  ;  in  the  other  class  they  would  place 
cases  of  angina  pectoris,  neuralgia,  or  neuritis  without  lesions  of  the  coronary 
arteries — that  is,  the  false  and  not  fatal  form. 

This  division  is,  however,  in  my  opinion,  too  absolute.  I  am  ready  to 
admit  that  stenosis  and  lesions  of  the  coronary  arteries  are  the  chief  cause  of 
the  disease  in  many  cases,  but  I  cannot  subscribe  to  a  classification  which 
would  di\'idc  angina  pectoris  into  two  well-marked  categories,  the  one  com- 
prising true  angina,  which  is  usually  grave  and  too  often  fatal,  while  the 
other  concerns  false  angina,  which  is  looked  upon  as  an  almost  neghgible 
quantity.  I  agree  that  a  patient  who  has  coronaritis  obhterans  mav  be 
harder  hit  than  one  who  has  not,  but  this  is  no  reason  for  sapng  that  the 
latter  is  a  false  angina  ;  indeed,  so  httle  is  this  form  a  false  angina  that  the 
attacks  may  be  acute,  painful,  and  fatal.  At  the  Saint- Antoine  and  Xecker 
Hospitals  I  witnessed  two  deaths  from  angina  pectoris  ;  the  autopsy  was 
made  with  every  possible  care.  Both  patients  had  chronic  aortitis  ;  in  one 
of  them  the  aortitis  was  syphihtic  and  accompanied  by  small  multiple 
aneurysms,  but  in  both  the  coronary  arteries  were  quite  free.  We  cannot, 
then,  speak  of  true  and  false  angina,  but  we  must  admit  cases  which  are  more 
or  less  formidable,  but  which  may  all  prove  fatal.  As  regards  prognosis,  how 
can  we  affirm  that  the  coronary  arteries  are  or  are  not  affected  during  life  ? 
I  tliink,  therefore,  practically  speaking,  that  every  patient  who  suffers  from 
angina  pectoris  may  die  of  it. 

Finally,  whatever  is  the  primary  cause  of  angina  pectoris,  whether  it  be 
ischemia  of  the  heart  or  not,  whether  the  initial  lesion  affects  the  aorta  alone, 
or  the  aorta  and  the  coronary  arteries,  or  the  coronary  arteries  without  the 
aorta,  the  cardiac  plexus,  with  its  afferent  and  efferent  nerves,  is  the  starting- 
})oint  of  the  symptoms.  The  whole  cardiac  plexus,  including  the  branches 
of  the  vagus,  the  great  sympathetic  and  the  gangUa,  may  take  part.  The 
richness  of  tliis  })lexus,  the  importance  of  its  nerves,  and  its  numerous 
anastomoses,  explain  both  the  gravity  and  the  diversity  of  the  symptumd. 


528  TEXT-BOOK  OF  MEDICINE 

The  radiations  of  pain,  or  synaesthesiae,  modify  the  symptomatic  expression 
of  the  attack,  which,  according  to  circumstances,  shows  itself  by  pain, 
dyspnoea,  or  syncope,  or  by  the  whole  symptom-complex.  The  cardiac 
plexus,  by  its  pneumogastric  or  its  sympathetic  branches,  holds  the  symptoms 
of  angina,  asphyxia,  precordial  pain  and  syncope  under  its  sway.  The 
reaction  on  the  brachial  plexus,  and  especially  on  the  ulnar  nerve,  explains 
the  pain  in  the  hand  and  the  little  finger.  When  the  attack  is  more 
generalized,  the  diversity  of  the  pains  is  in  relation  with  the  nerves  affected 
by  the  neuralgia,  and  in  this  way  we  can  explain  the  sensations  of  strangula- 
tion and  oesophagism  (fibres  of  the  pneumogastric),  the  thoracic  constriction 
and  pain  at  the  insertion  of  the  diaphragm  (phrenic  nerve),  the  pallor, 
sweating,  prostration,  and  chilling  of  the  extremities  (radiation  to  the  great 
sympathetic)  (Peter). 

Course. — The  first  attacks  of  angina  pectoris  are  generally  slight  or 
transient,  and  do  not  as  yet  show  the  severity  which  they  acquire  later.  In 
some  cases,  however,  the  first  attack  may  be  fatal.  I  was  present  at  the 
death  of  one  of  the  most  distinguished  physicians  at  the  Saint-Louis 
Hospital,  who  died  in  his  first  attack.  Some  individuals  (though  this  is 
rare)  remain  free  after  a  single  attack  ;  as  a  rule,  the  crises,  wliich  appear  at 
first  at  long  intervals,  occur  at  closer  intervals,  and  finally  come  on  every 
week  or  every  day.  Sometimes  the  patient  has  some  respiratory  distress, 
precordial  constriction,  numbness  of  the  arm,  or  aching  pain  in  the  region  of 
the  aorta  ;  tliis  condition  may  last  for  weeks  and  months,  quite  apart  from 
the  attacks.  The  attacks  are  frequently  periodic,  and  return  at  a  fixed  hour, 
whether  the  neuralgia  is  or  is  not  symptomatic  of  a;n  organic  lesion ;  the 
periodicity  is  not,  then,  a  distinctive  sign  in  favour  of  pure  neuralgia. 

The  chances  of  cure  are  greater,  and  the  prognosis  is  more  favourable 
when  angina  pectoris  is  not  associated  with  lesions  of  the  coronary  arteries 
or  of  the  aorta  ;  the  prognosis  is  certainly  less  grave  when  the  disease  is  only 
a  simple  neuritis  (hysteria,  smoker's  heart).  Angina  pectoris,  however,  is 
always  formidable,  for  sudden  death  and  fatal  syncope  are  only  too  frequent. 

Diagnosis. — The  diagnosis  of  angina  pectoris  is  sometimes  difficult, 
because  of  the  variations  in  the  symptoms.  Pleurodynia  of  the  precordial 
region  is  characterized  by  superficial  pains,  which  are  limited  to  the  muscles, 
and  do  not  radiate  beyond  the  invaded  parts.  Cervico- brachial  and 
thoracic  neuralgias  are  Hmited  to  the  course  of  the  diseased  nerves ;  they 
show  painful  fixed  points,  and  do  not  arise  with  the  suddenness  of  angina 
pectoris.  It  must  not  be  forgotten  that  angina  pectoris  is  often  only  an 
epiphenomenon  or  an  advance  sign  in  lesions  of  the  aorta  and  of  the 
mediastinum ;  it  is  frequently  the  first  warning  of  aneurysm  of  the  aorta, 
and  in  such  a  case  it  is  imperative  to  diagnose  the  cause.  At  other  times, 
instead  of  appearing  in  the  complete  form,  the  angina  is  only  indicated  by 


DISEASES  OF  THE  VESSELS  529 

one  of  its  symptoms,  such  as  numbness  in  the  left  arm,  pain  hmited  to  the 
Httle  finger,  or  a  sensation  of  constriction  and  agony  in  the  region  of  the 
heart.     These  defaced  forms  should  be  recognized. 

Neuralgia  of  the  phrenic  nerve,  whether  primary  or  consecutive  to 
diaphragmatic  pleurisy  or  to  acute  pericarditis,  shows  itself  by  a  complex 
of  symptoms  (situation  of  the  pain,  dyspnoea,  hiccough),  wliich  permits  the 
distinction  from  cardiac  neuralgia ;  but  neuralgia  of  the  phrenic  nerve  is 
sometimes  associated  directly  (neuritis)  or  indirectly  (reflex  radiation)  with 
neuralgia  of  the  cardiac  plexus.  There  is  in  these  cases  an  "  association  of 
pains  which  depends  on  the  innervation  of  the  circulation  by  the  cardiac 
plexus  and  on  that  of  the  respiration  by  the  phrenic  nerve"  (Peter). 

Hysterical  angina  pectoris  merits  special  mention,  and  the  diagnosis 
must  rest  on  the  following  considerations  :  The  attack  usually  occurs  at 
night ;  hysterogenic  zones  are  found  in  the  precordial  and  sternal  regions, 
and  the  aura  begins  with  hypersesthesia  at  these  spots.  Hysterical  angina 
pectoris  ends  in  tears,  and  is  provoked  by  moral  causes,  while  angina,  which 
is  not  hysterical,  is  brought  on  by  physical  causes  (fatigue,  walking,  strain). 

Treatment. — The  first  indication  is  to  eradicate  every  cause  (emotion, 
fatigue,  hearty  meals,  and  excess  of  tobacco)  that  is  capable  of  producing 
an  attack  ;  the  second  indication  is  to  treat  the  disease  (gout,  rheumatism, 
or  syphilis)  of  which  the  angina  is  sometimes  only  a  manifestation. 

During  the  attack  morphia  and  ice  appear  to  me  to  be  the  best  treat- 
ment. One  or  more  subcutaneous  injections  of  morphia  are  given,  and  ice- 
bags  are  apphed  to  the  precordial  region.  We  may  add  inhalations  of 
chloroform  or  of  ether  to  these  methods.  Local  blood-letting  and  the 
apphcation  of  leeches  or  cupping  to  the  painful  region  often  give  good 
results. 

Aspirin  renders  much  service.  Tliirty  grains  of  aspirin,  divided  into 
two  cachets,  are  given  every  two  hours.  I  must  also  mention  nitrite  of  amyl 
in  capsules;  inhalation  of  a  few  drops  at  times  brings  about  immediate 
improvement. 

Blisters,  issues,  or  the  cautery  may  be  applied  over  the  painful  region 
between  the  attacks.  In  a  case  in  which  painful  symptoms  had  persisted  for 
a  long  while,  I  ordered  ice-bags,  which  were  changed  day  and  night,  to  the 
precordial  region  for  several  weeks  ;  in  tliis  case  the  skin  must  be  carefully 
protected  by  means  of  lint  or  flannel  to  avoid  erythema.  In  the  case  to 
which  I  have  alluded  the  patient  found  such  relief  from  the  permanent 
application  of  ice  that  she  went  about  without  removing  the  bags. 

The  question  of  angina  pectoris,  when  associated  with  syphilitic  lesions 
of  the  aorta,  has  been  d^alt  with  in  one  of  the  preceding  sections,  so  I  shall 
not  refer  to  it  again  ;  but  the  physician  should  remember  the  possibility,  and 
give  injections  of  mercury  if  necessary. 

34 


530  TEXT-BOOK  OF  MEDICINE 

Every  individual  who  is  subject  to  angina  pectoris,  whatever  its  cause, 
must  give  up  tobacco,  tea,  alcohol,  and  coffee  ;  he  must  avoid  emotion, 
hearty  meals,  and  violent  exercise.  He  will  also  experience  benefit  from 
treatment  which  lowers  the  arterial  tension  (Huchard). 


XL  ARTERIAL  TENSION— HYPERTENSION- 
HYPOTENSION. 

The  study  of  arterial  tension  has  become  the  order  of  the  day,  and 
cUnicians  attach  special  importance  to  the  variations  which  the  tension 
undergoes  in  different  morbid  conditions. 

Professor  Potain  was  one  of  the  first  to  invent  a  practical  method  of 
estimating  the  arterial  tension  ;  his  researches  have  given  interesting  results, 
but  they  have  been  chiefly  confined  to  the  pressure  in  the  peripheral  vessels, 
such  as  the  radial  artery.  Mosso,  Bouloumie,  and  others,  have  recently  drawn 
attention  to  the  blood-pressure  in  the  smallest  vessels,  and  have  described  the 
changes  in  the  "  arterio-capillary  tension." 

Technique.^I  shall  describe  here  Potain  and  Bouloumie's  instruments 
for  measuring  the  arterial  or  arterio-capillary  pressure,  because  they  are  the 
most  practical.  The  first  apparatus,  called  the  "  sphygmomanometer,"  is 
composed  of  a  dial  manometer  and  an  indiarubber  tube,  which  ends  in  a 
small  ampulla  filled  with  air.  The  ampulla  is  applied  over  the  radial 
artery  so  as  to  obhterate  the  pulse  ;  the  number  indicated  by  the  needle 
expresses  the  arterial  pressure  in  centimetres  of  mercury. 

The  second  apparatus  has,  in  addition,  a  rubber  finger-stall,  with  which 
the  end  of  the  finger  is  compressed  till  the  anaemia  is  complete.  The  needle 
indicates  the  pressure  produced  by  the  reappearance  of  the  circulation  in 
the  pulp  of  the  finger. 

It  is  well  to  take  the  blood-pressure  apart  from  digestion,  and  in  the 
recumbent  position. 

The  mean  reading  in  a  normal  person  varies  from  14  to  18  for  the 
radial  jsressure,  and  from  11  to  13  for  the  arterio-capillary  pressure.  The 
tension  is  usually  higher  at  night  than  in  the  morning  ;  it  is  affected  by  food, 
emotion,  and  temperature.  It  is  not  as  high  in  women  as  in  men,  and 
increases  in  proportion  to  the  age. 

As  a  rule,  though  it  is  not  an  absolute  one,  the  heart-beats  are  slowed 
in  proportion  to  the  increase  of  the  blood-pressure. 

Ahmentary  products  and  certain  drugs  (adrenahn,  ergotin)  modify  the 
blood-pressure  in  a  more  or  less  lasting  manner ;  the  most  interesting 
variations,  however,  occur  in  pathological  conditions. 

Most  diseases  influence  the  arterial  tension ;  some  cause  a  rise,  others  a 


DISEASES  OF  THE  VESSELS  531 

fall.  The  limit  of  hypertension  and  of  hypotension  is  somewhat  artificial ; 
we  speak  of  hypertension  when  the  reading  exceeds  18  for  the  radial  and  14 
for  the  digital  pressure ;  of  hypotension  when  the  figures  are  below  14  and  10. 

Hypertension. 

Transient  hypertension  may  occur  in  many  morbid  states  :  eclampsia  and 
cerebral  haemorrhage,  lead-poisoning,  tobacco-poisoning,  acute  vascular 
affections,  aortitis,  pericarditis. 

Lasting  hypertension  depends  upon  two  factors — Bright's  disease  and 
arterio-sclerosis.  Potain  in  particular  has  called  attention  to  the  arterial 
hypertension  in  Bright's  disease  ;  it  may  be  as  high  as  24,  26,  or  even  30  centi- 
metres, and  it  is  so  common  as  to  be  an  indication  of  the  highest  importance. 

Atheroma  and  arterio-sclerosis  are  most  often  accompanied  by  notable 
increase  of  blood-pressure,  and  it  is  possible  that  in  some  cases  the  hyper- 
tension precedes  the  usual  manifestations  of  arterial  atheroma  (Huchard). 

Apart  from  these  two  factors,  diabetes  and  certain  forms  of  dyspepsia 
may  perhaps  play  some  part.  Bosc  and  Vedel  have  admitted  in  some 
subjects  a  kind  of  hereditary  predisposition  to  hypertension,  and  hydropathic 
hypertension  has  been  described,  though  its  nature  is  somewhat  indefinite  ; 
the  tendency  is,  however,  to  attribute  it  to  hypersecretion  of  the  suprarenal 
glands  and  of  the  pituitary  body. 

Symptoms. — The  first  symptom  of  hypertension  is  a  rise  in  the  arterial 
tension  to  20  centimetres  of  mercury  or  more,  and  in  the  capillary  ten- 
sion to  15  or  18. 

The  radial  pulse  is  hard  ;  the  temporal  artery  is  tortuous  ;  the  heart- 
beats are  violent,  and  the  second  sound  in  the  aortic  area  is  ringing  ;  a  white 
line  made  with  the  nail  on  the  abdominal  wall  lasts  only  one  or  two  seconds. 

In  addition  to  these  physical  signs,  Vaquez  has  grouped  certain  functional 
symptoms  into  a  syndrome  :  convulsions,  which  appear  in  eclampsia  as  well 
as  in  uraemia  and  saturnism,  and  resemble  general  or  partial  epilepsy ; 
amaurosis  without  change  in  the  fundus  oculi,  but  with  headache  and 
increased  ocular  tension ;  homonymous  hemianopsia ;  progressive  changes  in 
vision,  which  follow  the  variations  in  the  arterial  tension  ;  transient  aphonia, 
which  appears  and  disappears  suddenly ;  vertigo  ;  pulsation  in  the  arteries  of 
the  neck ;  hot  flushes ;  sweating ;  pallor  of  the  face ;  heaviness  in  the  limbs. 
Some  Avriters  would  set  down  to  hypertension  the  dead  fingers,  and  the 
crya3sthesia  I  have  noted  in  Brightism,  the  repeated  attacks  of  pulmonary 
congestion,  the  crises  of  angina  pectoris,  and  certain  troubles  of  a  neuras- 
thenic nature,  mental  depression,  transient  attacks  of  mania,  and  obsession. 
Shght  jaundice  may  exist  in  persons  whose  tension  is  high.  Sudden  death  is 
sometimes  seen,  and  lumbar  puncture  or  post-mortem  examination  may 
show  scattered  haemorrhages  in  the  meninges.    Hypertension,  therefore,  has 

34—2 


532  TEXT-BOOK  OF  MEDICINE 

a  varied  symptomatology,  which  has  been  gradually  enriched  by  signs 
formerly  attributed  to  the  diseases  which  it  accompanies.  The  pathogenesis 
of  hypertension  has  been  much  discussed.  It  is  often  due  to  peripheral  vaso- 
constriction, which  may  follow  true  lesions  or  spasmodic  troubles,  or  may  be 
the  result  of  toxic  or  mechanical  phenomena.  An  undeniable  part  is  played 
by  the  sympathetic  nerves,  the  lesions  of  arterio-sclerosis,  and  poisoning  due 
to  lead  or  tobacco. 

In  arterio-sclerosis  we  may  ask  whether  hypertension,  as  Huchard  says, 
is  the  cause,  and  not  rather  the  consequence,  of  vascular  lesions ;  in  renal 
impermeability  we  do  not  know  whether  it  results  from  retention  of  toxic 
products  or  simply  of  chloride  of  soda,  or  from  increase  in  the  mass  of  the 
blood. 

The  theory  of  Vaquez  deserves  special  mention.  He  has  found  changes  in 
the  suprarenal  glands,  and  has  set  down  hypertension  as  a  manifestation  of 
the  vasotonic  hypersecretion  of  these  glands.  As  the  hypertensive  action  of 
the  pituitary  body  is  well  known,  we  may  admit  the  existence  of  hypertension 
from  overactivity  of  this  body. 

The  prognosis  is  serious.  In  addition  to  the  immediate  complications 
already  noted,  we  must  not  forget  that  the  overwork  to  which  the  arteries 
are  subjected  may  lead  to  permanent  hypertrophy  of  the  muscular  coat, 
and  even  to  atheroma  (Huchard). 

Treatment. — Prophylaxis  consists  in  avoiding  tobacco,  spiced  foods, 
meat  diet,  and  alcohol.  Curative  treatment  comprises  lacto- vegetarian  diet 
and  rigid  hygiene  ;  we  must  give  drugs  which  lower  the  tension  and  dilate  the 
vessels— e.gr.,  nitrites  and  iodides,  purgatives,  diuretics;  in  severe  cases, 
bleeding  is  useful. 

Dechlorination  and  carbonic-acid  baths  are  often  of  service. 

Hypotension. 

Hypotension  may  be  transient  or  lasting.  In  the  former  case  it  appears  in 
most  infectious  maladies,  in  many  forms  of  poisoning,  and  in  acute  cardio- 
vascular affections  ;  in  the  latter  case  it  is  seen  in  Basedow's  disease,  in 
myocarditis  and  chronic  diseases  of  the  pericardium  and  the  heart,  and  in 
chronic  tuberculosis  ;  finally,  it  is  one  of  the  classical  symptoms  in  Addison's 
disease.  The  syndrome  of  arterial  hypotension  is  not  so  complete  as  that 
of  hypertension.  The  manometer  reading  may  be  as  low  as  8  or  10  centi- 
metres. The  pulse  is  small  and,  as  a  rule,  rapid ;  the  line  made  by  the  nail 
remains  white  for  a  long  while.  We  may  also  find  sluggish  peripheral 
circulation,  cyanosis,  coldness  of  the  extremities,  oedema,  passive  congestion 
of  the  liver,  and  oliguria.  This  syndrome  is  typical  in  Addison's  disease,  and 
may  be  called  the  syndrome  of  hypotension  or  asystole. 

The  pathogenesis  is  readily  summed  up  :  when  vascular,  it  is  due  to  some 


DISEASES  OF  THE  VESSELS  533 

obstacle  at  the  periphery ;  when  toxic,  it  may  be  put  down  to  the  action  of  the 
toxines  upon  the  vessels  and  the  vasomotor  system.  The  part  played  by 
the  tubercle  bacillus  and  its  products  in  these  cases  is  well  known.  The 
pathogenesis  of  hypotension  in  Addison's  disease  is  of  great  interest,  because 
it  is  proof  of  the  insufficiency  of  the  suprarenal  secretion.  It  is  possible  that 
similar  insufficiency  exists  in  acute  suprarenaUtis,  and  in  infectious  disorders 
and  that  we  must  give  to  it  its  share  in  the  production  of  the  hypotension 
which  is  often  found, 

Renon  and  Azam  have  recently  put  forward  a  similar  theory  as  to 
insufficiency  of  the  pituitary  secretion  in  the  infections. 

The  treatment  consists  in  the  exliibition  of  cardio -vascular  tonics,  when 
the  low  tension  is  dependent  on  some  cardiac  lesion. 

In  Addison's  disease  good  results  have  followed  the  use  of  suprarenal 
extract  and  of  adrenahn.  Opotherapy  has  been  employed  in  some  infectious 
diseases  ;  capsular  extract  has  appeared  to  be  of  some  slight  use.  Renon  and 
Debille  have  given  their  patients  pituitary  extract. 


PART  III 

DISEASES  OF  THE  DIGESTIVE  SYSTEM 

CHAPTER  I 
DISEASES  OF  THE  MOUTH 

I.  ERYTHEMATOUS  STOMATITIS. 

Description. — Inflammation  of  the  mouth  is  called  stomatitis  {arofxa, 
mouth).  Erythematous  stomatitis  (buccal  catarrh)  is  the  most  frequent 
variety ;  it  is  met  with  at  all  ages.  Its  usual  causes  are  dentition,  the 
eruption  of  the  wisdom  teeth,  dental  caries,  artificial  teeth,  abuse  of  tobacco 
and  highly-spiced  foods,  diinldng  of  hot  liquids,  accumulation  of  tartar,  and 
oral  sepsis.  The  various  micro-organisms  in  the  mouth  play  a  large  part 
in  its  causation.  Erythematous  stomatitis  is  also  associated  with  digestive 
troubles,  and  often  accompanies  catarrh  of  the  stomach.  Patients  with 
Bright's  disease  sometimes  have  stomatitis,  which  has  a  tendency  to  ulcerate. 
It  is  not  yet  decided  whether  this  is  due  to  the  elimination  of  toxic  principles 
or  to  the  association  of  the  microbes  in  the  mouth. 

Stomatitis  is  ushered  in  by  pain,  which  is  aggravated  by  heat,  cold, 
contact  with  food,  and  movements  of  mastication.  The  mouth  is  hot,  dry, 
and  clammy ;  the  breath  is  offensive,  and  the  sense  of  taste  blunted. 

The  inflammation  of  the  mucous  membrane  is  often  limited  to  a  specified 
region,  such  as  the  cheeks,  the  tongue,  the  roof  of  the  palate,  or  the  gums. 
The  inflamed  mucous  membrane,  which  is  red,  dry,  and  sliining,  is  covered, 
according  to,  the  region,  with  papillae,  or  swollen  glands.  On  the  edges  of  the 
gums  we  find  opalescent  epithelial  patches.  Where  the  mucous  membrane 
is  hned  with  loose  connective  tissue,  as  on  tlie  cheeks  or  on  the  hps,  swelhng 
and  oedema  are  seen.  In  places,  desquamation  of  the  epithelium  causes 
erosions  and  superficial  ulcers,  which  are  very  painful.  The  reaction  in  the 
Bubmaxillary  glands  is  but  sliglit. 

The  course  and  duration  of  the  disease  depend  on  the  cause.  Stomatitis 
may  be  kept  up  or  revived  by  dental  caries,  slow  eruption  of  the  wisdom 
teeth,  or  accumulation  of  tartar.  Chronic  gingivitis  is  frequent  in  diabetic 
patients  ;  the  teeth  often  fall  out  in  consequence.     Erythematous  stomatitis 

534 


DISEASES  OF  THE  MOUTH  535 

readily  yields  to  mouth-washes  of  borate  of  soda,  or  to  pastilles  and  lotions 
of  chlorate  of  potash.  Frequent  cleansing  of  the  mouth  with  antiseptic 
solutions,  such  as  thymol  (1  in  100),  or  chloral  hydrate  (1  in  100),  may  be 
prescribed.     The  cause  of  the  stomatitis  must  be  carefully  looked  for. 

II.  MERCURIAL  STOMATITIS. 

ffitiology. — Whether  mercury  is  introduced  into  the  system  by  the 
skin,  the  respiratory  organs  (mercurial  vapours),  the  mucous  membranes,  or 
the  digestive  system,  the  drug  is  partly  eUminated  by  the  saUvary  glands, 
and  its  action  on  the  mucous  membrane  produces  an  inflammation  called 
"  mercurial  stomatitis." 

Gilders,  fitters,  looking-glass  makers,  miners  who  live  in  the  midst  of 
metalhc  vapours,  and  hatters  who  handle  nitrate  of  mercury,  are  especially 
liable  to  poisoning.  Mercurial  preparations  given  in  syphihs  by  inunction, 
by  subcutaneous  injections,  or  by  the  mouth,  may  cause  stomatitis,  which 
varies  in  severity  according  to  the  susceptibility  of  the  individual.  One 
patient  can  tolerate  repeated  inunctions  of  mercury,  whilst  another  contracts 
stomatitis  after  a  single  inunction  of  mercurial  ointment.  Mercurial  stoma- 
titis is  almost  unknown  when  hypodermic  injections  of  the  biniodide  are 
used.  I  have  during  the  last  few  years  given  more  than  ten  thousand 
injections  of  biniodide  of  mercury,  and  I  have  not  noticed  the  least  accident. 

Pathogenesis, — The  nature  of  mercurial  stomatitis  has  been  much  dis- 
cussed. It  was  formerly  regarded  as  purely  toxic,  but  it  is  now  considered  a 
septic  condition  (Galippe).  It  seems'  to  me  difficult  not  to  admit  that  the 
condition  is  most  often  infective,  the  mercury  leading  to  more  rapid  multi- 
pUcation  of  the  microbes  in  the  mucous  membrane  when  previous  gingivitis 
and  dental  changes  have  occurred. 

Description, — Mercurial  stomatitis  may  be  acute  or  chronic.  The 
inflammation  usually  starts  behind  the  last  molar  tooth  of  the  side  upon 
which  the  patient  sleeps  (Ricord).  The  symptoms  are  most  marked  in  the 
lower  jaw  and  in  the  neighbourhood  of  decayed  teeth.  From  the  first  the 
patient  complains  of  a  metallic  taste  in  the  mouth,  of  irritation,  and  of  heat 
and  pain  at  the  angle  of  the  jaws.  The  breath  rapidly  becomes  foetid ; 
mastication  is  painful ;  the  gums  are  soft,  swollen,  and  bleed  easily.  The 
mouth,  which  is  at  first  dry,  is  soon  filled  with  saliva.  These  cases  have  been 
called  the  stomatites  d'alarme  (Fournier). 

When  tlie  above  symptoms  alone  are  present,  mercurial  stomatitis  yields 
to  treatment  in  a  few  days  ;  we  see,  however,  severe  forms,  which  were  more 
common  when  it  was  customary  to  provoke  and  keep  up  salivation  in 
the  treatment  of  syphilis.  In  these  grave  forms  (Fournier)  the  inflam- 
mation invades  the  alveolar  periosteum.     The  teeth  are  laid  bare  and 


536  TEXT-BOOK  OF  MEDICINE 

loosened.  The  inside  of  the  cheeks  becomes  swollen^  and  shows  the  mark  of 
the  teeth,  while  the  tongue  becomes  much  enlarged.  The  inflamed  parts 
are  reddish,  and  show  ulcers  which  are  covered  by  a  greyish  pultaceous 
fur.  The  sahva  flows  from  the  mouth  day  and  night  in  such  quantity  that 
it  may  amount  to  6  or  8  pints  in  twenty-four  hours.  The  saliva  contains 
mercury  in  small  quantities,  and  bleaches  gold.  Deglutition  becomes 
diflS.cult,  the  breath  is  horribly  foetid,  the  fever  is  high,  diarrhoea  appears, 
and  the  patient  sinks  into  profound  anaemia. 

We  may  see  still  more  terrible  forms,  in  which  the  oedema  extends  rapidly 
to  the  pharynx  and  the  sublaryngeal  tissues,  and  reaches  the  submaxillary 
region.  The  general  induration  and  the  enormous  swelhng  of  the  tongue 
make  deglutition  impossible,  and  threaten  the  patient  with  asphyxia. 
Sahvation,  fever,  and  insomnia  wear  out  the  suSerer,  and  at  times  bring 
about  a  fatal  termination.  When  mercurial  stomatitis  reaches  the  chronic 
stage,  the  acute  symptoms  disappear,  but  the  swelling  of  the  mucous  mem- 
brane and  the  ulcers  persist.  The  teeth  gradually  fall  out,  and  the  jaws  may 
become  necrosed.  In  some  cases  it  is  clironic  from  the  first.  The  acute 
symptoms  are  absent,  the  ptyalism  is  insignificant,  and  the  ulceration  of  the 
gums  is  not  marked  ;  but  the  alveolar  periosteum  is  attacked,  and  the  teeth 
are  laid  bare,  and  finally  fall  out.  This  exceptional  form  has  been  observed 
amongst  the  miners  of  Almaden  (Roussel). 

Pathological  Anatomy. — The  lesions  of  the  mucous  membrane,  formerly 
considered  as  due  to  common  stomatitis,  are  said  to  have  a  certain  specific 
character.  In  several  patients  Delbanco  has  noted  hypertrophy  of  the 
sebaceous  glands  in  the  mouth,  which  form  yellowish  grains  about  the  size 
of  a  pin's  head.  Histological  examination  has  proved  that  they  are  enlarged 
acinous  glands,  identical  with  the  sebaceous  glands  of  the  skin. 

Diagnosis. — The  diagnosis  rests  on  the  aetiology,  which  permits  us  to 
distinguish  the  mercurial  from  the  other  forms  of  stomatitis  with  severe 
ptyalism — e.g.,  uraemic  stomatitis. 

Treatment. — The  treatment  may  be  summed  up  as  follows  :  Limit  the 
inflammation  by  means  of  topical  emolhents,  give  chlorate  of  potash,  and 
cauterize  the  ulcers  with  nitrate  of  silver,  tincture  of  iodine,  perchloride  of 
iron,  or  hydrochloric  acid.  Chlorate  of  potash  has  the  advantage  of  being 
in  part  ehminated  by  the  salivary  glands,  and  thus  forms  a  kind  of  permanent 
mouth-wash.  It  may  even  be  given  with  the  mercury  as  a  preventative. 
Mercurial  preparations  should  never  be  prescribed  without  careful  examina- 
tion of  the  teeth  and  gums.  In  severe  cases,  where  the  nutrition  is  threat- 
ened by  the  difficulty  in  swallowing,  hquids  can  be  given  by  the  oesophageal 
tube.  Some  authors  have  recommended  iodide  of  potash,  which  seems  to 
facihtate  the  elimination  of  mercury.  Antiseptic  solutions  may  be  of  some 
use  when  the  infectious  element  is  predominant. 


DISEASES  OF  THE  MOUTH  537 


III.  ULCERO-MEMBRANOUS  STOMATITIS. 

History. — The  disease  which  to-day  is  described  under  the  name  of  ulcero-mem- 
braneous  stomatitis  has  for  a  long  time  been  confounded  with  other  affections  of  the 
mouth  under  the  misleading  names  of  stomacace  (crro/ia,  mouth  ;  koko?,  bad),  aquatic 
chancre,  scurvy  of  the  mouth,  membranous  stomatitis,  etc.  \Vhen  the  Vendean  Legion 
was  in  garrison  at  Tours  in  1818,  Bretonneau  described,  under  the  name  of  "  diphtheric 
buccale,"  certain  membranous  ulcerations  of  the  mouth  among  the  men,  and  he  con- 
sidered himself  the  more  certain  because  some  of  the  men  had  at  the  same  time  con- 
tracted pharyngeal  and  laryngeal  diphtheria.  Bretonneau's  doctrine  was  opposed. 
In  1853  RilUet  and  Barthez  rejected  the  theory  of  buccal  diphtheria,  which  they 
replaced  by  the  name  of  "  ulcero-membranous  stomatitis  " — a  disease  which  has  nothing 
in  common  with  diphtheria  ;  and  in  1859  Bergeron,  observing  an  epidemic  of  this 
disease  among  the  soldiers  in  the  Saint-Martin  Hospital,  gave  to  it  the  name  of  specific 
ulcerous  stomatitis.  This  difference  of  opinion  does  not  condemn  the  doctrine  of 
Bretonneau.  It  seems  to  prove  that  the  patients  observed  by  Bretonneau  were  suffering 
from  a  twofold  epidemic — ulcero-membranous  stomatitis  and  diphtheria.  Bretonneau 
did  not  understand  the  former,  but  he  was  correct  in  creating  "  diphtherie  buccale," 
and  it  would  be  a  grave  error  to  reject  this  manifestation  of  diphtheria,  which  has  been 
confirmed  by  recent  becteriological  researches. 

Description. — Ulcero-membranous  stomatitis  commences  like  the  other 
forms  of  stomatitis.  After  three  or  four  days  of  malaise  or  of  fever,  some- 
times even  without  prodromata,  the  symptoms  of  inflammation  appear — a 
feeling  of  burning  and  dryness,  redness  and  swelling  of  the  mucous  mem- 
brane.    The  ulcers,  however,  are  the  specific  stamp  of  the  disease. 

They  are  usually  hniited  to  the  left  side  of  the  mouth.  The  first 
ulcer  generally  affects  the  mucous  membrane  of  the  mouth  on  a  level  with 
the  last  molar  teeth.  The  ulcers  are  found,  in  order  of  frequency,  on  the 
gums,  cheeks,  and  lips,  especially  the  upper  lip  ;  more  rarely  on  the  tongue, 
roof  of  the  palate,  and  tonsils.  The  ulcers  on  the  gums  are  often  vertical, 
and  may  occupy  the  whole  edge  of  the  gum  ;  those  on  the  cheek  and  lips  are 
more  commonly  oval.  At  first  the  lesion  is  a  prominent  violet-coloured  disk, 
which  soon  becomes  soft.  The  surface  is  pulpy,  yellowish,  or  greyish,  and 
is  really  a  slough  composed  of  the  elements  of  tlie  mucous  membrane.  The 
slough  is  slightly  adherent ;  it  becomes  detached,  and  leaves  in  its  place  an 
ulcer,  which  bleeds  easily,  and  has  a  greyish  base,  with  irregular  and  ragged 
odges.  The  ulceration  spreads  by  the  progressive  elimination  of  the  foetid 
detritus  which  lines  its  cavity,  and  large  ulcers  sometimes  result  from  the 
confluence  of  smaller  ones.  The  surrounding  parts  are  more  or  less  oede- 
matous.  During  the  second  week  the  process  of  repair  commences,  the 
bottom  of  the  ulcer  becomes  clean,  the  greyish  membranes  are  detacjied, 
heaving  a  reddish  granulating  surface,  and  cicatrization  follows. 

To  sum  up,  ulcero-membranous  stomatitis  is  a  specific,  curable,  and 
more  or  less  superficial  gangrene  of  tlu^  mucous  membrane  of  the  mouth. 
The    ulcers,   however,   do  not  in   themselves  compri.se   the  entire   lesion. 


538  TEXT-BOOK  OF  MEDICINE 

Softening  and  swelling  of  the  mucous  membrane  of  the  gums,  which  becomes 
greyish  and  bleeding,  has  also  been  observed.  Some  authors  have  con- 
founded this  stomatitis  with  scurvy.  It  is  also  common  to  meet  with  the 
symptoms  and  the  lesions  of  sore  throat ;  ulcers  may  develop  at  the  back  of 
the  throat,  producing  an  ulcero-membranous  tonsillitis.  It  is  evident  that 
the  disease  is  not  simply  a  stomatitis  ;  it  is  an  ulcero-gangrenous  inflam- 
mation of  the  whole  bucco-pharyngeal  cavity. 

In  the  ulcerative  stage  the  local  symptoms  become  acute  :  pain  severe, 
mastication  impossible,  deglutition  difficult,  breath  horribly  foetid,  saHva 
profuse  and  streaked  with  blood,  yet  much  less  profuse  than  in  mercurial 
stomatitis.  The  submaxillary  and  retromaxillary  glands  are  often  swollen, 
and  remain  so  until  cicatrization  of  the  ulcers  occurs.  The  inflamed  glands 
do  not  suppurate,  but  in  scrofulous  subjects  they  may  persist  indefinitely. 
The  general  symptoms  of  fever,  and  gastro-intestinal  and  nervous  troubles 
are  more  marked  in  children  than  in  adults. 

Its  course  is  not  influenced  by  concurrent  diseases  (Bergeron).  Its 
duration  is  variable.  The  patient  recovers  in  a  week  or  ten  days  with 
proper  treatment ;  in  the  opposite  event  the  disease  may  be  prolonged  for 
weeks  and  months.  Complete  recovery  is  the  rule.  In  grave  cases,  how- 
ever, the  alveolar  edge  of  the  maxilla  becomes  necrosed  ;  the  teeth  are  laid 
bare,  and  fall  out  mthout  showing  any  trace  of  caries. 

Diagnosis — etiology. — The  situation,  course,  and  characters  of  the 
ulcero-membranous  patches  make  it  impossible  to  confound  this  disease 
with  other  forms  of  stomatitis.  In  "  diphtherie  buccale  "  pain  and  salivation 
are  practically  absent.  False  membranes  are  found  on  the  gums,  the  lower 
Hp,  and  the  labial  commissures.  These  membranes  are  at  first  whitish,  and 
then  grow  darker ;  when  they  are  removed,  the  mucous  membrane  is  found 
to  be  intact,  or  only  exulcerated,  which  is  in  striking  contrast  with  the 
ulceration  just  described.  Chnical  examination  is,  however,  generally  in- 
sufficient, and  bacteriological  investigation  is  necessary ;  it  may  reveal 
unsuspected  diphtheria. 

Syphilitic  mucous  patches  and  tubercular  ulcerations  of  the  mouth 
have  such  clearly  defined  characteristics  that  a  mistake  in  diagnosis  is 
impossible. 

Ulcero-membranous  stomatitis  often  assumes  an  epidemic  character. 
It  is  contagious,  but  does  not  appear  to  be  inoculable  ;  there  are,  however, 
positive  cases  of  inoculation.  It  attacks  children  of  from  four  to  ten  years 
of  age,  and  especially  adults,  when  it  finds  conditions  favourable  for 
development,  such  as  those  presented  by  bad  hygiene,  insufficient  food,  etc. 
This  explains  the  epidemics  among  soldiers,  sailors,  or  in  hospitals  and  in 
prisons.  Bacteriological  researches  concerning  this  variety  of  stomatitis 
and  the  tonsillitis  which  often  accompanies  it,  have  always  revealed  the 


DISEASES  OF  THE  MOUTH  539 

presence  of  two  micro-organisms — a  spirillum  and  a  fusiform  bacillus 
(Vincent).  Up  to  the  present  it  has  not  been  possible  either  to  cultivate  this 
bacillus  or  to  reproduce  the  lesion  experimentally.  For  the  time  being  it  is 
impossible  to  assign  a  specific  role  to  them.  "Their  constant  presence, 
however,  in  almost  pure  culture  in  the  exudation  is  sufficient  presumption 
to  legard  them  as  the  causes  of  the  disease,"  Prophylaxis  demands  the 
removal  of  persons  from  all  causes  of  contagion  and  from  the  scene  of  the 
epidemic.  For  an  adult,  chlorate  of  potash  should  be  administered  daily, 
and  if  necessary  the  ulcers  should  be  touched  with  nitrate  of  silver,  or, 
better  still,  with  small  tampons  of  absorbent  -wool,  moistened  with  a  solution 
of  sublimate  (1  in  1,000). 

IV.  THRUSH 

Thrush  is  also  called  white  mouth  or  creamy  stomatitis.  At  first  sight 
it  resembles  a  whitish  and  creamy  layer,  which  lines  the  mucous  membrane 
of  the  mouth  at  different  points.  This  layer  is  formed  by  the  union  of  disks, 
which  look  like  curds  of  milk,  and  are  composed  of  a  seed-bed  of  projecting 
whitish  grains. 

The  description,  however,  would  be  very  incomplete  if  it  were  limited 
to  the  oral  variety.  The  mouth  is  doubtless  its  seat  of  election  ;  neverthe- 
less, recent  researches  have  proved  how  common  it  is  in  other  regions. 
Although  it  is  here  described  among  the  diseases  of  the  mouth,  I  must 
mention  the  other  manifestations  of  the  disease,  I  shall  therefore  trace  the 
life-history  of  thrush^  and  shall  then  mention  the  modifications  seen  according 
to  the  region  affected. 

Life -History  —  Pathological  Anatomy.  —  Under  the  microscope  a 
particle  of  thrush  shows  two  distinct  elements  :  the  one  is  the  stroma,  in 
which  you  find  neither  pus  nor  fibrin,  formed  by  pavement  cells  of  every  age, 
mostly  degenerated  and  granular  ;  the  other,  the  specific  element,  is  formed 
of  interwoven  filaments  and  of  rounded  corpuscles.  These  filaments  were 
formerly  considered  as  a  mycelium,  and  the  rounded  corpuscles  were  looked 
upon  as  the  spores.  At  that  period  thrush  was  described  as  a  vegetable, 
belonging  to  the  mushroom  family,  a  cryptogram  of  the  genus  Oidium  aphfJio- 
fhyta  (Gruby),  O'idmm  albicans  (Robin),  Oidium  syrincjos'pora  (Quinquaud), 
The  researches  of  Audry  have  shown  thrush  to  be  a  yeast.  He  classes  thrush 
amongst  the  saccharomycetes,  describes  its  yeast-like  form,  gives  the  results 
obtained  from  cultures  on  solid  (potatoes)  and  liquid  media  (Koch's  broths), 
and  proposes  to  call  the  parasite  Saccliaromyces  albicans.  More  recent 
researches  tend  to  show  that  thrush  is  not  a  true  saccharomyces.  A  case  of 
pharyngeal  thrush,  caused  by  a  yeast  comparable  to  the  industrial  yeasts, 
has  been  published,  and  proves  once  more  tliat  "  a  naturally  inoffensive 


540  TEXT-BOOK  OF  MEDICINF. 

micro-organism  can  on  a  prepared  medium  become  pathological,  and  give 
rise  to  a  characteristic  disease."  Cultures  of  thrush  on  sterile  carrot  give 
snow-white  colonies  in  forty-eight  hours.  Microscopic  examination  reveals 
the  saccharomyces  in  the  form  of  rounded  cells,  in  groups  or  chains,  covered 
by  an  envelope  which  does  not  stain.  In  broth  the  microphyte,  after  a  few 
days,  forms  long  filaments  and  oval  cells  ;  on  a  solid  medium,  however,  the 
culture  no  longer  shows  filaments,  but  only  rounded  corpuscles.  True  spores 
only  appear  in  a  mineral  fluid  containing  sugar. 

As  an  accessory  element  we  often  find  an  alga  in  the  shape  of  little  rods 
without  any  trace  of  articulation,  known  as  the  leptothrix ;  it  has  nothing 
to  do  with  thrush,  and  exists  in  many  morbid  conditions  of  the  mouth. 

The  fungus,  when  inoculated  into  the  veins  of  an  animal,  causes  mycotic 
lesions,  which  are  very  interesting  (Klemperer,  Linossier  and  Roux, 
Grasset).  Experimental  oidian  infection  chiefly  attacks  the  kidneys  (Roger, 
Noisette),  which  are  riddled  with  Httle  white  granulations  (Roger).  The 
serum  of  animals,  vaccinated  against  Saccharomyces  albicans,  causes  aggluti- 
nation of  the  parasite,  which  covers  itself  mth  a  thick  cuticle  (Roger), 
behaving  like  Eberth's  bacillus,  with  this  difference,  that  in  the  case  of  the 
bacillus  the  agglutinative  reaction  is  one  of  infection  (Widal). 

We  may  now  consider  the  distribution  and  the  behaviour  of  thrush. 

Thrush  is  usually  found  in  the  mouth.  Its  appearance  is  announced  by 
a  pecuhar  state  of  the  mucous  membrane,  which  I  shall  describe  in  a 
moment.  The  relations  between  thrush  and  the  mucous  membrane  are 
variable,  according  as  the  thrush  is  epithelial  or  dermic  (Parrot).  In 
epithelial  thrush  the  filaments  go  down  into  the  epithehal  layer,  the  pave- 
ment cells  are  separated  by  a  pile  of  cells,  and  the  thrush  rises  in  the  shape 
of  tufts.  In  dermic  thrush  the  filaments  go  down  as  far  as  the  derma  of 
the  mucous  membrane,  and  the  papillae  show  nuclear  prohferation.  The 
epithelial  variety  of  thrush  is  only  found  on  the  velum  palati  and  on  the  roof 
of  the  palate. 

In  the  pharynx  thrush  may  be  primary,  and  precede  that  in  the  mouth, 
but  this  is  very  rare  indeed. 

Thrush  is  very  common  in  the  oesophagus,  where  it  forms  yellowish  or 
brownish  patches  ;  the  elements  go  down  deeply,  through  the  tunica  mucosa, 
as  far  as  the  muscular  layer.  The  connective  tissue  shows  abundant  pro- 
liferation at  the  affected  points. 

In  the  stomach  the  thrush,  covered  by  a  tliick  layer  of  mucus,  appears  in 
the  form  of  greyish  papillae.  It  adheres  firmly  to  the  walls,  which  it  pene- 
trates deeply.  .  The  superficial  portions  of  the  gastric  glands  are  destroyed, 
but  the  culs-de-sac  are  dilated,  and  resemble  gourds  full  of  spores  (Parrot). 
The  vessels  show  thrombosis,  due  perhaps  to  the  penetration  of  the 
filaments. 


DISEASES  OF  THE  MOUTH  5il 

The  csecum,  with  its  acid  reaction,  offers  conditions  favourable  to  the 
development  of  thrush. 

The  lower  vocal  cords  offer  a  good  soil  for  the  propagation  of  tlirush, 
because  they  are  pro\dded  with  pavement  epithehum,  whilst  thrush  does 
not  develop  on  mucous  membranes  with  columnar  epithehum,  no  doubt 
because  the  cilia  prevent  the  parasite  from  gaining  a  hold.  Parrot  has 
found  nodules  of  thrush  in  the  infundibula  of  the  lungs. 

It  is  not  exceptional  to  find  thrush  on  the  vulva,  vagina,  anus,  or  the 
prepuce,  and  on  the  nipples  of  wet-nurses. 

Thrush  is  also  a  pyogenic  agent.  Grasset  has  found  it  in  an  abscess  of 
the  gums,  and  Charrin  in  a  submaxillary  abscess.  In  man,  as  in  animals,  it 
may  produce  a  general  infection  in  the  lungs,  the  spleen,  the  Iddneys,  and 
the  brain  (Schmorl,  Zenken,  Ribbert,  Pineau), 

^Etiology — Pathogenesis. — Thrush  often  appears  mthin  the  first  two 
weeks  of  birth.  It  may  develop  as  a  purely  local  affection,  favoured  by  dirty 
bottles  and  acidity  of  the  milk ;  in  this  form  it  presents  no  grave  features. 
These  rare  cases  excepted,  thrush  is  a  secondary  affection,  indicative  of 
general  ill-health.  Thrush  is  more  general  at  the  two  extremes  of  Hfe,  and 
any  cause  of  organic  decay  favours  its  development.  In  the  new-born  it  is 
associated  with  digestive  troubles,  enteritis  (Seux),  bad  hygiene,  defective 
feeding,  and  in  the  state  of  malnutrition  wliich  Parrot  has  called  athrepsia. 
In  the  adult  and  the  aged  it  accompanies  cachexia,  phthisis,  cancer,  chronic 
diarrhoea,  prolonged  suppuration,  etc.  It  is  likewise  associated  with  acute 
diseases  (pneumonia,  pyelo-nephritis,  cystitis,  typhoid  fever,  and  the  puer- 
peral state).  Thrush  is  contagious,  but  the  soil  must  be  favourable  to  its 
development.  It  was  very  common  in  children's  hospitals,  but  is  much  less 
so  to-day,  owing  to  the  rigid  observation  of  prophylaxis  and  antisepsis. 

Gubler  has  rightly  attached  great  importance  to  the  acidity  of  the 
medium.  This  assertion  remains  true,  though  we  know  that  thrush  may 
grow  in  alkahne  media.  Tlirush  cannot  be  cultivated  in  the  sahva  (Roux 
and  Linossier) ;  consequently  dryness  of  the  mouth  and  absence  of  saliva 
favour  its  development,  as  is  seen  in  cachexia,  infectious  fevers,  hectic 
fever,  etc. 

Description.  -The  mouth  is  the  seat  of  election  in  thrush.  The  patches 
develop  on  tiie  tongue,  oji  the  inside  of  the  cheeks,  and  at  other  points  of  the 
nmcous  membrane,  and  it  is  easy  to  detach  them  by  rubbing.  The  appear- 
ance of  thrush  in  the  mouth  is  preceded  by  a  peculiar  state  of  the  mucous 
membrane,  which  is  dry,  shiny,  and  painful.  It  becomes  rea  and  glossy  anti 
desquamates,  wliilst  the  papilla)  of  the  tongue  stand  out ;  tiie  little  wliitish 
islands  theii  appear,  and  unite  to  form  the  patches  of  thrush  previously 
described.  Thrush  is  often  discrete  and  localized  to  the  tongue,  which 
appears  covered  by  nit^re  or  less  irregular  creamy  patches.     In  other  cases 


542  TEXT-BOOK  OF  MEDICINE 

the  thrush  is  confluent ;  it  spreads  over  the  inside  of  the  cheeks,  soft  palate, 
tonsils,  and  pharynx,  and  may  assume  a  yellowish  or  greyish  tint,  which  at 
first  sight  resembles  diphtheritic  concretions.  The  reaction  of  the  saliva  is 
acid. 

In  the  adult,  mastication  and  deglutition  become  difficult  and  painful. 
The  new-born  infant  cries,  takes  the  breast  with  difficulty,  and  at  last 
refuses  it.  The  development  of  thrush  in  young  children  coincides  with 
digestive  troubles,  vomiting,  and  diarrhoea,  which  in  grave  cases  are  accom- 
panied by  rigors,  erythema  of  the  buttocks,  and  cutaneous  ulcerations. 
The  enteritis  may  precede  the  thrush,  or  their  development  may  be  simul- 
taneous. The  gra^dty  of  the  case  is,  however,  subordinate  to  the  general 
condition  of  the  patient.  If  thrush  is  purely  a  local  symptom,  the  prognosis 
is  benign,  and  restoration  to  health  is  not  far  off.  Some  cases  of  secondary 
thrush  are  not  of  too  unfavourable  a  prognosis.  In  a  marasmic  infant  or  in 
a  cachectic  individual  the  appearance  of  thrush  is  of  evil  omen,  and  though 
it  may  be  possible  to  cure  the  local  mischief  its  appearance  is  almost  always 
the  index  of  approaching  catastrophe. 

To  sum  up,  as  regards  evolution  and  prognosis,  tlirush  presents  certain 
differences  in  children  and  in  adults.  In  the  adult,  and  much  more  so  in 
the  aged,  thrush  nearly  always  indicates  a  fatal  issue.  In  a  young  child 
thrush  often  has  the  same  serious  signification ;  in  some  cases,  however,  it 
is  primary,  and  is  simply  a  variety  of  stomatitis  easily  cured. 

Diagnosis— Treatment. — The  diagnosis  is  easy.  In  default  of  micro- 
scopical examination,  which  immediately  removes  all  doubts,  thrush  must 
not  be  confounded  with  the  flakes  of  curdled  milk  which  may  be  removed  by 
gentle  friction,  leaving  the  mucous  membrane  underneath  absolutely 
healthy.  Thrush  should  not  be  confounded  with  diphtheritic  stomatitis, 
where  the  exudation  occurs,  not  in  projecting  isolated  grains,  but  in  whitish 
adherent  patches,  which  are  quite  different  from  thrush, 

Alkahs  must  be  given,  as  thrush  does  not  flourish  so  well  in  alkaline 
media.  After  detaching  the  patches,  the  affected  parts  are  painted  several 
times  a  day  with  glycerine  and  borate  of  soda  in  equal  parts.  In  very  young 
children  we  must  find  a  good  wet-nurse,  or  give  milk  of  good  quahty.  If 
dyspeptic  or  intestinal  troubles  accompany  thrush,  two  or  three  teaspoon- 
fuls  of  Ume-water  in  the  milk  should  be  prescribed,  or  a  drop  of 
Sydenham's  laudanum  in  a  little  syrup  and  water.  CleanHness  is  im- 
perative as  regards  the  feeding-bottle,  the  breast  of  the  nurse,  and  the 
mouth  of  the  chUd. 


DISEASES  OF  THE  MOUTH  543 

V.  APHTHA. 

Description. — Aphthae  are  sometimes  described  under  the  name  of 
"aphthous  stomatitis,"  a  term  which  is  not  strictly  correct,  because  the 
stomatitis  is  merely  secondary.  The  name  "  aphthous  fever  "  would  be 
more  suitable.  In  benign  cases,  which  are  the  rule,  prodromata  are  absent. 
The  mucous  membrane  of  the  Kps,  the  tip  and  edges  of  the  tongue,  the  mucous 
membrane  of  the  cheeks  and  palate,  show  red  spots,  on  which  vesicles,  like 
those  of  herpes,  develop.  The  vesicles  become  filled  with  a  milky  Hquid, 
and  are  surrounded  by  an  area  of  swollen  mucous  membrane.  They  break, 
and  by  the  second  or  third  day  ulcers  are  formed. 

The  ulcers  are  circular  ;  their  size  varies  from  a  pin's  head  to  a  lentil ; 
some  may  be  more  extensive.  The  floor  of  the  ulcer  is  greyish,  and  formed 
by  a  mass  of  degenerated  cells.  Its  edges  are  irregular,  fixed,  and  clean-cut. 
The  ulceration  rarely  lasts  more  than  a  week,  and  heals  without  leaving  scars. 

The  lesion  produces  burning  pain,  which  becomes  very  acute  at  the 
moment  of  ulceration.  The  breath  is  fcetid,  and  salivation  is  marked ;  as 
mastication  and  sucking  are  painful,  a  child  refuses  the  breast,  and  an 
adult  must  be  satisfied  with  liquid  nourishment.  The  submaxillary  glands 
are  rarely  enlarged.  The  general  symptoms  are  trifling  in  slight  cases  ; 
when  the  aphthae  are  discrete,  the  symptoms  comprise  digestive  troubles, 
accompanied  or  preceded  by  shght  fever.  They  are,  however,  more  marked 
when  the  aphthae  are  confluent,  and  the  name  aphthous  fever  is  then 
applicable.  In  this  confluent  form,  which  may  be  epidemic,  fever  and 
general  symptoms  precede  the  eruption. 

The  ulcers  attack  the  roof  of  the  palate,  the  velum  palati,  the  tonsils, 
and  the  pharynx,  and  unite  to  form  large  ulcerated  areas.  In  some  cases 
ulcers  are  seen  on  the  hmbs,  especially  on  the  hands.  The  fever  is  high,  the 
digestive  troubles  (vomiting  and  diarrhoea)  are  severe,  and  the  disease, 
especially  in  children  and  old  people,  assumes  an  adynamic  form  which  may 
be  fatal. 

iEtiology. — The  aetiology  is  not  well  known.  The  disease  is  observed 
at  all  ages,  sometimes  in  an  epidemic  form ;  in  some  individuals  the 
coincidence  of  aphtha;,  with  certain  eruptions — herpes,  impetigo,  and 
eczema — has  been  noticed,  and  a  diathetic  origin  has  therefore  been 
suspected.  We  now  take  a  different  view  of  the  question.  In  the  seven- 
teentli  century,  physicians  spoke  of  contagion,  and  recent  researches  tend  in 
effect  to  show  that  aphthous  fever  is  an  infectious  disease  of  microbic  origin. 
CHnically,  there  are  striking  analogies  between  the  disease  in  man  and 
aphthous  fever  in  cattle.  Numerous  cases  seem  to  prove  that  the  disease 
may  be  transmitted  from  animals  to  man,  and  unboiled  milk  seems  to  be  the 
most  usual  mode  of  contagion. 


544  TEXT-BOOK  OF  MEDICINE 

It  is  certain  that  in  bottle-fed  cliildxen  the  eruption  is  symmetrical  on 
both  sides  of  the  median  raphe  of  the  palate. 

Treatment. — When  the  disease  is  sHght,  the  treatment  consists  in 
washing  out  the  mouth  with  sootliing  lotions,  or  with  a  5  per  cent,  solution 
of  salicylate  of  soda  (Hirtz).  Chlorate  of  potash  sliould  be  given,  and  healing 
will  be  hastened  by  weak  applications  of  nitrate  of  silver.  Purgatives  are 
generally  indicated.  I  obtained  excellent  results  from  a  milk  diet  in  a 
hospital  patient  who  had  had  aphthae  for  several  years. 

VI.  GANGRENE  OF  THE  MOUTH— NOMA. 

Under  the  name  of  noma  it  is  customary  to  describe  a  form  of  gangrene 
which  runs  a  special  course  and  is  of  microbic  origin ;  it  occurs,  especially 
in  children,  between  the  ages  of  tlu-ee  and  five  years,  and  forms  a  definite 
morbid  entity. 

Description. — This  terrible  disease  commences  insidiously  and  without 
pain  in  the  mucous  membrane  of  the  cheek,  and  more  especially  of  the  left 
cheek.  The  mucous  membrane  assumes  a  cyanotic  tint ;  a  pimple,  filled 
with  ruddy  serum,  forms,  breaks,  and  leaves  in  its  place  a  greyish  ulcer, 
which  at  this  period  is  odourless.  The  ulceration  spreads  rapidly  in  depth 
and  in  extent.  It  assumes  a  greyish-black  tint,  and  the  breath  becomes 
extremely  foetid.  In  the  fortunate  but  rare  cases  the  process  then  stops  ; 
the  base  of  the  ulcer  grows  clean,  granulations  form,  and  cicatrization  takes 
place.  When  the  disease  pursues  its  course,  the  ulceration  extends.  The 
ulcer  becomes  putrilaginous,  black,  and  surrounded  by  an  inflamed  zone  ; 
from  the  third  to  the  seventh  day  an  indurated  nodule  forms  in  the  deep 
tissue  of  the  cheek,  and  indicates  the  seat  of  the  gangrene  and  the  region 
which  it  is  about  to  invade.  The  lip  and  the  cheek  are  oedematous.  The 
skin  of  the  cheek  grows  shiny  and  purple,  while  the  saUva  is  sanious  and 
foul-smelling. 

At  a  given  moment  the  cutaneous  eschar  appears  ;  it  is  dry  and  appears 
depressed.  The  gangrene  affects  the  entire  thickness  of  the  cheek,  and  may 
invade  the  hps,  the  nose,  and  the  eyelid.  The  dead  tissues  then  fall  out  in 
pieces,  and  leave  in  their  place  an  excavation,  wliich  communicates  with  the 
mouth,  and  allows  foetid  Hquid,  drinks,  or  gargles  to  pass  through.  The 
bones  of  the  face  are  not  always  respected.  Necrosis  attacks  the  bones  of 
the  neighbouring  regions  (maxilla,  vault  of  the  palate).  In  some  cases  the 
gangrene  does  not  limit  itself  to  the  face,  but  develops  simultaneously  in  the 
lungs,  the  vulva,  the  pharynx,  the  oesophagus,  and  the  extremities. 

The  general  symptoms,  which  are  sUght  at  first,  become  exceedingly 
grave  when  the  skin  is  invaded.  The  fever  may  be  intense  ;  prostration  and 
adynamia  follow  the  febrile  stage.     Diarrhoea  becomes  incessant :  the  loss  of 


DISEASES  OF  THE  MOUTH  545 

weight  is  considerable.  In  noma  the  lymphatic  glands  of  the  neck  are 
scarcely  enlarged.  Death  generally  occurs  between  the  fifth  and  fifteenth 
days,  and  in  case  of  cure  (which  only  happens  in  one  case  out  of  five)  the 
patient  shows  scars,  fistulae,  and  sometimes  hideous  deformities. 

yEtiology. — Xoma  is  seen  at  all  ages,  but  it  is  most  common  in  children 
of  from  two  to  five  years  of  age.  The  disease  is  always  secondary,  and  it  is 
remarkable  that  local  lesions  of  the  mouth,  such  as  stomatitis,  have  almost 
no  effect  on  its  development,  whilst  general  diseases,  such  as  measles, 
scarlatina,  typhoid  fever,  diphtheria,  and  scurvy,  are  favourable  to  its 
inception.  Noma,  however,  has  become  very  uncommon,  owing  to  anti- 
septic measures  which  were  previously  unknown.  Bacteriological  researches 
have  not  yet  given  conclusive  results. 

The  treatment  consists  in  washing  out  the  mouth  with  a  solution  of 
boric  acid  (4  in  100)  and  applying  the  thermo-cautery  daily,  care  being  taken 
to  sustain  the  strength  of  the  patient  by  tonics  and  stimulants. 

VII.  SYPHILIS  OF  THE  LIPS. 

Chancre. — Chancre  of  the  lips  is  so  common  that  in  Nivet's  statistics 
concerning  338  chancres  of  the  mouth  and  tliroat  labial  chancre  accounts 
for  260.  Not  a  single  year  passes  without  my  seeing  four  or  five  cases. 
This  chancre,  hke  those  of  the  oral  cavity,  may  result  from  direct  contact  or 
from  indirect  contagion  by  means  of  .'nfected  articles — e.g.,  spoons,  glasses, 
pipes,  etc.  Chancre  is  hkewise  seen  on  the  lips  of  the  new-born  infant  when 
the  nurse's  nipple  is  infected.  The  chancre  is  here,  as  elsewhere,  single  ; 
nevertheless,  multiple  chancres  are  not  rare.  Chancre  of  the  lip  commences 
as  a  trifling  lesion.  The  patient  fancies  that  it  is  a  crack,  a  scratch,  or  a 
pimple.  The  comparison  with  the  crack  and  the  scratch  is  particularly 
applicable  to  chancres  of  the  commissures  and  median  part  of  the  lip.  In 
a  few  days  its  development  is  complete,  and  it  then  assumes  various  forms. 
Some  chancres  are  papilUform,  like  a  small  slightly  ulcerated  tumour,  with 
a  reddish  floor,  which  is  indurated  and  bleeds  easily.  Other  chancres,  again, 
especially  on  the  commissures  of  the  hps,  present  the  appearance  of  a  flat, 
superficial,  smooth  ulcer,  which  is  flesh-coloured,  or  covered  at  times  by  a 
diphtlicritic  layer.  It  affects  the  angle  of  both  lips.  Movement  and  rubbing 
make  it  bleed  ;  at  first  sight  it  might  be  taken  for  a  patch  of  eczema.  Chancre 
of  the  lips  is  often  papular,  and  forms  an  indolent  tumour  indurated  at  its 
base.  It  usually  affects  both  mucous  membrane  and  skin.  It  is  covered  by 
a  crust,  especially  on  its  cutaneous  segment.  This  crust,  common  to  all 
chancres  of  the  skin,  is  brownish  ;  it  may  be  removed  after  preliminary 
softening,  and  leaves  exposed  a  red  eroded  surface,  which  bleeds  on  being 
rubbed.     At  first  sight  these  chancres  resemble  a  furuncle  or  an  epithelioma. 

35 


546  TEXT-BOOK  OF  MEDICINE 

All  these  chancres  are  aUke  in  that  they  are  painless,  indurated  at  their 
base,  and  accompanied  by  painless  satellite  glands.  The  adenopathy  is  uni- 
lateral in  lateral  chancres  and  bilateral  in  median  chancres  ;  it  is  submental 
in  chancres  of  the  lower  hp,  and  submaxillary  in  chancres  of  the  upper  lip, 
gums,  tongue,  and  cheek.  The  labial  chancre  lasts  from  four  to  six  weeks  ; 
it  disappears  without  scarring,  but  leaves  an  induration,  which  in  turn  dis- 
appears. The  diagnosis  of  chancre  must  be  made  from  labial  herpes, 
eczema,  furuncle,  and  epithehoma.  The  indolence  and  the  parchment-like 
induration  of  the  base  of  the  chancre,  with  the  early  and  painless  adenitis, 
are  sufficient  for  diagnosis. 

Secondary  Lesions. — Syphihdes  of  the  lips  appear  as  small  opahne-tinted 
erosions  (erosive  variety),  and  if  the  syphilide  attacks  the  skin,  as,  for 
instance,  the  commissures,  it  is  covered  with  little  crusts.  These  syphilides 
are  very  common  in  children  sufEering  from  hereditary  syiDliiUs.  Syphilides 
are  exceedingly  contagious. 

Tertiary  Lesions.— The  gumma,  which  is  rare  on  the  lips,  has,  however,  a 
special  predilection  for  the  upper  Up.  It  may  be  superficial  or  deep  and 
intramuscular ;  it  reaches  the  size  of  a  lentil  or  of  a  cherry.  The  more 
numerous  the  gummata,  the  more  is  the  hp  deformed.  The  gumma  goes 
on  to  the  formation  of  an  ulcer,  with  prominent  encrusted  edges  and  greyish, 
sloughy  floor. 

The  sclerous  syphiloma  is  seen  on  the  hps.  I  had  a  very  remarkable 
case  of  this  kind  under  my  care.  It  has  a  predilection  for  the  lower  lip  ; 
nevertheless,  both  lips  are,  as  a  rule,  invaded.  In  its  first  period  it  causes 
general,  and  sometimes  considerable,  hypertrophy  of  the  lip,  which  looks 
somewhat  like  a  strumous  Kp.  It  has  been  Ukened  to  a  horn  or  to  a  tapir's 
hp.  The  induration  of  the  tissues  is  uniform,  and  sometimes  mammillated. 
It  does  not  terminate,  Uke  the  gumma,  in  softening  and  ulceration.  It  ends 
when  imtreated  in  atrophy.  The  hp  grows  thin,  and  the  mouth  is  con- 
tracted. Tertiary  labiaUtis  is  not  accompanied  by  pain  and  glandular 
reaction.  The  hps,  which  are  rigid  and  deformed,  partially  lose  their 
functions  (articulation  of  sounds,  mastication,  deglutition). 

VIII.  SYPHILIS  OF  THE  TONGUE. 

Chancre. — Chancre  is  rare  on  the  tongue  ;  it  is  more  common  on  the  tip 
than  on  other  parts.  Sometimes  it  forms  a  bleeding  ulcer,  with  a  red  or 
greyish  floor  ;  at  other  times  an  ulcerated  tumour  inserted  in  the  tongue. 
The  base  of  the  chancre  is  always  indurated,  and  the  adenopathy  is  unilateral 
or  bilateral,  according  as  the  chancre  is  on  the  side  of  the  tongue  or  in  the 
median  line.  Chancres  of  the  tongue  are  not  indolent,  hke  those  of  other 
regions ;  they  are  sometimes  very  painful,  on  account  of  the  movements  of 


DISEASES  OF  THE  MOUTH  547 

mastication,  and  on  account  of  their  incessant  contact  with  saUva,  tobacco, 
drink,  and  food. 

Secondary  Lesions. — Mucous  patches  of  the  tongue  may  appear  as 
(erosions,  ulcers,  nipple-hke  projections,  and  smooth  patches.  Syphilides 
on  the  edge  of  the  tongue  readily  ulcerate  ;  those  which  occupy  the  dorsal 
surface  of  the  organ,  when  they  are  not  properly  treated,  ulcerate,  and  form 
fissures,  cracks,  or  furrows,  with  hard  and  swollen  edges.  Lingual  syphihdes 
are  sometimes  papular,  especially  on  the  back  of  the  tongue,  where  they  form 
bosses  and  nipple-like  projections  (toad's  back).  Some  form  vegetations, 
deform  the  tongue,  and  simulate  a  cancerous  growth. 

Yet  another  variety  of  syphihde  is  seen  on  the  tongue — viz.,  smooth 
patches,  which  are,  as  it  were,  varnished.  They  are  not  erosive,  but  it  may 
be  said  that  at  the  site  of  the  patch  the  mucous  membrane  is  shaved  off 
(Fournier)  hke  a  mown  field  (Cornil).  These  patclies,  which  are  fairly 
regular  in  contour,  are  only  fomid  at  the  back  of  the  tongue,  and  border  on 
the  neighbouring  regions  where  the  vilH  are  intact.  This  variety  very 
closely  resembles  eczema,  and  a  differential  diagnosis  becomes  therefore 
necessary.  Eczema  of  tlie  tongue  has  received  the  most  diverse  names  : 
lingual  pityriasis  (Rayer),  geographical  tongue  (Bergeron),  glossitis  ex- 
fohatrix  marginata  (Fournier),  areal  eczema,  or  desquamative  marginal 
eczema  (Besnier),  and  hngual  psoriasis. 

Eczema  generally  commences  at  the  edge  of  the  tongue.  At  first  we  see 
a  small  circle,  or  several  little  finely  desquamating  circles,  with  festooned  or 
polycyclical  outlines.  Fully  developed  eczema  is  characterized  by  a  raised 
patch,  with  a  red  or  rose-coloured  base.  The  patch  or  patches  are  surrounded 
by  a  border,  or  by  yellowish  and  greyish  ribbons,  which  are  the  remains  of 
the  normal  mucous  membrane.  The  eczema  may  remain  marginal  or  may 
attack  the  whole  tongue,  but  in  unequal  degree.  When  the  eczema  is 
general,  the  dorsal  surface  of  the  tongue  is  red  and  smooth ;  some  greyish 
islands,  in  the  shape  of  arabesques,  remain,  and  are  the  remnants  of  the 
normal  mucous  membrane.  This  eczema  has  an  acute  course  ;  it  may  last 
some  days  or  several  weeks.  It  always  remains  localized  to  the  tongue, 
and  does  not  attack  the  velum  palati,  floor  of  the  mouth,  or  cheeks,  like 
leucoplasia.  The  submaxillary  glands  are  never  enlarged.  Sometimes  the 
eczema  is  accompanied  by  such  symptoms  as  pruritus,  burning,  and  pain ; 
sometimes  these  symptoms  are  insignificant.  Such  is  the  lingual  eczema 
of  those  suffering  from  arthritis,  gout,  and  dyspepsia.  It  is,  however, 
certain  that  this  eczema  often  appears,  witii  the  reminders,  on  the  tr)ngue 
of  those  suffering  from  recent  or  old  syphilis.  Parrot  and  Kaposi  consider  it 
a  symptom  of  liereditary  syphilis  ;  syj)hilis  is  an  iin|)()rtHiit  fiict(»r,  and  it 
might  !)('  considered  a  secondary  parasyphilitic  manifestation. 

Tertiary  Lesions. —1.  Gummata  may  be  superficial,  in  the  dermis,  or 

35—2 


548  TEXT-BOOK  OF  MEDICINE 

deep,  in  tlie  muscles.  Intramuscular  gummata  are  2iowhere  so  frequent  as 
in  the  tongue.  The  gummata  always  affect  the  upper  surface  of  the  tongue, 
and  vary  in  size  from  a  pea  to  a  nut.  When  they  are  multiple,  the  tongue  is 
mammillated,  being,  as  it  were,  crammed  with  nodules  (Fournier).  It 
extends  beyond  the  teeth,  and  is  almost  too  large  for  the  mouth.  It  becomes 
elephantiasis-Uke,  and  hinders  articulation,  mastication,  deglutition,  and 
respiration. 

At  times  there  is  only  one  gumma,  the  rest  of  the  tongue  being  free.  At 
the  Hotel-Dieu  I  have  had  a  patient  whose  single  gumma*  formed  a  tumour 
of  the  size  of  a  small  nut  in  front  on  the  right  half  of  the  tongue.  His  speech 
was  spluttering ;  mastication  and  deglutition  were  extremely  painful.  He 
could  not  close  his  mouth,  and  the  saliva  drooled  away.  I  put  the  patient 
upon  injections  of  biniodide  of  mercury.  The  symptoms  improved  rapidly, 
and  cure  was  complete  in  eight  weeks.  Such  a  gumma  simulates  other 
tumours  of  the  tongue,  e.g.,  tubercular  cold  abscess,  interstitial  sarcoma, 
lipoma,  and  hydatid  cyst. 

'A.  Ulcerations  may  result  in  the  circumscribed  or  diffuse  gumma.  It 
seenus  that  tertiary  ulceration  may  appear  without  having  been  preceded  by 
any  gummatous  swelhng.  Gummatous  ulcers  are  hollow,  deep,  with  clean- 
cut  edges  and  a  sloughy  floor,  which  is  greyish,  yellowish,  or  greenish,  sanious, 
and  sometimes  covered  with  fungoid  growths  yielding  a  slight  resemblance 
to  cancer.  These  ulcerations  are  neither  bleeding,  like  epitheliomata,  nor 
purulent,  like  tuberculomata.  Mastication  and  deglutition  are  very  painful, 
or  almost  impossible. 

A  jiatient  under  my  care  for  syphilitic  ulceration  had  the  front  of  the  tongue  eaten 
away.  The  pain  was  so  severe  that  she  kept  the  tongue  quite  still.  She  had  great 
difficulty  in  drinking  a  cup  of  milk.  She  spluttered  instead  of  speaking.  She  drooled 
saliva,  and  was  unable  to  rinse  her  mouth  or  to  clean  her  teeth.  Contact  with  cold  air 
was  painful.  Insomnia  and  want  of  food  had  led  to  a  loss  of  20  pounds  in  a  few  weeks. 
This  proves  once  more  that  pain  is  not  the  appanage  of  tubercular  ulcers,  for  syphihtic 
ulcerations  of  the  tongue  and  throat  are  at  times  exceedingly  painful.  The  ulcer  was 
cured  with  injections  of  biniodide  of  mercury. 

After  a  variable  time  the  syphiloma,  if  treated,  cicatrizes,  but  the  tongue 
often  remains  furrowed. 

In  some  cases  the  gummatous  ulceration,  if  not  treated,  may  become 
stationary,  and  last  for  months  and  years,  without  extending  beyond  its 
first  limits.  Fournier  has  seen  ulcers  which  were  one  or  two  years  old.  He 
quotes  "  a  very  curious  case  of  a  tertiary  lingual  ulcer,  dating  back  no  less 
than  twenty  years,  during  which  time  the  patient  had  submitted  to  no 
treatment  whatsoever.  And  note  this,  as  a  proof  of  what  specific  medication 
can  do  in  such  cases — this  ulceration  had  lasted  twenty  years.   Mercury  was 

*  Dieulafoy,  "  La  Grosse  Gomme  Solitaire"  {Clinique  Medicale  de  V  Hotel-Dieu, 
1903,  9""=  levon). 


DISEASES  OF  THE  MOUTH  549 

administered,  and  in  four  days  the  ulceration  commenced  to  get  better  ;  in 
four  weeks  it  was  cured." 

Syphilitic  ulcers  of  the  tongue  may  in  exceptional  cases  become 
phagedaenic  or  serpiginous. 

Foumier  mentions  a  woman  who  had  thrice  had  tertiary  ulcers  at  the  back  of  her 
throat  ;  on  the  fourth  occasion  the  tongue  was  invaded  at  the  base  by  two  large,  deeply 
excavated  ulcers. 

A  patient  had  a  tertiary  ulcer  on  the  right  half  of  the  tongue.  The  ulcer  ate  in  deep, 
grew  larger,  assumed  a  gangrenous  aspect,  and  was  stopped  only  at  the  end  of  three 
months.  Fresh  ulceration  appeared  three  months  later.  The  hole  became  gangrenous, 
and  putrilaginous  shreds  were  detached  from  it.  "  The  tongue  vanished  in  a  kind  of 
deliquescence."     It  took  several  months  to  cure  the  patient. 

3.  The  sclerous  syphiloma  has  a  marked  preference  for  the  tongue  ;  it 
may  be  superficial  or  deep.  The  superficial  sclerous  glossitis  attacks  the 
mucous  membrane  ;  the  affected  parts  are,  as  it  were,  depapUlated  (Fournier), 
and  contrast  with  the  normal  mucous  membrane,  covered  with  papillae.  The 
affected  mucous  membrane  is  sometimes  of  a  \dvid  red,  at  other  times  whitish. 
Between  the  fingers  the  mucous  membrane  feels  as  if  doubled  over  a  cartila- 
ginous plate  ;  its  sensitiveness  is  lessened,  and  sometimes  quite  lost.  In 
deep  sclerotic  glossitis  the  tongue  is  enlarged  ;  its  dorsal  surface  is  divided 
by  more  or  less  deep  furrows  into  lobes  and  lobules.  The  tongue  is,  as  it 
were,  tessellated  (Fournier),  and  in  some  cases  the  median  furrow  may  attain 
a  depth  of  1  centimetre.  Ulceration,  unless  provoked  by  exterior  causes 
(alcohol,  tobacco,  friction  against  the  teeth),  is  not  seen.  The  disease  runs  a 
very  slow  course,  without  pain  and  glandular  enlargement,  when  there  is  no 
ulceration.  The  tongue,  which  is  as  rigid  as  a  piece  of  wood,  gradually  loses 
its  functions  ;  articulation  of  words,  mastication,  and  deglutition  are  badly 
performed.  The  gummatous  and  sclerotic  forms  are  often  associated  ;  the 
condition  is  then  a  sclero-gummatous  glossitis.  Syphilitic  glossitis  may 
appear  as  nacreous,  laminated  patches  of  a  smooth  or  mammillated  form  ; 
these  are  called  mucous  patches.  What  is  to  be  understood,  in  a  general 
way,  by  oral  leucoplasia,  a  name  invented  by  Vidal,  which,  with  advantage, 
has  replaced  the  faulty  term  of  psoriasis  ?  The  name  "  oral  leucoplasia  " 
(white  patches,  opaHne  patches,  or  smokers  patches)  is  given  to  the  silvery, 
laminated,  and  indurated  patches  which  are  found  in  smokers,  or  in  gouty 
and  syphilitic  persons.  Oral  leucoplasia  affects  not  only  the  tongue,  but 
may  also  attack  the  lips,  the  cheeks,  aiid  the  velum  palati. 

The  patches  are  formed  of  thick,  white  epitheUal  scales,  with  superficial 
induration  of  the  mucous  membrane.  These  patches,  which  take  years  to 
develop,  may  become  fissured  and  painful.  Buccal  leucoplasia  may  be 
cured  or  be  prolonged  indefinitely,  or  finally  end  in  epithelioma.  Debovo 
stated  this  fact,  which  is  generally  admitted  (Vidal).  In  such  a  case  the  j)atch 
assumes  a  papillomatous  aspect,  or  rather  is  accompanied  l)y  painful  detip- 


550  TEXT-BOOK  OF  MEDICINE 

seated  induration  ;  the  lesion  reacts  on  the  glands,  and  we  have  a  buccal 
epithelioma.  No  difference  exists  between  oral  leucoplasia  in  people  who 
are  or  are  not  suffering  from  syphiUs.  Kaposi  admits  leucoplasia  of  a 
syphilitic  nature.  Besnier  considers  syphilis  as  a  predisposing  cause.  It 
is  probable  that  we  have  here  one  of  those  lesions  in  which  syphilis  causes  an 
important  difference  (parasyphihtic  lesions).  At  the  Hotel-Dieu  I  had  a 
patient  suffering  from  sclerotic  syphiloma  of  the  tongue  with  leucoplasia. 
Both  lesions  were  cured  by  injections  of  biniodide. 

Diagnosis. — The  diagnosis  must  be  made  when  the  syphiloma  presents 
the  form  of  a  non -ulcerating  tumour,  of  ulceration,  or  of  sclerotic  glossitis. 
I  have  remarked  previously  that  the  lingual  gumma  at  times  causes  a  firm 
or  soft  tumour,  when  the  diagnosis  is  not  always  evident  at  first  sight.  This 
variety  of  hngual  syphiloma  closely  resembles  the  hngual  tuberculoma,  or 
the  intramuscular  tubercular  abscess,  also  called  the  tubercular  gumma. 
Each  presents  similar  localization,  size,  and  appearance  to  both  sight  and 
touch.  The  existence  of  concomitant  pulmonary  tuberculosis  is  a  probable, 
but  not  a  certain,  sign ;  puncture  of  the  tumour  and  examination  of  the 
liquid  are  sometimes  necessary  for  the  diagnosis  (Marion).  Interstitial 
sarcoma  of  the  tongue  may  simulate  gumma  so  closely  that  specific  treatment 
may  be  needed  to  decide  the  point.  Lingual  lipoma,  too,  somewhat  re- 
sembles submucous  lingual  gumma.  Vergely  says  :  "If  antisyphihtic  treat- 
ment is  prescribed,  the  rapid  change  in  the  gumma  cUnches  the  diagnosis." 

Let  us  now  consider  the  ulcerative  syphiloma.  The  tertiary  ulcer  must 
not  be  confounded  with  dental  ulcers.  The  latter  occupies  the  edge  of  the 
tongue,  is  generally  elongated,  and  disappears  if  care  is  taken  to  file  off  or 
remove  the  offending  tooth.  Tubercular  ulceration  of  the  tongue  differs 
from  tertiary  syphiHtic  ulceration.  The  edges  are  more  jagged  and  less 
clean  cut ;  the  ulcer  is  less  crateriform  ;  it  suppurates,  and  the  adjacent 
mucous  membrane  is  frequently  studded  with  yellow  tubercles.  Koch's 
bacillus  is  often  found  in  the  scrapings  from  the  ulcer. 

Epithelioma  of  the  tongue  and  tertiary  syphilis  have  common  character- 
istics which  at  times  make  the  diagnosis  difficult.  Fournier,  however,  says 
that  the  syphihtic  lesion  commences  with  an  internal  induration,  and  the 
epithelioma  with  an  external  tumour.  Syphilis  causes  deep  ulceration,  while 
epithehoma  ulcerates  on  the  surface.  Syphilis  forms  multiple  lesions,  but 
epithelioma  is  solitary.  Syphilitic  lesions  rarely  bleed  and  secrete  but 
little  ;  epithelioma  bleeds  easily  and  secretes  much.  The  pains  of  syphihtic 
ulceration  are  less  spontaneous  and  less  radiating  ;  the  ulcerous  syphiloma  is 
not  accompanied  by  adenopathy  (unless  from  secondary  infection),  while  the 
epithelioma  causes  marked  enlargement  of  glands.  Treatment,  so  beneficial 
in  syphilis,  has  no  effect  in  epithelioma.  Histological  examination  may 
prove  the  presence  of  epithehoma. 


DISEASES  OF  THE  MOUTH  551 

Do  not  let  us  forget  that  epithelioma  may  be  grafted  on  a  syphilitic  ulcer 
of  the  tongue,  just  as  on  an  ulcer  of  the  stomach.  In  1907,  a  patient  came 
into  the  Hotel-Dieu  with  gummatous  ulceration  of  the  tongue.  Under 
mercurial  treatment  the  improvement  was  rapid,  and  the  epitheliomatous 
change  took  place  during  cicatrization. 

Sclerous  syphilitic  glossitis  must  not  be  confounded  with  smoker's 
glossitis.  The  smoker's  tongue  may  be  indented  and  uneven,  with  greyish 
nacreous  islets,  especially  at  the  tip  ;  these  characteristics  recall  lingual 
syphilis,  and  hence  the  diagnosis  is  at  times  difficult. 

In  treatment  I  give  the  preference  to  oily  or  watery  injections  of  biniodide 
of  mercury  in  doses  of  ^  to  4  grain.  These  doses  may  be  exceeded  consider- 
ably. After  from  twelve  to  fifteen  injections  the  treatment  is  suspended, 
and  recommenced  in  a  fortnight. 


IX.  SYPHILITIC  PERFORATION  OF  THE  ROOF  OF  THE 

PALATE. 

Perforation  of  the  roof  of  the  palate  is  not  rare  in  tertiary  syphilis,  if  I 
judge  of  its  frequency  by  the  number  of  people  who  come  to  hosjjital  with  a 
hole  in  their  mouths.  I  quote  here  from  my  chnical  lecture*  on  tliis 
question  : 

A  patient  came  to  the  Hotel-Dieu  for  a  "  corroding  disease  "  in  his  mouth.  He 
had  had  syphilis  twenty  years  before  ;  ten  years  later  rhinitis,  followed  by  dacryo- 
cystitis. When  he  blew  his  nose,  sanious  fluid  and  thick  crusts  came  out.  Breath  was 
fa'tid.  The  oral  trouble  appeared  iasidiously  during  the  course  of  the  chronic  nasal 
syphilis.  He  found  one  day  that  he  could  not  inhale  the  smoke  properly,  and  the 
smoke  passed  through  the  nose.  This  was  the  first  hint  of  any  perforation.  A  little 
later  the  symptoms  of  perforation  became  evident :  the  voice  became  nasal,  food  and 
drink  regurgitated  into  the  nose.  The  perforation  increased  in  size,  and  he  noticed  a 
"  small  hole  "  in  the  roof  of  his  palate.  He  used  a  jiiece  of  gutta-percha  to  stop  the 
hole.  The  disease  growing  worse,  he  came  under  my  care.  The  breath  was  fa'tid  ; 
his  speech  was  rendered  almost  unintelligible  by  the  perforation  ;  rhinitis  not  cured  ; 
nasal  secretion  abundant  and  muco-purulent  ;  deglutition  difficult ;  saUva  running  from 
the  mouth  ;  food  retained  in  the  nasal  cavity  by  the  gutta-percha,  and  putrefying  there. 

On  removing  the  plug,  the  stench  was  horrible,  and  the  mucous  membrane  bled  pro' 
fusely.  After  extraction  of  the  foreign  body,  examination  of  the  perforation  and  of  the 
excavation  was  possible.  On  the  buccal  side  a  hole  about  the  size  of  a  florin  occupied 
the  centre  of  the  palatine  vault.  It  gave  access  to  a  conical  excavation,  the  bottom  of 
which  was  formed  by  the  vault  of  the  nasal  fossjc.  The  edges  of  the  perforation  did  not 
look  like  cicatricial  tissue.  The  active  progress  of  destruction,  whicli  liad  been  going 
on  for  seven  years,  was  evident. 

Examination  of  the  nasal  fossre  showed  the  extent  of  the  mischief:  vomer  almost 
completely  destroyed  ;  perpendicular  plate  of  the  ethmoid  laid  bare  ;  cartilaginous 
septum  almost  intact,  but  much  displaced  to  the  right ;  mucous  membrane  of  the  noso 
swollen  and  suppurating. 

♦  "  Syphilis  Naso-Buccale  "  {Clinique  Medicate  de  VHutel-Dieu,  1899,  4""'  le^on). 


552  .  TEXT-BOOK  OF  MEDICINE 

I  at  once  prescribed  mercurial  treatment  (oily  injections  of  biniodide  of  mercury). 
After  six  injections  the  rhinitis  grew  better  ;  after  fifteen  injections  the  nasal  mischief 
was  arrested,  and  the  ozaena  disappeared.  The  injections  were  then  suspended  for  about 
ten  days  and  renewed.  Collin  made  an  obturator,  so  that  the  patient  could  talk,  sing, 
drink,  and  eat  as  well  as  ever. 

In  another  case  I  witnessed  the  process.  A  woman  under  my  charge  told  us  that 
a  year  before  she  had  a  so-called  "  severe  cold  in  the  head  " — that  is,  syphiUtic 
rhinitis.  She  could  only  breathe  with  her  mouth  open,  because  the  nose  was  blocked  ; 
she  lost  her  sense  of  smell,  and  the  breath  became  foetid.  The  rhinitis  went  on  eight 
or  nine  months,  and  three  months  ago  her  attention  was  drawn  to  the  roof  of  her  palate. 
She  touched  it  with  her  tongue,  and  felt  an  abscess  in  course  of  formation.  Later  she 
noticed  at  the  same  spot  a  small  piece  of  bone.  This  was  a  sequestrum.  On 
swallowing,  liquids  came  back  through  the  nose,  and  though  the  perforation  was  not  yet 
complete,  since  the  sequestrum  was  still  in  situ,  a  fissure  had  established  communication 
between  the  nose  and  the  mouth. 

Examination  of  the  palate  showed  the  process  in  full  evolution.  In  the  median 
line,  in  the  centre  of  a  reddish  granulating  ulceration,  the  sequestrum  stood  out ;  it 
was  formed  by  a  fragment  of  the  maxilla,  to  which  part  of  the  vomer  was  ankylosed. 
There  was,  therefore,  between  the  mouth  and  the  nose  only  a  simple  fissure,  filled  in 
part  by  the  sequestrum  and  the  granulations  of  the  neighbouring  parts.  Symptoms 
were  absent,  but  when  the  communication  was  established  the  symptom-complex 
became  clear  :  nasal  voice,  defective  pronunciation,  reflux  of  liquid  and  solid  food 
through  the  nose,  etc.  Examination  of  the  nasal  fossae  showed  that  the  cartilaginous 
septum  was  almost  entirely  eliminated,  and,  in  the  absence  of  treatment,  the  dissolu- 
tion of  the  nose  was  close  at  hand. 

I  had  in  the  Hotel-Dieu  a  patient  nicknamed  "  The  Cornet-Player."  Two  years 
before  he  had  syphilitic  rhinitis,  when  the  following  incident  took  place  :  For  several 
weeks  he  had  felt  on  the  roof  of  his  mouth  a  small  painless  projection,  which,  however, 
gave  no  trouble,  until  one  evening,  when  he  was  jslaying  his  cornet,,  the  symptoms  of 
perforation  suddenly  appeared.  He  could  get  no  sound  from  his  cornet,  because  the 
air  passed  through  the  nose.  His  nasal  voice  amused  his  friends.  He  took  a  glass  of 
beer,  but  the  liquid  came  back  through  the  nose. 

Next  day  he  told  us  the  history  of  the  previous  evening.  We  found  in  the  roof  of 
the  palate  a  small  perforation.  His  voice  was  nasal  and  his  pronunciation  defective. 
Fluid  came  back  through  his  nostrils.  I  sent  for  his  cornet,  but  he  could  not  make 
a  sound.  The  expired  air  passed  through  a  hole  in  the  palate.  A  gutta-percha 
obturator  was  put  into  the  perforation  ;  the  symptoms  immediately  disappeared. 
In  this  case,  too,  the  perforation  supervened  suddenly  in  the  course  of  syphilitic 
rhinitis. 

The  following  case  also  presents  many  interesting  points  : 

"  For  the  last  seventeen  years,"  said  my  patient,  "  I  have  gone  about  with  a  hole 
in  my  mouth.  I  have  made  obturators  in  caoutchouc  and  in  gutta-percha  as  well  as 
I  could,  but  they  are  very  imperfect.  What  can  you  do  for  me  ?"  At  the  same 
time  he  removed  the  so-called  obturator.  His  speech  was  at  once  transformed  into 
a  kind  of  unintelligible  mumbling.  I  examined  his  mouth,  and  saw  on  the  roof  of 
the  palate  an  enormous  hole,  large  enough  to  take  in  a  hazel-nut.  The  perforation 
had  commenced  seventeen  years  before  as  a  small  opening  in  the  course  of  syphilitic 
rhinitis.  The  ulceration  had  gi-adually  destroyed  a  part  of  the  roof  of  the  mouth,  and 
yet  during  this  long  time  the  general  health  was  not  interfered  with,  and  the  syphilis 
did  not  manifest  itself  elsewhere.  The  necrosis  was  arrested  by  means  of  oily  injections 
of  biniodide  of  mercury.  Berger  made  an  obturator,  and  since  then  phonation, 
mastication,  and  deglutition  have  been  performed  to  perfection. 


DISEASES  OF  THE  MOUTH  553 

Description. — The  necrotic  process  shows  itself  first  on  the  floor  of  the 
nasal  fossae,  and  the  general  rule  is  that  syphilitic  rhinitis  almost  always 
precedes  the  perforation  of  the  roof  of  the  palate  (I  am  speaking  of  the 
roof,  and  not  of  the  velum).  It  was  beUeved  for  a  long  time  that  perforation 
of  the  roof  proceeded  from  the  mouth  towards  the  nose.  This  is  an  error. 
The  perforation  proceeds  from  the  nose  towards  the  mouth.  This  view  is 
held  by  Fournier  and  Duplay,  and  I  agree  with  them  entirely. 

Besides,  if  we  consider  syphiHs  of  the  nasal  fossae  as  a  whole,  we  see  that 
it  is  the  centre  frorn  which  syphilitic  lesions  of  the  neighbouring  parts  start 
out.  In  one  patient,  syphilitic  rhinitis  ends  in  necrosis  of  the  nasal  bones, 
and  the  bony  framework  collapses.  In  another,  nasal  syphiHs  attacks  the 
lachrymal  bone  and  the  nasal  process  of  the  superior  maxilla.  Dacryo- 
cystitis, watli  or  without  abscess,  is  the  result.  In  a  few,  happily  rare,  cases 
nasal  syphihs  attacks  more  dangerous  regions — the  upper  wall  of  the  nasal 
fossae  and  the  cribriform  plate  of  the  ethmoid  and  the  sphenoid  bones. 
Syphihtic  osteo-periostitis  readily  spreads  into  the  cranial  cavity,  and  may 
cause  meningo-encephalitis,  abscess  of  the  brain,  phlebitis  of  the  sinuses, 
or  "  naso-cranial  syphihs,"  as  Fournier  calls  it. 

Perforation  of  the  roof  of  the  palate  is  also  a  consequence  of  nasal 
syphihs.  "  In  consequence  of  tuberculo-ulcerous  sypliihdes,  or  of  gum- 
matous periostitis  of  the  floor  of  the  nasal  fossae,"  says  Fournier,  "  a  larger 
or  smaller  segment  of  the  superior  maxilla  is  denuded,  and  becomes  necrosed. 
An  eUminative  peripheral  phlegmasia  occurs,  and  an  abscess  is  formed  under 
the  mucous  membrane  hning  the  inferior  surface  of  the  diseased  bone.  Tliis 
abscess  points  in  the  mouth  as  a  small  hemispherical  tumour.  At  a  given 
moment  it  opens  spontaneously,  or  is  opened  by  the  surgeon.  The  orifice 
soon  enlarges,  and  then  a  part  of  the  necrosed  segment  appears  bare  on  the 
roof  of  the  palate.  Lastly,  the  necrosed  portion  separates,  and  in  a  moment, 
to  the  great  surprise  of  the  patient,  a  more  or  less  extensive  perforation  of 
the  palate  is  formed,  with  two  major  troubles,  which  are  its  necessary  conse- 
quence— alteration  of  the  voice  and  reflux  of  sohd  and  liquid  foods  introduced 
into  the  mouth." 

Two  distinct  phases  then  occur  in  this  syphilitic  process.  In  the  first 
phase,  which  is  often  slow  and  insidious,  the  process  is  nasal.  The  lesion 
betravs  itself  by  the  symptoms  of  chronic  coryza,  with  ozaMia,  crusts,  nuico- 
purulent  secretion,  and  the  formation  of  sequestra,  easily  distinguishable 
with  the  probe.  This  phase  is  followed  by  the  phase  of  perforation.  This 
])erforati()n  usually  occupies  the  median  line  of  the  roof  of  the  ])alate  a  little 
in  front  of  the  palate  bones.  It  follows  "  the  partial  necrosis  of  the  maxilla, 
or  of  the  two  njaxillae  and  the  vomer  at  their  point  of  meeting."  •  The  perfora- 
tion may  be  round  or  oval.  At  first  it  is  the  size  of  a  pin's  head  ;  later  it 
may  be  as  large  as  a  florin  or  more,  because  it  may  invade  a  portion  of  the 


554  TEXT-BOOK  OF  MEDICINE 

roof  of  the  palate.  On  the  side  of  the  mouth  the  lesion  in  the  palate  is 
also  very  indolent.  My  patient  noticed  nothing  until  the  smoke  from  his 
cigarette  came  out  of  his  nose,  and  revealed  the  perforation.  The  cornet- 
player  felt  no  pain  in  his  mouth  when  the  perforation  suddenly  occurred. 

At  the  moment  of  its  formation  the  perforation  does  not  always  look 
like  a  hole  ;  it  may  be  only  a  simple  fissure,  as  in  the  second  case.  "  The 
hole  "  only  exists  when  the  sequestrum  has  been  eliminated.  This  elimina- 
tion may  be  slow,  the  fragment  crumbling  gradually  ;  it  may  be  sudden,  the 
fragment  being  evicted  as  a  whole,  as  in  the  cornet-player.  The  elimination 
of  the  sequestrum  usually  leaves  but  a  small  perforation,  which  is  at  this 
time  perfectly  curable,  either  spontaneously  or  by  specific  treatment. 

As  a  rule,  a  syphilitic  perforation  left  to  itself  tends  to  enlarge.  The 
ulcero-necrosing  process,  which  is  slow  in  its  course,  recalls  both  rarefying 
osteitis  and  phagedsena.  In  two  or  three  years  the  perforation  attains  the 
size  of  a  halfpenny ;  in  four  or  five  years  it  is  as  large  as  a  florin.  It  is 
somewhat  surprising  that  syphiUs  persists  in  a  certain  region,  and  slowly 
pursues  its  ravages  for  ten  or  fifteen  years,  wliilst  it  leaves  the  rest  of  the 
organism  free.  The  same  process  is  seen  in  other  regions.  We  are  not 
sufficiently  familiar  with  these  elective  localizations  of  syphilis,  and  we  too 
often  make  mistakes,  because  we  beheve  syphiUs  to  be  incapable  of 
lasting  for  ever  in  one  spot,  and  of  respecting  the  remainder  of  the 
economy. 

The  symptoms  vary  according  to  the  size  of  the  perforation.  If  the 
perforation  is  a  simple  fissure  or  a  small  opening,  reflux  of  a  few  drops  of 
fluid  through  the  nose  and  slightly  nasal  timbre  of  the  voice  are  its  only 
symptoms  ;  if  the  perforation  is  larger,  nasal  voice,  defective  pronunciation, 
and  reflux  of  drink  and  food  through  the  nose  are  the  consequences.  These 
symptoms  recall  paralysis  of  the  velum  palati ;  in  both  cases  we  find  the 
same  difficulties  of  deglutition  and  pronunciation. 

Besides  the  nasal  sound  which  renders  the  voice  unnatural,  certain  words 
or  letters  cannot  be  pronounced.  Thus  "  b  "  and  "  p  "  are  pronounced 
"  m,"  for  the  following  reasons  :  Under  normal  conditions  the  letters  "  b  " 
and  "  p  "  are  formed  by  the  column  of  expired  air,  which  suddenly  separates 
the  lips  and  makes  them  vibrate.  When  the  roof  of  the  palate  is  perforated, 
the  column  of  expired  air  loses  its  strength,  because  it  is  divided  into  two 
parts  :  one  part  separates  the  lips,  and  only  succeeds  in  pronouncing  "  m," 
while  the  other  passes  into  the  nasal  fossae,  and  renders  the  voice  nasal. 
The  patient  can  partially  remedy  this  condition  by  pinching  his  nose. 
Deglutition  is  rendered  very  difficult  by  the  perforation  of  the  palate,  because 
the  sohds  and  liquids  which  are  passing  between  the  tongue  and  the  palate, 
and  are  being  pushed  from  before  backwards,  enter  the  hole  and  come  back 
through  the  nose.     Perforation  of  the  roof  of  the  palate  betrays  itself  by 


DISEASES  OF  THE  MOUTH  555 

other  symptoms,  such  as  the  impossibility  or  difficulty  of  sucking,  of 
whistUng,  of  blowing,  or  of  inhaling  the  smoke  of  a  cigarette. 

Pathogenic  Diagnosis. — Perforation  may  be  also  caused  by  tubercu- 
losis and  by  lupus,  but  it  is  extremely  rare.  "  Out  of  twenty  palatine  per- 
forations," says  Fournier,  "  nineteen  may  be  ascribed  to  sypliilis."  I  go 
even  further,  and  I  beheve  that  out  of  forty  perforations  syphilis  can  claim 
tliirty-nine.  Yet  this  considerable  disproportion,  notwithstanding,  the 
diagnosis,  must  be  made.  Tubercular  perforations  of  the  velum  palati  are 
more  common  than  those  of  the  roof.  The  latter  alone  demand  our  attention 
here. 

Case  observed  by  Quenu  : 

A  patient  suffering  from  phthisis  complained  of  the  passage  of  liquids  through  his 
nose.  On  examining  the  mouth,  an  antero-posterior  ulcer  was  observed  on  the 
middle  line  of  the  roof  of  the  palate,  behind  the  incisors.  The  surface  was  covered  with 
a  yellowish -grey  detritus.  In  the  centre  there  was  a  small  perforation.  On  the  posterior 
part  of  the  roof  of  the  palate  the  swollen  mucous  membrane  was  covered  with  the  tuber- 
cular granulations.  Post  mortem,  the  roof  and  the  velum  of  the  palate  were  removed. 
The  mucous  membrane  was  destroyed  ;  the  bone  formed  the  bottom  of  the  ulcer.  The 
perforation  was  due  to  the  destruction  of  the  fibro-mucous  tissue  which  closed  the 
anterior  palatine  canal.  This  perforation,  hke  the  bony  canal,  which  is  single  on  the 
side  of  the  mouth,  bifurcated  into  the  two  tubes  which  opened  on  either  side  of  the 
nasal  septum.     On  the  nasal  side  the  perforations  were  rounded. 

Caussade  has  sent  me  the  following  case  : 

He  had  under  his  care  a  tubercular  patient  who  complained  of  a  smarting  in  the 
roof  of  the  palate  and  of  sharp  pains  on  contact  with  food.  On  examining  the  mouth, 
the  general  pallor  so  frequent  in  tuberculosis  was  noticed.  On  the  roof  of  the  palate, 
to  the  left  of  the  middle  line,  and,  as  it  were,  grafted  on  to  the  cicatrix  of  old  lupus, 
there  existed  an  irregular  ulcer  of  the  size  of  a  florin.  Around  this  ulcer,  which 
had  a  sanious  floor  and  loose  edges,  were  some  yellowish  granulations.  A  probe 
readily  entered  the  nasal  fossae,  proving  the  existence  of  a  small  perforation.  Tubercle 
bacilli  were  found  in  the  purulent  liquid  bathing  the  ulcer  ;  they  were  also  present 
in  the  yellow  granules. 

To  sum  up  :  the  jagged,  loose  edges  of  the  ulceration,  the  sanious  fioor,  the  yellow 
peripheral  granules,  and  the  presence  of  the  bacilli  in  the  pus,  distinguished  the  tuber- 
cular from  the  syphilitic  ulceration. 

There  is  a  perforating  disease  of  the  mouth  which  must  be  distinguisliod 
from  syphiHtir-  porforations.  What  is  to  be  understood  by  perforating 
disease  of  the  mouth  ?  Fournier  thus  names  the  trophic  lesion,  which  is 
especially  seen  in  tabetics  ;  it  is  comparable  with  perforating  ulcer  of  the 
foot.  Baudot  has  collected  .seven  cases.  This  tropliic  trouble,  which  as  a 
rule  causes  no  pain,  runs  the  following  cour.se  :  progressive  absorption  of 
the  alveolar  arches  causes  the  teeth  to  fall  out  spontaneously.  The  falling 
out  of  the  teeth  is  followed  by  absorption  of  the  alveolar  border.  "  Per- 
forating disease  "  follows  this  bony  absorption  ;  it  commences  with  ulceration 
of  the  mucous  membrane,  and  burrows  down  into  the  tissues  until  it  per- 
forates the  bone.     This  perforation  only  affects  the  superior  ma.\illa  (though 


556  TEXT-BOOK  OF  MEDICINE 

trophic  troubles  are  met  with  in  both  maxillae).  It  may  be  unilateral  or 
bilateral ;  it  never  occupies  the  centre  of  the  roof  of  the  palate,  but  the  peri- 
phery, especially  at  the  site  of  the  first  molars  which  hav^e  fallen  out.  The 
perforation  is  elongated  in  its  antero-posterior  direction,  and  may  allow 
insertion  of  the  finger  ;  it  estabhshes  communication  between  the  mouth 
and  the  nasal  fossae  or  the  maxillary  sinus. 

Perforating  disease  difiers  from  syphihtic  perforations  of  the  palate  in 
the  trophic  troubles  wliich  precede  it— viz.,  casting  of  the  teeth  and  absorp- 
tion of  the  alveolar  borders  of  both  maxillae.  As  I  have  just  stated,  it  never 
occupies  the  centre,  but  the  periphery  of  the  roof  of  the  palate  ;  the  edges  are 
usually  insensitive.  It  is  a  trophic  trouble  almost  always  accompanied  by 
positive  or  aberrant  symptoms  of  tabes. 

Treatment. — Treatment  is  in  part  prophylactic.  As  the  perforation  is 
preceded  by  syphilitic  rhinitis,  we  should  recognize  and  treat  the  rhinitis. 
In  a  syphilitic  patient  chronic  coryza  is  always  open  to  suspicion.  Anyone 
tainted  with  syphilis  who  catches  "  a  persistent  cold  in  the  head,"  with 
purulent  mucus  and  crusts,  must  be  watched  closely,  because  the  rhinitis 
may  end,  for  want  of  specific  treatment,  in  ozaena,  in  destruction  of  the 
cartilages  and  the  bones,  and  in  perforation  of  the  palate.  With  all  the  more 
reason  must  treatment  be  commenced  without  loss  of  time  in  a  syphilitic 
patient  who,  during  a  chronic  coryza,  feels  a  swelUng  in  the  roof  of  the 
palate.  This  swelUng  is  the  prelude  of  a  process  which  will  terminate  in 
perforation  ;  the  lesion,  if  taken  in  time,  may  be  confined  within  limits. 

The  perforation  at  its  commencement  is  always  of  small  size,  perhaps  as 
large  as  a  pin's  head.  At  tlus  moment  it  is  sometimes  curable  by  mercury, 
with  or  without  the  addition  of  iodides.  When  the  perforation  is  large,  we 
have  only  two  means  of  remedying  it — surgical  intervention  or  a  well-made 
obturator.  In  either  case  the  patient  must  be  at  first  put  on  specific  treat- 
ment to  limit  the  necrotic  process  if  it  is  still  active.  This  treatment  con- 
sists in  mercury,  with  or  without  iodide  of  potassium.  As  regards  mercurial 
preparations,  I  give  the  preference  to  injections  of  an  oily  solution  of  bin- 
iodide  of  mercury. 

X.  TUBERCULOSIS  OF  THE  MOUTH. 

Some  years  ago  tuberculosis  of  the  digestive  canal  was  practically 
unknown  ;  tubercular  lesions  and  ulcers  of  the  intestine  had  alone  been 
described,  but  the  other  parts  of  the  digestive  tube  had  not  been  explored. 
Bayle  had  seen  tubercular  ulcerations  of  the  mouth  without  giving  them 
their  real  significance.  Tliis  question,  first  studied  by  Ricord,  was  at  his 
inspiration  undertaken  by  Buzenet,  and  was  clearly  stated  by  Julliard  ;  since 
these  early  researches  of  French  origin,  numerous  investigations,  both  in 


DISEASES  OF  THE  MOUTH  557 

France  and  abroad,  have  rendered  the  question  of  bucco-pharyngeal  tuber- 
culosis classical. 

The  ulcerations  of  the  mouth  and  the  throat,  which  are  sometimes  met 
with  in  tubercular  subjects,  are  not  ulcerations  of  a  cachectic  nature,  as  was 
at  first  beheved ;  they  are  really  tubercular  ulcerations,  resulting  from 
tuberculosis  in  situ  (Trelat).  By  choice  their  seat  is  on  the  tongue,  the 
pharynx,  and  the  isthmus  of  the  gullet.  They  may  be  sohtary  or  multiple, 
and  show  the  most  varied  forms.  I  shall  study  them  separately  in  the 
mouth  and  in  the  throat.  This  distinction  is,  furthermore,  necessary,  because 
the  ulcerations  of  these  different  regions  have  a  somewhat  different  course. 

Tongue. — Tuberculosis  of  the  tongue  shows  two  chief  forms — tumour 
and  ulcer.  The  tumour,  called  also  tubercular  gumma,  lingual  tubercu- 
loma, or  tubercular  intramuscular  abscess,  is  a  soft  tumour  which  is  not 
painful,  projects  from  the  surface  of  the  tongue,  and  may  be  as  large  as  a 
cherry-stone  or  a  nut. 

Tubercular  ulcers  of  the  tongue  are  more  common ;  they  occupy,  in  order 
of  frequency,  the  tip,  upper,  and  lower  surfaces  of  that  organ.  They  develop 
in  the  following  mamier  :  A  rounded  yellowish  spot,  about  2  Unes  in  diameter, 
is  seen  on  the  mucous  membrane.  The  epithelium  falls  off,  and  the  result  is 
an  ulceration,  wliich  increases  in  size  and  depth.  The  ulcer  sometimes  com- 
mences as  a  fissure,  and  brings  about  hypertrophy  of  the  papilla?.  When  the 
ulcer  has  formed  the  edges  are  scalloped  and  clean-cut ;  the  floor  is  covered 
with  a  layer  of  mucus  and  sahva,  wliich  on  removal  leaves  a  yellowish  uneven 
surface  exposed.  Around  the  ulcer  a  bed  of  yellowish  points  is  frequently 
seen ;  they  were  incorrectly  considered  to  be  folUcular  orifices,  but  they  are 
really  small  subepitheUal  abscesses,  or  masses  of  tubercular  follicles,  having 
the  structure  of  tubercular  tissue,  ulcerating  in  their  turn,  and  becoming 
part  of  the  principal  ulcer. 

Histological  examination  reveals  the  following  characteristics  :  A  section 
through  an  ulcer  of  the  tongue  shows  that  the  granulating  portions  of  the 
ulcer  are  formed  of  embryonic  tissue.  The  surface  of  the  ulcer  is  likewise 
infiltrated  with  embryonic  tissue,  and,  deeper  still,  bundles  of  muscular  fibres 
are  seen,  between  and  around  which  the  embryonic  connective  tissue  shows 
hero  and  there  little  islands  of  more  or  less  developed  tubercular  granula- 
tions. The  granulations,  or  rather  the  tubercular  folHcles  (giant  cells, 
eml^ryonic  cells,  and  bacilh),  invisible  to  the  naked  eye,  are  deeply  seated  in 
the  nniscular  tissue  of  the  tongue  ;  they  are  found  as  much  as  f-  inch  or  more 
beyond  the  ulcerated  surface. 

The  tubercular  ulcer  of  the  tongue  is  almost  always  sohtary  at  its  onset, 
thus  differing  from  ulcers  of  the  pharynx,  the  isthmus  and  the  velum, 
which  are  often  multiple.  As  the  ulcer  grows  older,  it  becomes  deeper,  an- 
fractuous, and  deeply  excavated,  in  distinction  to  the  ulcers  of  the  pharynx. 


558  TEXT-BOOK  OF  MEDICINE 

which  are  generally  superficial.  On  the  tongue  the  ulcers  make  slow  progress , 
and  coincide  with  the  chronic  forms  of  pulmonary  phthisis,  whilst  the  tuber- 
cular ulcers  of  the  pharynx  coincide  rather  with  the  rapid  and  general  forms 
of  tuberculosis.  The  ulcers  in  the  mouth  in  some  cases  seem  to  precede  the 
lesions  in  the  lung  ;  they  may  heal  and  cicatrize.  The  ulcers  of  the  tongue 
are  very  painful  upon  contact  with  hquids  or  food,  and  patients  have  much 
pain  in  the  acts  of  mastication  and  deglutition. 

These  pains  are,  however,  not  so  acute  as  those  occasioned  by  ulceration 
of  the  pharynx.  Contrary  to  what  might  be  supposed,  tubercular  ulcers 
of  the  tongue  are  rarely  followed  by  adenopathy. 

The  tubercular  ulcer  of  the  tongue  must  not  be  confounded  with 
chancre.  The  chancre  has  not  a  greyish  and  granular  surface  ;  it  is  not  sur- 
rounded by  a  bed  of  yellowish  points  ;  its  floor  is  more  in  relief,  and  it  is  not 
painful  on  pressure.  Its  base  is  much  more  indurated ;  the  adenitis  which 
it  provokes  is  painless.  Tubercular  ulceration  of  the  tongue  is  distinguished 
from  epithelioma  by  the  following  signs  :  The  surface  of  the  epithehoma 
shows  more  vegetations;  it  bleeds  easily,  and  gives  rise  to  an  oozing  of 
foetid  liquid.  Its  edges  are  very  much  raised  and,  as  it  were,  everted.  It 
it  often  the  seat  of  spontaneous  lancinating  pains.  It  produces  painful 
adenitis  of  slow  course. 

Tubercular  ulcers  are  very  rare  on  the  lips  and  gums.  They  are  some- 
times consecutive  to  tubercular  ulcers  of  the  mucous  membrane  of  the 
cheeks.  Reclus  records  a  case  in  which  ulcers  on  the  gums  led  to  falhng  out 
of  the  teeth.  Giraudeau  cites  a  case  in  which  osteo-pei;iostitis,  falling  out  of 
the  teeth,  and  necrosis  of  the  maxilla  occurred. 

Roof  of  the  Palate. — Tubercular  ulcers  of  the  roof  of  the  palate  are 
more  common  than  was  formerly  supposed.  Hermandier  has  collected 
eight  cases.  One  or  more  ulcers  may  be  found  ;  they  are  situated  indiscrimi- 
nately on  all  parts  of  the  roof,  and,  as  a  rule,  the  velum  palati,  the  pillars  of 
the  fauces,  and  the  hps  present  at  the  same  time  ulcers  of  a  like  nature. 
Here,  as  elsewhere,  the  outhnes  are  well  defined  when  the  ulcer  is  sohtary ;  but 
when  several  ulcers  unite,  as  frequently  happens,  the  ulcerated  surface 
presents  a  sinuous  outhne,  and  may  be  some  inches  in  extent.  The  edges  of 
the  ulcers  are  reddish,  pufEed,  and  clean-cut ;  they  are  rarely  indurated. 
Tubercular  ulceration  of  the  roof,  hke  that  of  the  tongue,  is  frequently 
surrounded  by  projecting  )^ellowish  points,  which  are  tubercular  nodules. 

The  formation  of  the  ulcers  is  accompanied  by  smarting  and  pain,  par- 
ticularly on  contact  with  food.  In  some  cases  (Quenu,  Caussade)*  the  ulcers 
end  in  perforation  of  the  roof  of  the  palate.     The  ulcer  is  rarely  cured. 

Painting  with  a  solution  of  lactic  acid  (1  in  10)  gives  good  results. 

*  This  question  has  been  treated  in  the  section  dealing  with  perforation  of  the 
roof  of  the  palate,  as  regards  differential  diagnosis. 


CHAPTEE  II 
DISEASES  OF  THE  THROAT  AND  PHARYNX 

In  studying  the  diseases  of  the  throat  and  pharynx  we  shall  at  every 
moment  meet  with  the  word  angina.  This  word  angina  (from  ayx^,  I 
strangle)  was  formerly  employed  to  designate  every  disease  which  was 
accompanied  by  troubles  of  deglutition  and  respiration  and  was  seated 
above  the  lung  and  the  stomach.  Though  the  word  angina  does  not 
answer  to-day  to  the  ideas  which  created  it,  it  has,  nevertheless,  been 
retained,  and  writers  have  essayed  to  make  it  comprehensible  by  associating 
with  it  certain  adjectives  which  give  it  species  and  varieties. 

I.  ACUTE  CATARRHAL  ANGINA— ACUTE  ERYTHEMATOUS 

ANGINA. 

Under  the  name  of  erythematous  angina  and  acute  anginal  catarrh, 
we  describe  inflammation  of  the  raucous  raembrane  of  the  posterior  portion 
of  the  mouth  and  the  pharynx,  which  is  superficial,  sometimes  limited  to  a 
diffuse  redness,  as  the  name  "  erythematous  "  indicates,  and  sometimes 
accompanied  by  a  pultaceous  covering.  The  localization  of  the  angina  is 
somewhat  variable  :  sometimes  it  is  diffuse,  and  occupies  both  the  pharynx 
and  the  posterior  portion  of  the  mouth  ;  at  other  times  it  affects  certain 
points,  as  the  isthmus  of  the  gullet,  the  tonsils,  or  the  pharynx. 

Description. — Acute  catarrhal  angina  commences  with  shivering, 
fever,  lassitude,  headache,  and  loss  of  appetite,  wliich  are  slight  in  some 
subjects,  but  in  others  (in  children  especially)  become  so  severe  that  we  are 
liable  to  suspect  the  onset  of  some  serious  disease.  The  general  troubles, 
which  may  be  accompanied  or  not  by  gastric  disturbance,  precede  the  angina 
by  a  day  or  so  ;  they  may  appear  simultaneously.  The  angina  is  ushered  in  by 
a  sensation  of  dryness  and  smarting  in  the  throat.  Deglutition  is  painful ; 
the  mucous  membrane  is  red,  dry,  sniny,  and  close  set  with  projections  due 
to  swelling  of  the  muciparous  glands  ;  while  the  serous  infiltration  of  the  sub- 
mucous tissue  produces  swelling  of  parts  rich  in  loose  cellular  tissue,  such  as 
the  uvula  and  istlimus  of  the  gullet.  The  angina  may  remain  simply 
erythematous,  but  sometimes  as  early  as  the  second  or  tiiird  day  the  liypiir- 

559 


560  TEXT-BOOK  OF  MEDICINE 

secretion  of  the  mucous  membrane  is  shown  by  mucus  on  the  pharynx  and 
by  caseous  concretions,  or  pultaceous  layers  on  the  tonsils.  These  products, 
which  are  not  adherent,  do  not  resemble  the  membranes  of  diphtheria,  and 
yet  they  may  be  associated  with  the  diphtheria  bacillus,  as  bacteriology 
has  proved. 

Acute  angina  is  most  frequently  accompanied  by  a  gastric  or  bihous 
condition.  The  tongue  is  white  and  coated,  the  anorexia  is  complete, 
attacks  of  nausea  are  frequent,  and  constipation  is  the  rule.  The  fever  falls 
from  the  second  to  the  fifth  day.  The  submaxillary  glands  are  but  slightly 
enlarged.  Acute  catarrhal  angina  does  not  last  more  than  a  week  ;  it  gener- 
ally ends  in  resolution,  but  relapses  and  passage  into  the  chronic  state  may 
occur  in  patients  predisposed  by  some  diathetic  condition.  Paralysis  of  the 
velum,  and  even  general  muscular  paralysis  have  been  described  (Gubler) ; 
these  cases  are  obviously  diphtheria. 

JEtiology,  diagnosis,  and  treatment  will  be  studied  in  the  following 
chapter.  For  the  time  being  let  me  remark  that  the  better  prepared  the 
soil,  the  more  important  the  role  of  the  micro-organisms. 

Mouth-washes  and  antiseptic  gargles  are  indicated.  I  generally  employ 
very  weak  solutions  of  boric  acid  (6  per  cent.). 


II.   ACUTE   TONSILLITIS— SIMPLE  TONSILLITIS— SUPPURATIVE 
TONSILLITIS— ULCERO-MEMBRANOUS  TONSILLITIS- 
VINCENT'S  ANGINA. 

Inflammation  of  the  tonsils,  or  amygdahtis,  is  also  called  tonsillar  angina. 
In  order  to  facihtate  description  I  shall  describe  three  varieties — simple, 
suppurative,  and  infectious  amygdalitis — but  these  three  varieties  have 
common  characteristics  which  are  often  blended  chnically. 

1.  Simple  Acute  Tonsillitis. 

Description. — Acute  tonsilhtis  constitutes  an  important  variety,  and  is 
the  most  common  form  of  catarrhal  angina.  When  the  tonsilhtis  is  shght, 
its  description  blends  in  part  with  the  symptoms  enumerated  in  the  previous 
section.  When  it  is  severe,  it  may  commence  with  a  sharp  rigor  ;  the 
temperature,  particularly  in  children,  rises  to  104°  F.,  and  the  face  becomes 
red  and  feverish.  Deglutition  soon  becomes  very  painful,  and  its  every  move- 
ment is  accompanied  by  contortions  and  grimaces.  Liquids  often  regurgitate 
through  the  nose,  and  the  patient  refrains  from  swallowing  liis  sahva. 
The  voice  becomes  tonsillar ;  the  opening  of  the  mouth  and  the  move- 
ments of  the  jaw  are  very  painful.  The  exterior  and  lateral  regions  of  the 
neck  are  painful  and  brawny,  and  the  tonsils  become  so  swollen  that  respira- 


DISEASES  OF  THE  THROAT  AND  PHARYNX  561 

tion  may  be  obstructed.  Pains  in  the  ear  and  auditory  troubles  occur  only 
when  the  inflammation  reaches  the  Eustachian  tube. 

Examination  of  the  throat  is  not  always  easy,  because  the  pain  on  opening 
the  mouth  causes  contraction  of  the  masseters.  The  tongue  is  thickly 
coated.  The  tonsils,  wliich  are  red  and  bulky,  are  unequally  affected  by  the 
inflammation,  and  present  whitish  concretions  in  the  follicular  crypts,  so 
that  the  disease  has  received  the  name  of  "  follicular  tonsillitis."  These  con- 
cretions are  yellowish-white,  soft,  caseous,  easily  detached,  and  have  httle 
tendency  to  reproduce  themselves  ;  they  sometimes  appear  to  be  encysted. 
In  spite  of  the  acuteness  of  the  symptoms,  the  disease  ends  in  a  few  days  by 
resolution,  though  it  ends  in  suppuration  in  the  form  which  I  shall  describe 
next. 

Acute  tonsilhtis  attacks  all  ages,  but  principally  youth.  When  it  is 
primary,  its  cause  is  cold  and  chills  ;  when  secondary,  it  is  associated  with 
other  affections,  such  as  coryza  or  grippe.  Some  people  are  predisposed  to 
it,  and  amongst  them  second  attacks  are  frequent.  Spring  and  autumn 
and  the  menstrual  periods  are  favourable  to  its  appearance.  The  disease  is 
often  contagious  and  epidemic.  Tliis  question  will  be  discussed  under  the 
Bacteriology  of  Angina. 

2.  Suppurative  Tonsillitis— Phlegmonous  Angina. 

I  shall  next  describe  parenchymatous  tonsilhtis  terminating  in  sup- 
puration. 

Description.  —  The  name  phlegmonous  tonsillitis  would  lead  us  to 
suppose,  incorrectly,  that  the  tonsil  itself  is  the  seat  of  the  suppuration.  The 
tonsil  may  suppurate  in  certain  cases,  when  we  see  on  the  surface  little 
abscesses  filUng  the  folhcular  crypts,  but  this  is  the  exception.  As  a  rule, 
the  abscess  forms  in  the  peritonsillar  tissue,  at  its  upper  and  outer  part,  so 
that  the  tonsillitis  becomes  a  peritonsillitis. 

Phlegmonous  tonsillitis  may  have  an  acute  onset ;  more  often  it  com- 
mences as  a  simple  catarrhal  angina,  and  the  subsequent  symptoms  announce 
the  formation  of  pus.  These  symptoms  are  a  violent  rigor,  rise  of  temperature 
to  104°  F.,  intense  pain  in  the  tonsil,  and  extreme  difficulty  in  moving  the 
jaw.  During  the  next  few  days  the  fever  remains  high,  and  tlio  pain  spreads 
to  the  neck,  the  jaws,  and  the  ears.  Loss  of  appetite  is  complete  ;  swallowing 
is  extremely  painful  or  impossible  ;  the  breathing  is  laboured,  the  voice  is 
nasal,  and  tlie  sahva  flows  continuously.  Tlie  patient  can  neither  open  his 
mouth  nor  move  his  tongue  ;  he  can  hardly  speak  ;  his  neck  is  bent,  im- 
movaljlo,  brawny,  and  painful.  The  head  is  retracted  towards  the  liealthy 
side,  and  movement  is  almost  impossible.  Examination  of  the  tiiroat  is 
very  difficult,  because  the  patient  has  the  greatest  difficulty  in  opening  tlie 
moutii.     Wiien  the  throat  is  seen,  the  tonsils  are  often  found  to  bo  covered 

36 


562  TEXT-BOOK  OF  MEDICINE 

with  whitish  exudate,  and  when  the  abscess  is  in  process  of  formation,  the 
colour  is  sometimes  purple.  The  breath  is  foetid,  and  the  tongue  covered 
with  a  thick  coat.  The  velum  palati  is  lowered  and  pushed  back ;  the  isthmus 
of  the  gullet  is  narrowed  by  the  oedema  of  the  mucous  membrane  and  the 
projection  of  the  affected  tonsil.  The  patient  experiences  a  sort  of  suffoca- 
tion, which  caused  the  name  of  "  esquinancia  "  to  be  given  formerly  to  the 
disease.  Two  or  three  days  later  the  pain  becomes  shooting,  and  we  may 
perhaps  feel  a  soft  swelling  indicating  pus.  Artificial  or  spontaneous  opening 
of  the  abscess  is  followed  by  considerable  rehef .  Spontaneous  rupture  occurs 
generally  from  the  sixth  to  the  eighth  day  at  the  intersection  of  the  pillars  of 
the  fauces,  and  the  patient  expectorates  bloody  foul-smelling  pus. 

Phlegmonous  tonsillitis  is  not  serious  as  a  rule,  and  recovery  occurs  in 
about  a  week  ;  nevertheless,  gangrene,  oedema  of  the  larynx,  phlebitis  of  the 
jugular  vein  with  suppuration,  and  opening  of  the  abscess  into  the  cellular 
tissue  of  the  neck,  thrombosis  of  the  jugular  veins,  and  ulceration  of  the 
arteries,  followed  by  fatal  hsemorrhage,  have  been  noted.  In  spite  of  their 
great  rarity  some  of  these  complications  deserve  notice.  Vergely  has  collected 
sixteen  cases  of  ulceration  of  the  internal  carotid  artery,  or  of  the  branches 
which  run  from  the  inferior  pharyngeal  and  palatine  arteries  to  the  tonsils. 
In  some  cases  the  haemorrhage  is  lightning-Hke  in  its  rapidity,  and  the 
catastrophe  occurs  without  any  warning.  Sometimes  the  haemorrhage  recurs 
several  times,  and  it  is  necessary  to  Ugature  the  carotid  artery.  In  one 
case  a  terrible  haemorrhage  ceased  spontaneously,  and  was  not  followed  by 
death. 

The  aetiology  of  phlegmonous  angina  is  in  part  blended  with  that  of 
simple  tonsillitis  ;  it  is  hkewise  subject  to  recurrences,  and  is  often  grafted 
on  a  chronic  catarrhal  or  subacute  angina,  which  has,  so  to  say,  acted  as  the 
port  of  entrance. 

3.  Infectious  Tonsillitis. 

Description. — During  the  past  few  years  several  cases  of  tonsilHtis  have 
been  classed  amongst  the  infectious  diseases,  and  rightly  so  (Bouchard). 
Simple  or  suppurative  tonsillitis  may  be  one  of  the  numerous  locaHzations  of 
"  tonsillar  fever."  Other  local  manifestations  of  the  disease  may  be  found 
in  the  testicle,  ovary,  or  kidneys,  and  in  this  respect  they  bear  a  Ukeness  to 
the  locaHzations  produced  by  other  infectious  diseases,  such  as  mumps. 
Tonsillar  fever  is  an  infectious  disease,  hke  pneumonia,  which  chooses  the 
lung  as  its  seat  of  election,  but  also  exerts  its  action  on  the  pleura,  the  endo- 
cardium, the  meninges,  the  kidneys,  etc. 

Attention  having  been  drawn  to  this  point,  it  is  certain  that  tonsilUtis 
sometimes  resembles  an  infectious  disease.  In  some  cases  the  local  angina 
is  slight,  and  yet  we  find  that  the  general  symptoms,  including  rigors,  fever. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  563 

lassitude,  and  want  of  appetite,  show  an  intensity  and  a  duration  which  are 
more  in  accordance  with  the  hypothesis  of  a  general  infection,  than  of  a 
simple  inflammation  of  the  tonsil. 

Orchitis  is  one  of  the  manifestations  of  tonsillar  fever,  and  it  is  not  with- 
out analogy  to  the  orchitis  of  typhoid  fever  and  of  mumps.  Orchitis  occurs 
both  in  the  sUght  and  in  the  severe  forms  of  angina.  It  appears  especially 
during  the  dechne  of  the  tonsiUitis  ;  it  is  unilateral,  painful,  and  characterized 
by  inflammation  of  the  testicle  and  effusion  into  the  tunica  vaginaUs.  It 
lasts  from  one  to  three  weeks  ;  it  terminates  by  resolution,  rarely  by  suppura- 
tion, but  it  may  leave  beliind  slight  atrophy  of  the  testicles.  Ovaritis  has 
likewise  been  observed. 

The  nephritis  that  appears  in  the  course  of  tonsillar  fever  is  character- 
ized by  albuminuria,  and  in  some  cases  by  lumbar  pain,  cedema,  and  ursemic 
symptoms.  Although  tliis  nephritis  is  generally  transitory  and  superficial, 
it  may  in  some  cases  result  in  Bright's  disease. 

Articular  pains,  pseudo-rheumatism,  cutaneous  eruptions,  polymorphous 
erythema,  purpura,  ulcerative  endocarditis,  purulent  pericarditis  or  pleurisy, 
peritonitis,  meningitis,  broncho-pneumonia,  phlebitis,  suppurative  otitis, 
nephritis,  orcliitis,  and  ovaritis  may  occur  in  the  course  or  the  decHne  of 
tonsillitis.  Some  of  these  comphcations  are  more  usually  associated  with 
suppurative  tonsilUtis ;  others,  again,  are  rather  the  appanage  of  follicular 
tonsilUtis.  Some  of  these  comphcations  are  the  index  of  a  very  grave 
prognosis  ;  they  may  appear  in  the  course  of  acute  tonsilhtis  wliich  began 
with  mild  symptoms. 

These  facts  prove  that  many  varieties  of  tonsilhtis  are  ordinarily  infec- 
tious diseases.  We  shall  see  what  bacteriology  teaches  on  this  subject. 
For  the  moment  it  is  important  to  remember  that,  clinically  speaking, 
tonsillitis  may  vary  in  its  severity  and  its  course.  It  may  behave  like  a 
local  inflammation,  and  comprise  the  whole  disease  ;  it  may  be  accompanied 
by  multiple  manifestations,  like  the  infectious  diseases. 

Bacteriology.— Bacteriological  researches  have  taught  us  that  in  every 
catarrhal  or  phlegmonous  angina  the  exudate  and  the  caseous  masses  in 
the  cryj)ts  of  the  tonsils  contain  numerous  microbes,  wliich  may  likewise 
be  met  with  in  the  mouths  of  healthy  persons. 

Micrococci,  diplococci,  streptococci,  staphylococci,  pneumococci,  pneumo- 
bacilli,  Bacillus  coli,  tiitragenous  pseudo-diphtheritic  bacilli,  and  all  tiie 
saprophytes  of  the  mouth,  may  be  found  in  the  different  varieties  of  angina 
just  described.  The  principal  share,  however,  belongs  to  the  streptococcus, 
in  the  following  proportions  : 

In  twenty-two  cases  of  angina  and  tonsilhtis  Veillon  found  patho- 
genic microbes  in  the  following  proportions  :  the  streptococcus  was  present 
twenty-two  times,  the  pneumococcus  was  associated  witii  it  sixteen  times, 

3G— 2 


564  TEXT-BOOK  OF  MEDICINE 

and  the  staphylococcus  was  associated  with  it  twice.  Not  a  single  one  of 
these  microbes  is  specific.  What  part  do  they  play  in  angina  and  ton- 
sillitis ?     Why  and  how  do  they  become  virulent  and  pathogenic  ? 

Sometimes  there  is  contagion,  and  a  healthy  individual  receives  the 
pathogenic  agent  from  the  outset.  In  other  cases  we  must  have  recourse  to 
the  old  ideas  of  "  morbid  spontaneity,"  but  we  call  it  "  auto-infection." 
Under  the  influence  of  conditions  wliich  concern  both  the  seed  and  the 
soil,  some  of  which  conditions  are  known  to  us  (cold,  overwork,  microbic 
associations)  and  some  of  which  are  unknown,  the  microbe  or  microbes 
increase  in  virulence,  and  disease  results.  The  pharyngeal  mucous  mem- 
brane is  rich  in  lymphoid  tissue  and  in  macrophages  and  microphages,  which 
are  in  a  continual  state  of  defence.  If  the  defence  weakens,  phagocytosis 
is  in  default  (Metchnikoff),  and  the  individual  is  "  in  a  state  of  morbid 
receptivity." 

In  some  cases  the  pathogenic  agents  do  not  invade  the  tonsils  from  the 
surface,  but  may  enter  on  the  deep  side.  In  such  a  case  the  angina  is 
secondary ;  the  patient  has  been  suffering  from  an  infectious  disease,  and 
as  the  tonsils  "  retain  and  destroy  the  microbes,  it  is  not  surprising  that 
they  suffer  in  consequence  from  time  to  time." 

However  this  may  be,  the  pathogenic  agents,  and  notably  the  strepto- 
coccus, act  according  to  their  virulence  and  according  to  the  soil  they  meet 
with.  The  results  and  the  compHcations  enumerated  may  be  due  either  to 
the  streptococcal  toxine  or  to  the  passage  of  the  streptococcus  into  the 
blood  and  the  organs.  Perhaps  injections  of  antistreptococcal  serum, 
which  are  so  efficacious  in  erysipelas,  may  be  utilized  in  streptococcal 
angina. 

Diagnosis. — On  principle,  examination  of  the  throat  in  a  patient  attacked 
by  even  the  simplest  angina  must  never  be  omitted.  Examination  of  the 
throat  is  painful,  and  at  times  difficult.  Children  undergo  it  with  ill-grace, 
but  it  must  be  insisted  on,  for  fear  of  error  in  the  diagnosis.  The  throat  is 
freed,  by  means  of  a  gargle,  from  the  mucus  which  encumbers  it,  and  then 
explored,  either  by  a  direct  or  reflected  hght. 

In  one  of  the  following  chapters  I  shall  give  the  diagnosis  between 
tonsilhtis  and  diphtheritic  angina.  In  many  cases,  however,  it  can  only 
be  decided  by  bacteriological  examination.  Angina  may  precede  or  accom- 
pany the  articular  manifestations  of  acute  rheumatism.  It  causes  great 
difficulty  in  swallowing  when  the  muscles  of  the  pharynx  are  affected 
(Chomel). 

The  initial  angina  of  scarlatina  precedes  the  cutaneous  eruption,  and 
may  even  be  present  alone,  without  any  eruption.  This  angina  is  charac- 
terized by  the  severity  of  the  fever  and  the  purple  coloration  of  the  mucous 
membrane,  due  to  the  scarlatinal  eruption,  which  occupies  not  only  the 


DISEASES  OF  THE  THROAT  AND  PHARYNX  565 

isthmus  of  the  fauces,  but  also  the  cavity  of  the  mouth  and  the  inner  surface 
of  the  cheeks.  Scarlatinal  angina  is  sometimes  remarkably  indolent.  It 
is  often  accompanied  by  a  pultaceous  exudation  formed  of  soft,  whitish 
patches,  which  are  readily  detached,  and  leave  the  subjacent  mucous 
membrane  quite  intact.  This  exudate,  wliich  is  also  found  in  the  angina 
of  typhoid  fever,  is  formed  by  the  accumulation  of  degenerated  epitheUal 
cells. 

The  exanthem  of  measles  is  characterized  by  a  red  stippling,  and  by 
prominent  spots  upon  the  roof  of  the  mouth,  and  later  the  back  of  the 
pharynx  and  the  posterior  pillars  of  the  fauces  (Lasegue).  The  bucco- 
pharyngeal exanthem  is  preceded  or  accompanied  by  ocular,  nasal,  and 
laryngo-bronchial  catarrhs,  which  announce  the  invasion  of  measles. 

Erysipelatous  angina  may  be  consecutive  to  erysipelas  of  the  face, 
or  may  commence  in  the  pharynx.  It  is  ushered  in  by  a  more  violent 
rigor  than  that  of  catarrhal  angina.  The  difficulty  of  swallowing  is  very 
great,  and  pustules  are  sometimes  present  on  the  mucous  membrane,  which 
is  of  a  claret  colour  (Cornil).     The  submaxillary  glands  are  very  congested. 

The  angina  which  sometimes  accompanies  urticaria  is  easily  recognized 
on  account  of  the  rash  on  the  face  and  the  body. 

Pharyngeal  syphilis  must  not  be  confounded  with  non-syphilitic  angina. 
I  am  not  speaking  of  those  cases  in  which  more  or  less  abundant  mucous 
patches  are  found  in  the  throat— rin  such  cases  the  diagnosis  is  evident — 
but  I  allude  to  those  cases  characterized  by  a  diffuse  or  circumscribed 
erythema  of  the  velum  palati,  pillars,  tonsils,  and  pharynx,  which  has 
often  a  bright  red  shade,  and  fairly  often  coincides  with  syphilitic  erythema 
of  the  larynx. 

I  shall  describe  tuberculosis  of  the  tonsil  in  one  of  the  following  sections. 
For  the  moment  I  shall  confine  myself  to  mentioning  a  form  of  acute  tuber- 
culosis of  the  tonsil  which  exactly  resembles  follicular  tonsilUtis.  The 
diagnosis  can  only  be  decided  by  bacteriological  examination.  Ulcero- 
membranous tonsillitis  occurs,  and  is  often  associated  with  ulcero-mem- 
branous  stomatitis.  It  is  due  to  fusiform  bacilU  and  spirilla,  described  by 
Vincent,  and  runs  the  following  course  :  An  adult  or  a  child  is  taken  ill 
with  pains  in  the  throat.  The  mucous  membrane  is  red  and  oedematous. 
Two  or  three  days  afterwards  there  appears  on  one  tonsil  (more  rarely  on 
both)  a  greyish  membrane,  which  may  be  removed  by  scraping,  and  leaves 
bare  a  reddish  and  bleeding  surface.  The  false  membrane,  which  has  a 
nauseating  smell,  may  extend  to  the  uvula  and  the  pillars.  "  The  large 
number  of  fusiform  bacilli  and  spirilla  in  the  false  membrane,  the  repro- 
duction of  the  false  membrane  as  long  as  these  microbes  are  present,  and  the 
clearing  up  of  the  mucous  membrane  as  soon  as  they  commence  to  decrease, 
are  sound  arguments  for  admitting  their  action  in  the  genesis  of  ulcero- 


566  TEXT-BOOK  OF  MEDICINE 

membranous  tonsillitis  and  stomatitis."  The  shedding  of  the  false  mem- 
brane leaves  a  deep,  anfractuous  ulcer  with  prominent  edges.  The  breath 
is  foetid,  and  the  glands  are  enlarged.  The  disease  lasts  from  one  to  three 
weeks.  Ulcero -membranous  tonsilhtis  must  not  be  confounded  either  with 
diphtheria  or  with  chancre  of  the  tonsil.  The  search  for  fusiform  bacilli 
and  spirilla  can  alone  confirm  the  diagnosis. 

Treatment. — The  treatment  of  angina  and  of  catarrhal  tonsillitis 
consists  at  first  in  the  use  of  lukewarm  gargles  of  decoction  of  mallow,  which 
are  alternated  with  the  following  g  trgle  : 


1^  Water 
Boric  acid 
Essence  of  mint 


O.i.ss. 
3ii.ss. 
ITlii. 


on 


The  pain  in  the  throat  is  relieved  by  the  following  loti 

1^  Glycerine  . .  . .  . .  . .  , .     3v. 

Borate  of  soda     . .         . .         . .         . ,         . .     3ss. 

Chlorhydrate  of  cocaine . .  . .  . .  . .     gr.  iv. 

The  inflamed  parts  are  moistened  every  hour  with  this  lotion. 

Cold  compresses,  covered  with  oiled  silk,  to  the  throat  give  good  results. 
Saline  purgatives  and  emetics  are  to  be  reserved  for  cases  in  wliicli  the 
angina  is  associated  with  some  gastric  or  bilious  condition.  In  phlegmonous 
angina  the  best  thing  to  do  i^  to  make  use  of  the  means  previously  men- 
tioned. As  to  opening  the  abscess  with  a  bistoury,  we  must  not  overlook 
the  possibility  of  severe  haemorrhages  which  sometimes  occur  in  peri- 
tonsillar phlegmon. 


III.  RETROPHARYNGEAL  ABSCESS. 

Acute  retropharyngeal  abscess  is  frequent  in  very  young  children ;  it 
is  sometimes  the  result  of  post-pharyngeal  adenitis  (Verneuil).  At  the  com- 
mencement these  abscesses  look  hke  a  simple  pharyngeal  angina  ;  later  the 
intensity  of  the  fever  and  of  the  pain  indicates  the  formation  of  pus.  At 
tliis  period  the  local  symptoms  are  very  variable,  according  as  the  abscess 
occupies  the  upper  or  the  lower  region  of  the  pharynx. 

In  the  former  case  (superior  retropharyngeal  abscess),  deglutition  is 
painful,  and  the  posterior  wall  of  the  pharynx  shows  a  swelhng  wliich  may 
be  reached  with  the  finger,  and  may  yield  fluctuation. 

In  the  latter  case  (inferior  retropharyngeal  abscess)  it  is  difficult  to 
feel  the  tumour,  because  the  patient  does  not  lend  liimself  to  manipulation. 
Compression  of  the  larynx  by  the  abscess  causes  respiratory  troubles,  which 
have  often  led  to  a  wrong  diagnosis  of  croup,  oedema  of  the  glottis,  or  a 
foreign  body  in  the  larynx.     To  avoid  this  error,  we  should  ever  remember 


DISEASES  OF  THE  THROAT  AND  PHARYNX  567 

the  rigidity  of  the  neck  and  the  early  appearance  of  severe  dysphagia.  The 
fever  is  very  high,  dehrium  is  frequent,  and  the  patient  becomes  comatose, 
collapses,  and  dies  suddenly.  ''  In  view  of  the  alarming  prognosis  of 
untreated  retropharjTigeal  abscess,  the  practitioner  must  intervene  in 
every  case  which  comes  under  his  notice.  The  fear  of  sudden  death,  wliich 
is  always  possible,  demands  intervention  as  soon  as  the  diagnosis  has  been 
estabhshed." 

Post-mortem  examination  reveals  general  purulent  infiltration  of  the 
walls  of  the  pharynx.  The  infiltration  may  reach  the  mediastinum,  spread 
along  the  oesophagus  and  the  vertebral  column,  and  dissect  out  the  muscles 
of  the  neck. 


IV.  CHRONIC  ANGINAL  CATARRH— GRANULAR  ANGINA 
CHRONIC  TONSILLITIS. 

Description. — I  shall  include  chronic  anginal  catarrh  and  granular 
angina  in  one  description,  because  they  are  frequently  seen  in  the  same 
patient,  and  are  not  sufficiently  distinct  to  deserve  a  separate  description. 

The  symptoms  of  chronic  angina  show  themselves  slowly  and  without 
pain.  The  patient  experiences  a  sensation  of  dryness,  tickhng,  or  pricking 
in  the  throat  and  nasal  fossa3,  which  is  most  marked  in  the  morning.  The 
pharynx  is  covered  with  tliick,  viscid  masses  of  mucus,  which  cause  a  kind 
of  hawking,  and  are  only  expectorated  after  several  attempts. 

The  throat  is  dry  ;  deglutition  is  sometimes  difficult,  and  sUght  deafness 
occurs  if  the  inflammation  has  reached  the  Eustachian  tube. 

The  soft  palate  and  the  wall  of  the  pharynx  are  red,  shiny,  granular, 
sometimes  swollen,  and  streaked  with  varicose  veins.  Tlie  uvula  is  long 
and  ojdematous.  The  granulations  are  formed  by  the  hypertrophy  of  the 
glandular  folUcles  ;  they  may  be  discrete  or  confluent,  and  occupy  the 
posterior  wall  of  the  pharynx,  the  anterior  pillars  of  the  fauces,  and  the 
uvula.  They  have  a  red  tint,  and  are  rarely  larger  than  a  hemp-seed. 
The  large  granulations  are  due  to  the  hypertrophy  of  the  adenoid  tissue, 
which  is  so  abundant  in  this  region.  The  presence  of  small  pustules  charac- 
terizes acneiform  angina  (Lasegue). 

Tiie  nasal  fossse  and  the  larynx  often  participate  in  the  inflammation. 
Chronic  coryza  and  laryngitis  result  therefrom,  and  their  symptoms  are 
added  to  those  of  pharyngitis.  Posterior  rhinoscopy  shows  the  pharyngeal 
tonsil  to  be  raspberry-like,  and  covered  with  muco-purulent  secretion, 
which  flows  down  the  pharynx.  The  posterior  extremity  of  the  turbinate 
bones  is  often  hypertrophied. 

Headache  and  neuralgia  of  t]w  occipital  nerve  are  often  present  in 
chronic  pharyngitis,  as  Vergely  has  pointed  out. 


568  TEXT-BOOK  OF  MEDICINE 

Granular  angina  is  essentially  chronic.  It  is  subject  to  subacute  attacks 
and  to  relapses.  It  is  brought  on  by  repeated  irritation  of  the  mucous 
membrane  of  the  pharynx  (tobacco,  alcohohc  beverages,  and,  in  singers, 
contact  with  the  air).  It  is  especially  frequent  in  people  suffering  from  gout, 
rheumatism,  and  herpes. 

The  local  treatment  consists  in  cauterization,  pigments,  and  gargles. 
Mineral  waters  containing  sulphur,  alkaUs,  and  arsenic  find  their  appHca- 
tion  in  constitutional  conditions. 

Chronic  Tonsillitis. — The  disease  has  a  marked  predilection  for  youth. 
It  is  common  up  to  the  age  of  puberty,  but  very  rare  in  the  adult,  unless  it 
be  a  relic  of  early  years.  It  is  especially  met  with  in  lymphatic  and  scrofu- 
lous patients.  It  is  sometimes  the  result  of  acute  tonsilhtis,  but  it  is  more 
often  a  recrudescence,  for  it  may  be  said  that  the  disease  never  stops  com- 
pletely in  predisposed  persons.  Each  crisis  is  marked  by  similar  symptoms, 
but  in  different  degrees,  according  as  the  attack  is  more  or  less  acute. 

The  chronic  inflammation  often  induces  hypertrophy  of  the  tonsils. 
The  hypertrophy  involves  the  lymphoid  folhcles,  the  connective  tissue,  and 
the  mucous  membrane  which  covers  the  tonsil,  and  penetrates  into  its  crypts. 
The  hypertrophied  tonsil  weighs  from  40  to  100  grains  (Chassaignac).  It 
is  soft  if  the  hyperplasia  affects  the  lymphoid  tissue  ;  indurated  if  the  hyper- 
plasia involves  the  connective  tissue.     It  is  a  chronic  fibrous  inflammation. 

The  hypertrophied  tonsils  project  more  or  less,  and  may  touch  the 
uvula.  They  present  all  possible  shadings,  from  rose  to  deep  red.  The 
pultaceous  secretion,  rich  in  microbes,  lodges  in  the  sulci  on  the  surface. 
The  hypertrophy  of  the  tonsils  is  accompanied  by  chronic  adenitis  of  the  sub- 
maxillary glands,  which  may  break  down.  Corj^za  and  chronic  blepharitis 
are  also  seen  in  lymphatic  and  scrofulous  subjects.  When  the  hypertrophy 
is  considerable,  the  breathing  is  embarrassed,  particularly  during  sleep. 
This  dyspnoea  produces  violent  contractions  of  the  diaphragm,  which,  in 
their  turn,  depress  the  lower  ribs,  and  contribute  to  the  deformity  of  the 
thorax  (Dupuytren,  Lambron). 

With  this  question  of  tonsillar  hypertrophy  is  connected  the  hypertrophy 
of  the  pharyngeal  tonsil  and  of  the  adenoid  tissue  in  the  pharynx.  Kuault 
has  described  these  infantile  forms.  Certain  infants,  even  though  hardly 
weaned,  show  a  tendency  to  breathe  and  to  sleep  with  their  mouths  open, 
accompanied  by  characteristic  ratthng  and  snoring.  These  signs  indicate 
hypertrophy  of  the  pharyngeal  tonsil,  wliich  may  develop  later  into  the 
adenoid  growth.  In  other  infants  the  adenoid  hypertrophy  spreads,  and 
is,  so  to  speak,  "  a  hypertrophic  pharyngitis,  affecting  all  the  adenoid 
tissue  at  the  back  of  the  mouth." 

The  diagnosis  of  enlarged  tonsils  in  infants  and  youths  may  present 
many  difficulties.      A  simple  hypertrophy  of  the  three  tonsils  is  often  in 


DISEASES  OF  THE  THROAT  AND  PHARYNX  569 

reality  latent  tuberculosis.     I  shall  discuss  this  point  in  detail  under  Larval 
Tuberculosis  of  the  Three  Tonsils. 

The  medical  treatment  of  chronic  tonsilUtis  consists  in  toucliing  the 
tonsils  frequently  with  alum,  nitrate  of  silver,  or  tincture  of  iodine.  Surgical 
treatment  is  only  of  use  in  hypertrophy.  The  tonsils  are  removed,  or 
cauterization  is  employed  by  means  of  Paquelin's  thermo  -  cautery  or 
Krishaber's  galvano-cautery.  This  method,  wliich  I  have  often  found 
effective,  gives  excellent  results.  The  tonsil  is  destroyed  after  a  small 
number  of  sittings. 

V.  DIPHTHERIA. 

History. — Diphtheria  has  been  knowoi  since  the  days  of  antiquity,  but  its  various 
manifestations  were  regarded  as  so  many  distinct  diseases.  Often,  indeed,  the  nature 
of  the  disease  was  misunderstood.  For  instance,  epidemics  of  diphtheria,  raging  in 
the  form  of  angina,  had  given  birth  to  the  names  "  Egyptian  ulcer,"  "  Syrian  ulcer," 
"  ulcera  pestlfera  "  (Areteus),  observers  mistaking  for  ulcerations  the  local  lesions 
in  the  throat,  which  sometimes  assume  an  ulcerous  appearance.  Epidemics  of  diph- 
theria raging  as  laryngitis  (croup)  created  the  names,  '*  garrotillo  "  (epidemics  of  the 
end  of  the  sixteenth  century  in  Spain),  "  morbus  strangulatorius  "  (ejiidemics  at  the 
commencement  of  the  seventeenth  century  in  Italy),  "suffocating  angina" — names 
which  thoroughly  prove  the  localization  of  the  disease  in  the  larynx.  No  relation, 
however,  had  been  established  by  observei"s  between  the  laryngeal  and  pharyngeal 
forms  of  the  disease  ;   they  looked  on  them  as  distinct  diseases. 

Fothergill,  during  the  epidemics  in  England  (1774),  and  Huxham,  during  the  Ply- 
mouth epidemic  (1751),  fell  into  a  similar  confusion,  and  spoke  of  gangrene  of  the 
throat.  Home  (17Go),  a  Scotch  physician,  invented  the  name  "croup";  he  deserves 
the  credit  of  having  clearly  separated  the  strangulatory  affections  of  the  larynx  from 
the  pellicular  maladies  of  the  pharynx,  but  he  was  wTong  in  not  recognizing  the  identical 
nature  of  angina  and  of  croup,  and  on  this  point  confusion  still  continues. 

Samuel  Bard  (1771)  introduced  some  order  into  the  chaos,  in  that  he  clearly  estab 
lished  the  identity  of  the  different  local  forms  of  diphtheria.  The  work  of  Bard,  how- 
ever, remained  in  an  unfinished  state,  and  found  no  response.  It  was  reserved  for 
Bretonneau  to  establish  by  clinical  and  pathological  proofs  the  common  origin  of  these 
various  morbid  conditions,  to  prove  that  they  are  one  specific  disease,  to  which  he  gav 
the  name  of  '*  diphtheritis."  Bretonneau  likewise  showed  that  gangrenous  angina 
was  in  most  cases  diphtheria,  and  he  completed  his  work  by  creating  stridulous  laryn- 
gitis (false  croup) — a  disease  which  simulates  croup,  but  which  has  nothing  in  common 
with  it. 

Bretormeau's  teaching  was  spread  by  Trousseau,  who  adopted  the  doctrine  of  liis 
master,  whilst  slightly  modifying  it.  Trousseau,  however,  substituted  for  diphtheritis, 
which,  according  to  Bretonneau,  gave  a  kind  of  preponderance  to  the  inflammatory 
element,  the  word  "  diphtheria,"  because  ho  considered  the  inflammatory  element  of 
less  account. 

He  described  malignant  diphtheria,  wliich  had  not  been  previously  classified  ;  made 
the  operation  of  tracheotomy  popular,  and  foresaw  the  toxic  origin  of  diphtheritic 
paralysis.  Ho  studied  the  disease  in  its  entirety,  and,  witli  a  master  Jiand,  wrote  u 
marvellous  description  of  it. 

The  ideas  of  Bretonneau  and  Trousseau  found  opponents  in  CJermany.  Viroliow 
and  Rokitansky  tried  to  overturn  the  tlieory  of  identity  advanced  by  Bretonneau  ; 


570  TEXT-BOOK  OF  MEDICINE 

they  invoked  the  aid  of  pathological  anatomy,  but  they  only  succeeded  in  re-establish- 
ing the  confusion.  They  admitted  croupous  and  diphtheritic  inflammations — croupous 
in  the  case  of  superficial  fibrinous  exudates  developed  on  a  simple  eiDithelium,  like 
that  of  the  respiratory  passages  ;  diphtheritic  in  the  case  of  deep  fibrinous  infiltration, 
which  developed  on  the  thick,  stratified  epithelia,  and  ended  at  times  in  necrobiosis  of 
the  tissue.  The  German  school  was  in  the  wrong,  and  the  idea  of  unity  and  the  specific 
nature  of  diphtheria,  so  well  set  forth  by  our  great  French  masters,  received  a  brilUant 
confirmation  from  the  discovery  of  the  pathogenic  microbe  of  diphtheria,  just  as  the 
unity  and  specific  nature  of  the  difl:erent  forms  of  tuberculosis  (tubercular  and  caseous 
products),  the  work  of  Laennec,  attacked  by  the  German  school,  were  proved  by  the 
discovery  of  the  tubercle  bacillus. 

In  1883  Klebs  discovered  the  bacillus,  cultivated  it,  and  recognized  its  aptitude  to 
form  membranes,  but  he  could  not  give  proof  of  its  sjiecific  nature.  The  irrefutable 
demonstration  of  the  specific  nature  of  the  diphtheria  bacillus  is  due  to  Rcux  and  Yersin, 
who  in  three  successive  papers  have  given  us  the  results  of  their  admirable  labours. 
These  results  may  be  formulated  in  a  few  sentences.  The  bacillus  of  diphtheria  pro- 
duces the  diphtheritic  membranes,  but  it  is  not  the  sole  agent  capable  of  producing 
false  membranes.  Other  micro-organisms,  such  as  the  streptococcus,  pneumococcus, 
staphylococcus,  and  especially  a  small  diplococcus,  are  apt  to  produce  false  membranes. 

It  is,  then,  not  in  the  false  membrane  that  the  specific  nature  of  the  diphtheritic 
bacillus  must  be  looked  for.  Its  specific  nature  lies  in  the  toxine  which,  amongst  other 
complications,  determines  paralysis.  In  some  cases  the  diphtheria  bacillus  may  cause 
toxic  symptoms  and  paralysis,  without  any  previous  production  of  false  mem- 
branes. 

Diphtheria  is  eminently  a  toxic  disease  ;  it  readily  becomes  infectious  by  association 
with  micro-organisms  wliich  increase  the  virulence  of  the  diphtheria  bacillus,  or  which 
add  their  own  share  of  virulence.  The  streptococcus  is  the  most  active  agent, 
and  many  complications  that  occur  during  the  course  of  pharyngeal  or  laryngeal  diph- 
theria are  due  to  the  secondary  infections  which  these  agents  produce. 

These  views  are  given  in  detail  in  the  sections  on  Diphtheritic  Angina  and  Pseudo- 
Diphtheritic  Membranous  Angina,  as  well  as  in  the  section  on  Croup. 

The  Bacillus  of  Diphtheria. — A  particle  of  false  membrane  is  taken  with  a  platinum 
loop  from  the  throat  of  a  child  suffering  with  diphtheria,  and  spread  out  on  slides.  The 
films  thus  obtained  are  dried  by  passing  them  through  the  flame  and  stained  with 
Roux's  blue  or  with  gentian  violet.  The  preparation  is  washed  in  water  and  placed 
under  the  microscope.  The  Klebs-LStfier  bacillus  is  seen  in  the  midst  of  numerous 
micro-organisms  (coccus,  streptococcus,  bacteria).  It  is  a  straight  or  sHghtly  curved 
bacillus,  as  long  as  the  tubercle  bacillus,  but  thicker  ;  its  rounded  extremities  stain 
more  deeply  than  its  middle  portion.  "  In  diphtheria  of  rapid  course,  after  staining 
with  methylene  blue,  the  superficial  parts  of  the  false  membrane  are  seen  to  be  formed 
by  a  layer  of  small  diphtheria  bacilH,  almost  in  a  pure  state.  They  are  separated  from 
the  mucous  membrane,  which  has  lost  its  epithelium,  by  a  layer  of  granular  fibrin, 
and  by  a  fibrinous  network  adherent  to  the  mucous  tissue.  The  most  superficial  zone 
of  the  false  membrane  often  contains  different  microbes,  rods,  and  micrococci  in 
chains,  mixed  with  masses  of  diphtheria  bacilh,  which,  on  the  other  hand,  predominate 
immediately  below  "  (Roux  and  Yersin). 

The  diphtheria  bacillus  is  readily  cultivated  in  tubes  of  gelatinized  serum. 
By  means  of  a  platinum  wire  a  particle  of  mucus  or  of  false  membrane  is 
taken  from  the  throat,  and  smears  are  made  with  this  wire  on  the  surface 
of  the  coagulated  serum.  It  is  advisable  to  inoculate  two  or  three  tubes 
without  taking  fresh  material.     We  thus  obtain  in  the  second  or  third  tube 


DISEASES  OF  THE  THROAT  AND  PHARYNX  571 

colonies  which  are  more  discrete  and  characteristic.  The  tube  is  closed  by 
a  plug  of  wool  and  put  into  the  oven  at  a  temperature  of  from  35°  to  37°  C. 
At  the  end  of  eighteen  hours,  or  even  earlier,  colonies  appear  ;  when  well 
developed  and  sufficiently  isolated,  they  are  characterized  by  rounded  dis- 
crete or  confluent  spots  of  a  grepsh-white,  more  opaque  at  the  centre  than 
at  the  periphery.  I  call  these  colonies  papular,  because,  when  they  are  well 
developed,  they  project  from  the  surface  of  the  serum.  We  shall  see  in  the 
following  sections  that  the  diagnosis  of  diphtheritic  angina  and  pseudo- 
diphtheritic  angina  can  only  be  made  by  cultures  and  bacteriological  ex- 
amination. For  the  moment,  therefore,  I  will  leave  the  distinctive  signs  of 
their  microbes. 

The  diphtheritic  colonies  having  been  obtained  by  culture,  it  suffices  to 
take  a  particle  and  stain  with  Roux's  blue.  When  the  preparation  is  finished, 
it  is  examined  A\ith  an  immersion  lens,  and  the  diphtheria  bacillus,  which 
is  always  immovable,  is  then  seen. 

The  bacilli  are  often  disposed  in  groups  of  three  or  four.  They  may  be 
arranged  in  parallel  fines,  or  may  represent  the  letters  V,  X,  L  ;  they  may 
resemble  an  acute  or  circumflex  accent,  but  are  never  placed  end  on.  They 
look  like  short,  squat  needles  which  have  been  allowed  to  fall  in  small  heaps 
on  a  table  (Martin).  "  The  diphtheria  bacillus  remains  alive  in  cultures  for 
a  long  time.  Bacilfi  contained  in  closed  tubes  without  air,  and  protected 
from  the  light  for  thirteen  months,  Jiave  given  active  cultures  "  (Roux  and 
Yersin). 

In  virulfMit  diphtlicria  the  bacilfi  are  generally  long,  numerous,  and 
sometimes  curved.  They  form  numerous  colonips.  When  the  disease  is 
less  virulent,  the  colonies  are  less  numerous,  and  the  bacilli  are  shorter  and 
less  curved. 

A  very  short,  bacillus  has  been  desoribod  by  Eschorich,  who  calls  it  the  pseudo- 
diphtheria  bacillus.  Opinions  are  divided  as  to  whether  it  is  a  diphtlieria  bacillus 
which  has  been  attenuated  and  robbed  of  its  virulence,  or  whether  it  represents  a 
different  species,  havingnothing  in  common  with  the  bacillus  of  diphtheria.  This  bacillus 
is  found  in  the  mouth  of  healthy  subjects,  and  is  present  in  the  angina  of  scarlatina 
and  of  measles.  I  have  found  it  in  a  contagious  angina,  accompanied  by  herpes  and 
membranes.  Cultures  inoculated  into  guinea-pigs  never  cause  the  death  of  the  animal ; 
thus  this  characteristic  is  said  to  differentiate  the  psoudo-diphtheria  bacillus.  The 
experiments  of  Martin,  however,  show  tliat  th(>se  bacilli,  which  are  non-virulent  in  the 
case  of  the  guinea-pig,  kill  small  })irds  that  are  protected  by  a  preventive  injection  of 
antidiphtheritic  serum.  Martin  has  further  proved  that  these  non-virulent  bacilli  can 
secrete  the  diphtheritic  toxine  in  suitable  media.  Finally,  several  experimenters  have 
been  able  to  increase  the  virulence  of  these  originally  inoffensive  microbes. 

These  facts  show  tiiat,  before  creating  a  group  of  j)seudo-diphthcria  l)acilli,  very 
doHned  characteristics  have  to  be  found,  which  will  enable  us  to  diiTerontiate  tlu^m 
from  the  dij)lithcria  bacillus. 

Tho  diphtlieria  bacillus  has  no  tendency  to  ponotrato  the  organs  ;  Barbicr  and 
ToUoraer    maintain,    however,    that    they    have    discovered    the    bacillus    in    the 


572  TEXT-BOOK  OF  MEDICINE 

cervical  and  bronchial  glands,  the  spleen,  and  in  tlie  medulla  (post-mortem 
researches). 

Experiments. — The  diphtheria  bacillus  is  readily  cultivated  in  alkaline  veal  broth. 
Half  a  cubic  centimetre  of  culture  injected  into  the  cellular  tissue  of  a  pigeon  kills  it 
in  less  than  sixty  hours.  A  rabbit  dies  in  a  few  days  from  an  injection  of  2  to  4  c.c. 
of  culture.  The  guinea-pig  is  usually  selected,  and  dies  in  less  than  thirty -six  hours 
from  a  very  small  injection. 

In  a  few  hours  local  oedema,  with  a  h?emorrhagic  patch,  develops  at  the  seat  of 
inoculation.  The  bacilU  remain  confined  to  the  cedematous  region  ;  they  do  not  enter 
the  bloodvessels,  the  lymphatics,  or  the  organs,  and,  in  spite  of  their  rapid  diminution 
in  the  inoculated  region,  the  disease  continues  its  course,  by  reason  of  the  toxine 
which  has  been  formed  in  situ. 

After  death  the  inoculated  animals  present  identical  lesions  :  general  dilatation  of 
the  small  vessels,  congestion  of  the  suprarenal  capsules  and  the  kidneys,  swelling  of  the 
glands,  pleurisy  in  the  guinea-pig,  and  degeneration  of  the  liver  in  the  rabbit. 

By  means  of  pure  cultures,  it  is  possible  to  reproduce  the  diphtheritic  membrane 
on  the  trachea,  the  conjunctiva,  or  the  pharynx  of  pigeons  and  hens,  and  on  the  vulva 
of  the  female  guinea-pig  ;  all  that  is  required  is  to  paint  the  mucous  membrane,  which 
has  been  previously  excoriated.  It  is  possible  to  cause  lesions  and  symptoms  re- 
sembUng  croup  in  the  trachea  of  the  rabbit.  Diphtheria  of  the  skin  may  likewise  be 
produced  in  animals,  provided  the  epidermis  has  been  previously  removed. 

Diphtheritic  Membranes. — In  tlie  pathological  condition  the  membranes  invade 
the  mucous  membrane  and  the  skin,  provided  always  that  the  skin  has  been  denuded 
of  its  epidermis  and  the  mucous  membrane  of  its  epithelium.  The  membranes  appear 
spread  out,  and  reform  with  extreme  facility.  The  membranes  are  much  less  common 
on  the  skin  than  on  the  mucosa  ;  they  may  develop  on  the  surface  of  blisters,  leech- 
bites,  herpetic  vesicles,  cracks  in  the  nipple — in  short,  wherever  the  integument  is 
denuded  of  its  epidermis. 

Cutaneous  diphtheria  (for  example,  diphtheria  which  develops  after  a  blister)  pre- 
sents the  following  characteristics  :  The  invaded  part  becomes  painful,  red,  and  covered 
with  a  firm,  greyish  membrane,  which  is  difficult  to  detach.  '  The  edges  of  the  wound 
swell  and  take  on  an  erysipelatous  tint.  Pustules  form  ;  the  epidermis  falls  off,  and 
the  bared  skin  is,  in  its  turn,  invaded.  The  false  membranes  fall  off  and  reform,  but 
finally  disappear  ;  the  cutaneous  surface,  however,  has  a  feeble  tendency  to  cicati'iza- 
tion,  and  may  remain  red,  bleeding,  and  painful  for  a  long  time.  Cutaneous  diphtheria 
is  usually  grave,  because  it  is  often  associated  Math  secondary  infections  (streptococci), 
and  is  sometimes  followed  by  gangrene,  but  esj^ecially  because  it  is  prone  to  be  the 
starting-point  of  general  intoxication  and  malignant  diphtheria  (Trousseau).  The 
membranes  invade  the  mucous  membranes  of  the  pharynx,  nasal  fossae,  larynx,  bronchi, 
conjunctiva,  eyelids,  cornea,  vulva,  prepuce,  anus,  gums,  mouth.  Eustachian  tube, 
and  oesophagus.  These  various  locaHzations  of  diphtheria,  however,  are  far  from 
being  frequent ;  the  usual  locaUzations  are  in  the  nasal  fossae  (diphtheritic  coryza),  the 
back  of  the  mouth,  the  pharynx,  which  we  shall  study  under  the  name  of  Diphtheritic 
Angina,  and  in  the  larynx,  which  we  have  described  elsewhere  under  the  name  of 
Croup.  The  false  membranes  are  only,  as  I  have  just  said,  local  manifestations  of 
diphtheria  ;  they  are  the  most  frequent  and  formidable  manifestation,  for  the  mem- 
branes in  the  larynx  and  respiratory  passages  may  choke  young  patients  who  are  not 
treated  in  time.  Diphtheria,  however,  reveals  itself  also  by  toxic  manifestations 
caused  by  a  poison  which  we  shall  stud^  later. 

Diphtheritic  Toxine. — The  pathogenic  microbe,  so  plentiful  in  diphtheritic  mem- 
branes, does  not  enter  the  blood  or  the  organs  of  patients  who  have  fallen  victims  to 
diphtheria.  How  are  we  to  explain  the  fact  that  colonies  of  bacilli,  localized  to  some 
part  of  the  mucous  membrane  or  the  skin,  can  cause  the  organic  lesions  (kidney,  liver. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  573 

nerves),  the  poisoning  and  the  paralysis  which  so  often  occur  ?  "In  diphtheria  the 
infection  is  not  produced  by  microbic  invasion  of  the  tissues,  but  by  diffusion  within  the 
body  of  a  toxic  substance  formed  on  the  surface  of  the  mucous  membrane  outside  the 
body,  as  it  were." 

This  poison,  discovered  by  Roux  and  Yersin,  "  has  been  the  subject  of  a  series  of 
researches,  considered  even  to-day  as  the  best  monograph  which  has  ever  appeared 
in  bacteriology,  and  rightly  so."  Funk,  in  speaking  thus,  echoes  the  general  opinion. 
Roux,  by  discovering  the  diphtheritic  toxine,  prepared  the  way  for  the  discovery  of 
the  antitoxin. 

The  toxine  is  obtained  by  cultivating  the  virulent  diphtheria  bacillus  on  broth,  in 
contact  with  air.  In  order  to  prepare  an  active  toxine,  it  is  necessary  to  make  use  of  a 
very  virulent  culture.  It  is  also  necessary  to  secure  the  exact  alkalinity  of  the  broths  ; 
for  this  purpose  the  peptonized  broth  must  be  made  alkaline,  until  it  no  longer  reddens 
blue  Utmus  paper.  The  broth  is  placed  in  Fernbach  flasks  with  a  flat  bottom,  so  that 
the  layer  of  liquid  may  be  shallow.  After  sterihzation  in  the  autoclave,  fresh  virulent 
bacilli  are  sown  in  the  broth,  and  heated  in  the  stove  to  37°  C.  Roux,  liaving  proved 
that  the  diphtheritic  poison  was  produced  more  rapidly  and  in  greater  quantity  when 
the  cultures  were  made  in  contact  with  air,  invented  an  ingenious  method  of  passing 
a  current  of  moist  air  into  the  culture. 

For  this  purpose,  he  connected  the  side  aperture  of  Fernbach's  flasks  with  a  tube, 
so  as  to  make  a  vacuum.  In  three  or  four  weeks  a  culture  rich  in  virulent  toxine  is 
obtained.  A  layer  of  whitish  sediment,  like  a  crust  of  ground-glass,  is  deposited  at  the 
bottom  of  the  flask.  This  is  a  deposit  of  bacteria,  and  on  the  surface  of  the  broth  a 
whitish-looking  scaly  veil,  composed  of  younger  bacilU,  is  formed.  The  liquid  between 
those  two  layers  is  turbid  at  the  commencement  of  the  culture,  but  gradually  becomes 
more  and  more  clear. 

The  finished  cultures  are  filtered  through  a  Chamberland  candle,  and  the  clear 
liquid  is  stored  in  well-filled  corked  flask^,  and  kept  in  the  dark  at  the  ordinary  tem- 
perature. The  toxine  thus  prepared  generally  kills  a  guinea-pig  of  500  grammes  in 
forty-eight  hours  after  a  dose  of  -i.  c.c. 

The  inoculation  of  the  toxine  into  certain  animals,  such  as  the  guinea-pig,  rabbit, 
etc.,  produces  symptoms  and  lesions  similar  to  those  seen  in  patients  who  have  suc- 
cumbed to  toxic  diphtheria.  Subcutaneous  injection  in  these  animals  produces  a 
fibrinous  sanguinolent  oedema  at  the  point  of  inoculatioii,  followed  by  swelling  of  the 
glands,  diarrhoea,  and  hurried,  shallow  breathing.  The  post-mortem  lesions  are : 
congestion  of  the  intestine  and  bloody  fluid  in  the  bowel,  hsemorrliagic  congestion  of 
the  suprarenal  capsules  and  the  kidneys,  yellow  staining  and  fatty  degeneration  of 
the  liver,  pleuritic  effusion,  very  marked  dilatation  of  the  vessels,  myocarditis,  and 
imperfect  coagulation  of  the  blood.  Injections  of  toxine  not  only  produce  the  acute 
intoxication  just  described,  but  also  paralysis  (and  this  is  one  of  the  most  interesting 
sides  of  the  work  of  Roux  and  Yersin),  that  closely  resembles  diphtheritic  paralysis, 
which  we  shall  discuss  in  one  of  the  following  sections.  The  diphtheritic  toxine  is 
closely  related  to  the  diastases  and  the  venoms. 

Microbic  Associations. — We  have  just  studied  the  products  of  the  diphtheria  bacillus 
— i.e.,  the  membranes  and  the  toxine — but  the  secondary  infections  play  a  great  part 
in  the  symptoms  of  diphtheria.  The  streptococcus,  the  staphylococcus,  other  cocci, 
the  pneumococcus,  and  the  bacteria  of  putrefaction  assist  in  the  morbid  process.  Tlicso 
microbes,  and  especially  the  streptococcus,  give  rise  to  suppurative  adenitis,  bronclio- 
pulmonary  complications,  otitis,  and  gangrene. 

Clinical  observation  has  taught  us  that  the  membranes  play  quite  a  secondary 
part  in  some  cases.  From  the  very  onset  the  malady  has  all  the  syni|)t()nis  of  the  most 
septic  and  infectious  diseases  ;  it  is  accompanied  by  all)Uininuriii  and  lia'inonliage, 
an(i   iuviides  the  entire  economy,  causing  adynamia  and  often   killing  by  syncope. 


574  TEXT-BOOK  OF  MEDICINE 

Trousseau,  on  account  of  its  extreme  gravity,  gave  to  this  disease  the  name  of  toxic 
or  malignant  diphtheria.  Bacteriology  has  confirmed  clinical  research  in  every  point  ; 
it  has  given  us  the  reasons  and  taught  us  the  causes  of  the  different  forms  of  diphtheria. 
The  production  of  the  membranes  is  due  to  the  presence  of  the  bacillus.  The  symptoms 
of  intoxication  are  due  to  the  poison  elaborated  by  the  bacillus.  The  infectious  symp- 
toms are  due  principally  to  the  associated  microbes.  We  shall  study  later  the  associa- 
tion of  the  diphtheria  bacillus  with  the  streptococcus — an  association  which  reciprocally 
increases  the  virulence  of  the  pathogenic  agents,  and  causes  malignant  and  fatal  diph- 
theria. 


VI.  DIPHTHERITIC  ANGINA. 

Diphtheritic  angina  does  not  always  show  the  same  course  and  symptoms. 
In  its  most  common  and  favourable  form,  which  has  been  called  since 
Trousseau's  time  normal  diphtheritic  angina,  the  intoxication  and  the  infec- 
tion are,  fortunately,  of  secondary  importance.  The  disease  invades  the 
throat  to  a  greater  or  less  extent ;  it  often  reaches  the  larynx,  especially 
in  children,  and  sometimes  engenders  severe  paralysis,  especially  in  adults. 
This  proves  that  the  disease  is  not  without  danger  ;  but,  after  all,  the  course 
and  comphcations  of  the  so-called  normal  angina  can  be  nearly  always 
cured  with  serum,  and  the  rapid  and  fatal  comphcations  that  are  so 
frequent  in  the  malignant  form  need  not  usually  be  feared. 

In  the  latter  form,  which  is  rightly  known  as  toxic  infective  angina, 
and  which  I  shall  continue  to  call  malignant,  the  general  symptoms  are  far 
more  important  than  the  local  ones.  From  the  outset  the  malady  has  the 
appearance  of  a  grave  infectious  disease.  The  entire  economy  is  invaded  in 
a  few  hours  or  in  a  few  days.  It  is  not  the  false  membrane  nor  death  by 
croup  that  is  to  be  feared,  but  the  rapid  poisoning  and  collapse,  to  which 
patients  often  succumb. 

Some  authors  have  attempted  to  classify  diphtheritic  angina  according 
to  bacteriological  examination.  Normal  diphtheritic  angina  would  thus 
be  a  monomicrobic  angina,  in  which  the  bacillus  exists  in  a  pure  state.  On 
the  other  hand,  malignant  angina  would  be  a  polymicrobic  angina,  in  which 
the  diphtheritic  bacillus  is  associated  with  other  microbes — notably  the 
streptococcus.  There  is  some  truth  in  these  assertions,  and  these  mono- 
microbic and  polymicrobic  forms  will  be  described  in  this  section,  but  I 
would  hasten  to  say  that  such  a  radical  bacteriological  classification  would 
be  erroneous.  I  admit  that  the  normal  angina  is  often  monomicrobic,  but 
in  many  other  cases  it  may  be  associated  with  cocci,  diplococci,  staphylo- 
cocci, and  even  streptococci  (as  I  have  just  proved),  and  yet  the  angina 
does  not  lose  its  characteristics  as  a  frank  or  normal  angina.  Per  contra, 
it  is  not  only  a  polymicrobic  angina  which  can  be  malignant.  I  shall  quote 
fatal  cases  of  diphtheritic  angina  which  were  not  polymicrobic,  the  diph- 
theria bacillus  being  present  in  a  pure  state  (Roux,  Martin). 


DISEASES  OF  THE  THROAT  AND  PHARYNX  575 

It  is  therefore  best  to  retain  the  cUnical  classification,  and  describe 
normal  angina,  which  is  but  little  toxic,  and  a  malignant  angina,  which  may 
be  subdivided  bacteriologically  into  angina  with  toxic  symptoms  and 
diphtheritic  angina  witli  infective  symptoms.  And  yet  these  two  cUnical 
forms— normal  and  mahgnant  angina — are  not  always  clearly  defined, 
and  we  find  mixed  forms.  The  disease  may  commence  with  mild  symptoms, 
and  yet  after  a  few  days  it  becomes  mahgnant.  Here,  as  in  all  toxic  and 
infectious  diseases,  the  poison  and  infectious  agents  show  degrees  and 
reserve  surprises  for  us.  Without  affecting  the  truth  of  the  description,  it 
Ls  possible  to  conform  to  the  custom  established  by  Trousseau,  and  to 
describe  separately  the  two  varieties. 

1.  Normal  Diphtheritic  Angina. 

Description. — While  normal  diphtheritic  angina  spares  no  period  of 
hfe,  it  is  much  more  frequent  between  the  ages  of  three  and  seven  years.  Its 
onset  is  usually  insidious  and  less  acute  than  that  of  acute  tonsilhtis.  It 
installs  itself  by  stealth.  The  fever  is  moderate,  and  may  fall  in  three  or 
four  days  ;  the  sore  tlixoat  is  not  severe,  and  the  patient  may  feel  hardly  any 
pain  on  swallowing.  While  the  above  statement  is  practically  true,  we  find 
many  exceptions,  since  bacteriology  has  taught  us  not  to  be  deceived  by  the 
multiple  disguises  of  diphtheritic  angina. 

The  disease  (in  my  description  I  borrow  from  Trousseau)  commences 
with  more  or  less  vivid  redness  of  the  pharynx  and  swelhng  of  one  tonsil ; 
in  some  cases  both  are  involved.  A  well-defined  white  spot  is  soon  visible 
on  the  affected  organ.  This  spot  at  first  consists  of  a  layer  resembling 
coagulated  mucus,  which  rapidly  becomes  thickened  and  of  a  membranous 
consistency.  At  the  commencement  this  exudate  is  readily  detached  from 
the  surface,  to  which  it  is  adherent  by  filaments  penetrating  the  follicles 
of  the  tonsil. 

The  underlying  mucous  membrane  is  healthy,  except  for  the  destruction 
of  the  epithcUum.  The  mucosa  may  appear  to  be  hollowed  out  because  it 
is  swollen,  and  forms  a  kind  of  pad  around  the  exudate.  Ulceration  is 
exceptional.  After  some  hours  the  pseudo-membrane  is  more  prominent, 
and  covers  the  greater  part  of  the  tonsil.  It  becomes  more  and  more  ad- 
herent at  the  points  first  invaded,  and  takes  on  a  yellowish  or  greyish-white 
tint.  As  a  rule,  the  roof  of  the  palate  commences  to  become  inflamed. 
The  uvula  swells,  and  is  often  covered  with  membrane  witliin  twenty-four 
hours.     The  membrane  now  appears  on  the  other  tonsil  and  the  pliarynx. 

We  find,  however,  many  exceptions,  since  bacteriology  has  taught  us  not 
to  be  misled  by  the  polymorphism  of  diphtheritic  angina.  We  often  see, 
not  membranes,  but  erythematous,  pultaceoiis,  lacunar,  or  herpetic  angina. 

From  the  first,  or  in  a  short  while,  we  notice  enlargement  of  the  glands 


676  TEXT-BOOK  OF  MEDICINE 

at  the  angle  of  the  jaw  on  the  same  side  as  the  affected  tonsil.  This  adenitis 
is  of  great  importance,  because  it  is  rarely  absent.  The  glands  are  hard 
and  movable,  the  periglandular  tissue  being  unaffected.  The  adenopathy 
is  due  to  the  diphtheritic  toxine,  and  we  shall  see  that  it  changes  in  character 
in  the  streptococcal  forms. 

The  symptoms  of  angina  are  more  pronounced  by  the  second  or  third 
day ;  the  dysphagia  is  more  severe,  but  the  fever  is  shght,  and  may  even 
disappear  at  this  period.  The  child  often  has  an  ansemic  look,  due  to 
diminution  in  the  haemoglobin,  as  Quinquaud  has  shown. 

On  examining  the  throat,  the  uvula,  the  pillars  of  the  fauces,  both  tonsils, 
and  the  pharynx  are  in  some  cases  covered  with  false  membranes,  which 
may  have  a  lardaceous  aspect.  The  membranes  are  produced  so  readily 
that  they  reappear  in  a  few  hours  upon  an  area  which  has  been  entirely 
cleaned.  This  rapid  development  is  often  seen  in  young  subjects.  The 
throat  may  be  completely  covered  with  false  membranes  in  thirty-six  hours 
in  a  child  of  three  years,  whilst  several  days  are  necessary  in  an  adult. 
The  patches  grow  thicker  from  the  addition  of  new  layers,  which  are  formed 
below  the  old  ones.  The  most  superficial  layers  are  readily  detached,  but 
the  deeper  ones  adhere  to  the  mucous  membrane,  and  cannot  always  be 
removed  without  causing  slight  bleeding.  Some  patches  are,  as  it  were, 
let  into  the  surrounding  mucous  membrane,  which  projects,  and  gives  the 
false  impression  of  an  ulceration. 

The  membranes  do  not  long  preserve  their  whitish  or  yellowish  aspect, 
because  their  colour  is  altered  by  liquids,  vomited  matter,  drugs,  or  blood, 
which  has  come  from  the  nasal  fossse.  They  then  take  on  a  greyish  or 
blackish  tint,  wliich,  joined  to  the  foetor  present,  leads  to  the  wrong  idea  of 
gangrene.  This  gangrenous  appearance  is  common  in  the  adult,  but  rare 
in  children,  and  explains  the  name  gangrenous  sore  throat  given  to  diph- 
theritic angina  by  several  authors.  Gangrene  is  exceptional  in  diphtheria. 
Bretonneau  was  loath  to  admit  it,  but  it  may  be  seen  in  grave  cases  and  in 
certain  epidemics. 

Normal  diphtheritic  angina  is  often  accompanied  by  albuminuria.  This 
symptom  is  not  of  serious  import. 

In  favourable  cases  the  disease  is  not  of  long  duration.  After  eight  to 
ten  days  the  glandular  swelhng  diminishes,  the  membranes  no  longer  reform, 
the  mucous  membrane  becomes  clean,  and  the  difficulty  in  swallowing 
disappears.  If  the  patient  has  not  been  treated  in  time  with  serum,  con- 
valescence is  long,  and  may  be  comphcated  by  serious  troubles. 

In  the  adult  extension  of  the  angina  to  the  larynx  is  rare,  but  croup 
consecutive  to  the  angina  is  very  common  in  children  when  serum  has 
not  been  used.  Tliis  terrible  comphcation  occurs  when  the  angina  has 
scarcely  terminated — in  fact,  croup  often  arises  while  membranes  are  still 


DISEASES  OF  THE  THROAT  AND  PHARYNX  577 

present  in  the  throat.     It  is  announced  by  changes  in  the  voice  and  by 
fits  of  dry  cough  at  short  intervals  (see  Croup). 

The  frec[uency  of  croup  in  children  makes  diphtheritic  angina  much  more 
serious  in  them  than  in  adults.  When,  however,  croup  occurs  in  the  adult, 
it  is  more  dangerous  than  in  the  child.  The  termination  of  the  disease  with 
syncope,  which  is  so  common  in  mahgnant  forms,  is  unusual  in  normal 
diphtheritic  angina. 

Angina  is  not  always  the  initial  manifestation  of  diphtheria.  It  often 
follows  diphtheria  of  the  nasal  fossse,  which  has  been  latent  for  some  days. 
It  may  also  follow  diphtheria  of  the  mouth,  larynx,  or  skin,  but  this  sequence 
is  very  rare. 

Prognosis. — Normal  diphtheritic  angina  is  generally  benign.  It  may, 
indeed,  be  said  that,  apart  from  the  comphcations  of  croup  and  broncho- 
pneumonia, which  are  much  more  common  in  children  than  in  adults,  normal 
diphtheritic  angina  is  almost  exempt  from  danger.  It  is,  therefore,  im- 
portant to  distinguish  it  from  the  grave  toxic  variety.  When  the  angina  is 
normal,  the  fever  is  slight,  and  abates  in  a  few  days.  The  submaxillary 
adenitis  is  moderate,  and  rarely  appears  early.  The  colour  is  not  from  the 
first  pale  and  leaden.  Albuminuria  is  transient  or  absent.  The  pulse  is 
of  good  quality.  The  bacteriological  examination  does  not,  as  a  rule, 
reveal  the  long,  curved  bacilh,  and  when  other  microbes  are  associated 
with  the  diphtheria  bacillus,  they  are  unimportant  (Brisou's  coccus),  or 
are  present  in  very  small  numbers  (staphylococci,  streptococci). 

Nevertheless,  although  normal  diphtheritic  angina  excludes  up  to  a 
certain  point  the  idea  of  toxicity,  it  is  none  the  less  true  that  in  the  most 
normal  case  of  diphtheritic  angina  some  toxic  symptoms  exist.  The 
glandular  swelling,  the  albuminuria,  and  the  decoloration  of  the  tissues 
are  evidence  of  poisoning  by  the  diphtheria  toxine. 

These  toxic  symptoms,  which  are  sUght,  I  admit,  I  shall  call  primary, 
because  they  are  contemporary  with  the  angina.  Diphtheritic  angina, 
however,  may  be  normal  and  benign  in  appearance,  and  yet  excite  secondary 
toxic  symptoms.  The  poison  accumulates  insidiously  in  the  system,  and 
causes  diphtheritic  paralysis. 

Lastly,  in  very  rare  cases  an  angina  which  seemed  to  be  normal  may 
become  grave,  or  even  fatal,  if  not  treated  in  time  with  serum,  as  the  cases 
cited  by  Roux  and  Yersin  and  by  Chaillou  and  Martin  prove. 

We  see,  then,  that,  for  different  reasons,  diphtheritic  angina,  even 
when  normal  and  but  slightly  toxic,  is  not  exempt  from  danger.  There  is, 
therefore,  all  the  more  reason  to  diagnose  and  treat  the  disease  without  delay. 

When  we  discuss  the  treatment,  there  is  one  point  on  which  I  siiall  lay 
stress.  It  is  not  sufficient  to  treat  diphtheria  with  injections  of  scrum.  The 
earlier  the  treatment,  the  better  it  succeeds. 

37 


578  TEXT-BOOK  OF  MEDICINE 

2.  Toxic  or  Infective  Diplitlieritic  Angina — Trousseau's  Malignant 

Diphtlieria. 

In  the  preceding  section  I  described  the  action  of  the  bacillus  in  producing 
false  membranes  which  are  harmless  in  the  throat,  but  dangerous  in  the 
respiratory  passages,  where  they  may  produce  croup  and  asphyxia.  Normal 
diphtheritic  angina  is  the  most  common  form,  and  is  generally  seen  in 
sporadic  cases.  It  may  be  seen,  however,  in  certain  epidemics,  even  when 
mahgnant  diphtheria  is  raging.  "  In  fact,"  says  Trousseau,  "  in  a  family 
of  whom  four,  five,  or  six  individuals  are  stricken  with  the  disease,  normal 
diphtheritic  angina,  with  or  without  croup,  will  be  the  general  rule.  The 
malignant  form,  which  poisons  patients  in  the  same  way  as  septic  diseases 
do,  will  be  the  exception." 

In  principle,  as  I  stated  above,  the  most  normal  case  of  diphtheritic 
angina  is  always  accompanied  by  some  toxic  symptoms.  The  pallor  of  the 
face,  the  rise  of  temperature,  the  swelling  of  the  cervical  glands,  and  the 
albuminuria,  are  symptoms  due  to  absorption  of  the  diphtheritic  poison. 
These  symptoms  do  not  entail  danger  when  they  are  moderate  ;  they  are 
more  or  less  a  part  of  the  common  description  of  many  cases  of  normal 
diphtheritic  angina,  and  do  not  afEect  the  prognosis.  In  some  cases,  however, 
the  toxic  symptoms  are  so  acute  that  the  patient  hterally  dies  of  infective 
poisoning,  or,  as  Trousseau  said,  of  malignant  diphtheria.  The  following 
examples  will  show  how  rapid  the  evolution  of  mahgnant  diphtheria 
may  be. 

Description. — "  One  of  my  colleagues,  Walleix,"  says  Trousseau,  "was  in  charge  of  a 
child  suffering  from  diphtheritic  angina,  which  was  improving.  While  he  was  examining 
the  child's  throat,  she  coughed  up  some  sahva,  which  entered  his  mouth.  He  took  the 
disease.  Next  day  he  noticed  a  small  pelhcular  concretion  on  one  of  his  tonsils.  Fever 
developed,  and  in  a  few  hours  the  tonsils  and  the  uvula  were  covered  with  false  mem- 
branes. Serous  Hquid  began  to  flow  from  the  nose.  The  glands  and  the  cellular  tissue 
of  the  neck  swelled  considerably.  He  became  delirious,  and  died  forty-eight  hours 
later,  without  any  laryngeal  complication." 

A  country  practitioner  was  attending  a  child  suffering  from  croup,  for  which  trache- 
otomy became  necessary.  During  the  operation  the  entrance  of  blood  into  the  trachea 
caused  fears  of  suffocation.  The  anxious  physician  apphed  his  mouth  to  the  wound 
in  the  throat  in  order  to  suck  out  the  fluid  which  was  entering  the  trachea.  He  inocu- 
lated himself  with  the  disease,  and  died  forty-eight  hours  later  of  mahgnant  diphtheria. 

Henri  Blache  was  in  charge  of  a  child  who  had  undergone  tracheotomy.  At  the 
end  of  the  third  night  he  complained  of  slight  sore  throat.  Acute  fever  was  present, 
and  false  membranes  on  the  tonsils.  In  a  few  hours  enormous  swelhng  of  the  neck 
and  continuous  discharge  from  the  nose.  In  twenty-four  hours  deUrium,  and  death 
seventy-two  hours  later  from  malignant  diphtheria,  without  having  sho\\Ti  the  slightest 
symptom  in  the  respiratory  passages.  Some  years  ago  Potain  asked  me  to  see  a 
family  suffering  from  diphtheria.  On  my  arrival,  I  was  told  that  the  two  children 
had  died  from  diphtheritic  angina.  The  mother  had  been  taken  the  previous  day  with 
sore  throat  and  prostration.  My  examination  gave  me  a  very  bad  impression.  She 
was  deadly  pale  ;  her  lips  were  blue  ;  her  pulse  wretched.     The  cervical  glands  and  the 


DISEASES  OF  THE  THROAT  AND  PHARYNX  579 

cellular  tissue  formed  a  brawny  mass.  Marked  albuminuria.  Throat  covered  with 
diffluent  fcetid  membranes  ;  sanious  nasal  discharge.  She  was  quite  lucid,  and  had  no 
illusions  as  to  her  condition.  "  Whatever  you  do,"  said  she,  "  I  shall  die  of  the  disease 
which  has  just  killed  my  two  children."  She  passed  away  next  day.  The  respiratory 
passages  were  quite  free  from  any  infection. 

The  fulminant  form  is,  fortunately,  very  rare.  In  other  cases  the  disease  runs  its 
course  in  eight  or  ten  days,  as  in  the  following  example  from  Trousseau's  writings  : 
A  child,  twelve  years  of  age,  had  been  attacked  by  slight  angina  three  days  previously. 
She  was  taken  to  the  hospital.  On  examination,  the  fcetor  of  the  breath  was  very 
striking.  Putrilaginous  membranes  at  the  back  of  the  throat  and  on  the  roof  of  the 
palate.  On  the  right  side  much  swelling  of  the  cervical  and  maxillary  glands.  This 
glandular  swelling,  which  from  the  first  meant  a  grave  prognosis,  increased  during  the 
next  few  days,  and  involved  the  cellular  tissue  of  the  cervical  and  submaxillary  regions. 
A  most  alarming  phenomenon  supervened — viz.,  erysipelatous  redness  of  the  skin, 
pointing  to  deep  inflammation  of  the  parts.  On  the  third  day  diphtheritic  coryza 
and  profuse  epistaxis  made  the  outlook  very  gloomy. 

With  such  formidable  symptoms,  although  the  respiration  remained  normal,  the 
prognosis  was  most  grave.  She  grew  cold,  just  like  a  cholera  patient.  She  had  a  ten- 
dency to  syncope.  Her  pulse  was  extremely  feeble  and  slow.  The  respiration  remained 
free,  and  the  respiratory  passages  were  not  affected  by  the  diphtheria.  She  refused 
to  take  any  nourishment.  The  glands  became  smaller,  the  nasal  lesions  improved, 
and  the  erysipelatous  redness  disappeared  ;  but  yet,  in  spite  of  this  deceptive  improve- 
ment in  the  local  signs,  the  child  died  on  the  tenth  day,  "  poisoned  by  the  diphtheritic 
venom  which  had  infected  her."  She  died  of  syncope  whilst  turning  round  and  refusing 
to  take  a  drink.  The  picture  of  malignant  diphtheria  is  not  always  as  complete  as 
it  was  in  the  above  case.  The  horrible  fcetor  of  the  breath,  the  brauTiy  induration  of 
the  cellular  tissue  of  the  neck,  and  the  erysipelatous  tint,  on  which  Trousseau  and 
Borsieri  have  laid  such  stress,  may  be  absent ;  in  spite  of  the  absence  of  these  symptoms, 
however,  the  excessive  pallor,  the  weak  pulse,  the  obstinate  refusal  to  take  food  or  drink, 
the  diarrhcea,  the  severe  and  early  albuminuria,  the  rapid  loss  of  strength,  point  to 
malignant  diphtheria  of  most  grave  prognosis,  although  the  respiratory  passages  are 
absolutely  free. 

We  may  now  ask  how  bacteriological  researches  can  explain  these 
malignant  cases. 

1.  Toxic  Malignant  Diphtheria. — In  some  cases  the  grave  or  fatal 
eomphcations  are  due  to  the  diphtheria  toxine  alone,  and  other  microbes 
are  absent.  Roux  and  Yersin  report  half  a  dozen  cases  in  their  monograph 
of  1888.  Cases  1,  3,  5,  6,  7,  10,  concern  young  patients  who  died  of  toxic 
angina.  Bacteriological  examination  yielded  pure  cultures  of  the  diphtheria 
baciUus. 

Martin  lias  collected  twenty-eight  cases  of  fatal  toxic  diphtheria,  in 
wliich  bacteriological  examination  showed  only  the  existence  of  long  and 
curved  diphtheria  bacilli,  without  other  microbes.  Chaillou  and  Martin 
(in  their  memoir,  July,  18()4)  have  collected  ten  fatal  cases  of  toxic  diph- 
theria, in  which  pure  cultures  of  diphtheritic  bacilU  were  found,  without 
other  microbes.     The  long  curved  bacillus  was  most  frequently  present. 

In  the  above  ca.ses  clinical  observation  was  always  confirmed  by  bacterio- 
logical examination.    It  is  therefore  possible  for  us  to  give  an  exact  clinical 

37—2 


580  TEXT-BOOK  OF  MEDICINE 

description  of  this  pure  toxic  angina,  which  constitutes  one  of  the  varieties 
of  mahgnant  angina. 

Tlie  temperature  is  higher  than  in  normal  diphtheritic  angina.  It 
oscillates  between  102°  and  104°  F.,  and  remains  at  this  point  for  some  days. 
It  is  a  bad  sign  if  the  temperature  does  not  fall  after  the  fourth  or  fifth  day 
(Martin).  The  changes  in  the  pulse  follow  the  oscillations  of  the  tempera- 
ture. The  false  membranes  are  thick,  adherent,  and  of  a  greyish-white 
colour.  They  generally  cover  the  tonsils,  the  uvula,  the  pillars,  and  the 
back  of  the  throat,  leaving  no  intervals  of  healthy  mucosa.  In  some  cases, 
however,  the  false  membranes  are  discrete. 

The  swelling  of  the  cervical  glands  is  more  rapid  and  more  marked  in 
toxic  than  in  normal  diphtheria.  Nevertheless,  it  is  rare  to  see  such  marked 
swelhng  as  in  diphthero-streptococcal  angina. 

Albuminuria  is  more  constant  in  toxic  than  in  normal  diphtheria,  though 
it  does  not  usually  appear  before  the  third  day,  and  it  does  not  disappear 
when  the  disease  is  about  to  end  fatally. 

In  toxic  diphtheria  the  colour  is  more  pale  and  leaden.  The  Ups  are  at 
times  cyanosed,  even  though  there  is  no  danger  of  asphyxia.  Diarrhoea  is 
frequent.  Distaste  for  food  and  drink  is  usually  present.  Rapidly  increasing 
weakness,  compressible  pulse,  and  tendency  to  syncope,  which  do  not  exist, 
or  are  only  slight  in  normal  diphtheria,  are  a  marked  feature  in  these  cases. 

Bacteriological  examination,  without  being  quite  conclusive,  shows 
that  numerous  colonies  of  long  curved  bacilH  belong  to  toxic  diphtheria. 
Experimental  cultures  on  broth  furnish  valuable  information  as  to  the 
degree  of  toxicity.  Brieger  and  Wasserman  were  able  to  extract  from  the 
blood  of  a  child  who  died  of  toxic  diphtheria,  with  collapse  and  cardiac 
failure,  a  quantity  of  diphtheria  toxine,  and  to  prove  its  specific  action  by 
inoculation  of  guinea-pigs.     Martin  has  obtained  similar  results. 

Let  us  now  compare  the  experimental  lesions  due  to  the  injections  of 
diphtheria  toxine  with  those  found  in  patients  who  have  died  from  toxic 
diphtheria.  They  are  quite  similar  :  heart  flabby  and  yellow,  parenchy- 
matous and  interstitial  myocarditis,  ecchymotic  pericarditis,  congested  Hver, 
dilatation  of  the  capillaries,  and  fatty  infiltration  of  the  hepatic  cells  ; 
infiltration  of  the  tubuli  contorti  of  the  kidney  and  dilatation  of  the 
glomerular  vessels  ;  enlarged  spleen  and  hypertrophy  of  the  Malpighian 
corpuscles ;  swelhng  of  Beyer's  patches  and  of  the  follicles  ;  infiltration 
of  the  intestinal  mucous  membrane. 

The  symptoms  and  the  lesions  explain  the  action  of  the  toxine  in  the  case 
of  toxic  diphtheria.  Let  us  now  see  how  malignant  diphtheria  behaves 
when  other  organisms  are  also  present. 

2.  Malignant  Diphtheria  with  Microbic  Associations. — In  most  cases 
the  mahgnant  forms  of  diphtheria  are  both  toxic  and  infective.     They  are 


DISEASES  OF  THE  THROAT  AND  PHARYXX  581 

due  to  the  reciprocal  exaltation  of  the  diphtheria  bacillus  and  of  the  microbes 
which  are  associated  with  it.  The  streptococcus  plays  the  principal  part, 
as  the  following  experiments  of  Roux  and  Yersin  show  : 

Prepare  a  weak  culture  of  diphtheria  baciUi,  so  that  inoculation  produces 
sUght  local  oedema  in  a  guinea-pig.  Prepare  another  culture  of  virulent 
streptococci,  so  that  1  c.c.  will  kill  a  rabbit  in  twenty-six  hours.  Prepare 
Ukewise  a  broth  culture  containing  a  combination  of  attenuated  diphtheria 
bacilU  and  virulent  streptococci.  Take  two  guinea-pigs  and  inoculate  them 
\vith  ^  c.c.  of  the  attenuated  diphtheria  culture  ;  take  two  others  and 
inoculate  them  with  |  centimetre  of  the  streptococcus  culture,  and  two  more 
Anth  1  c.c.  of  a  mixture  containing  equal  parts  of  the  two  cultures.  In  a 
few  days  the  guinea-pigs  inoculated  \\-ith  the  weak  culture  show  slight 
oedema  and  a  little  scab  at  the  point  of  inoculation,  but  no  other  compU- 
cations.  The  guinea-pigs  inoculated  with  the  streptococcus  show  an  abscess 
at  the  point  of  inoculation,  but  the  guinea-pigs  which  have  been  inoculated 
with  the  mixture  die  two  days  later. 

At  the  point  of  inoculation  false  membranes  and  oedema  containing 
diphtheria  bacilh  and  streptococci  appear.  The  lesions  found  post  mortem 
comprise  dilatation  of  the  vessels,  congestion  of  the  suprarenal  capsules, 
and  effusion  into  the  pleurae.  Tubes  of  serum  are  inoculated  with  the 
oedema  fluid.  Next  day  the  diphtheria  colonies  are  well  developed,  while  the 
streptococcus  has  only  grown  to  a  ,very  small  extent.  It  is,  therefore,  easy 
to  separate  the  two  microbes.  We  can  now  see  how  much  the  harmless 
diphtheria  bacillus  has  been  reinforced  by  contact  with  the  streptococcus. 
For  this  purpose  two  cultures  are  made — one  with  the  inojffensive  diphtheria 
bacillus,  and  the  other  with  the  reinforced  bacillus.  The  cultures  are  heated 
in  the  oven  for  a  fortnight  at  35°  C.  in  a  current  of  air,  filtered  through 
porcelain,  and  injected  into  the  veins  of  four  rabbits.  Two  rabbits  are  given 
10  c.c.  of  the  cultures  of  the  reinforced  bacillus.  They  die  in  thirty  hours, 
so  virulent  is  the  culture.  The  other  two  rabbits  are  each  given  twice  as 
large  a  dose  of  the  culture  of  the  weakened  bacillus,  and  Uve  two  months. 
It  is  only  after  a  long  time  that  they  grow  thin  and  succumb  to  paralysis. 

The  streptococcus  and  the  diphtheria  bacillus,  when  separated,  are 
incapable  of  killing  guinea-pigs  ;  when  associated,  they  kill  rapidly,  owing 
to  the  lesions  of  diphtheria. 

When  we  compare  the  cUnical  and  experimental  facts  (Roux,  Yersin, 
T'arbier,  Martin,  Chailh)u),  we  find  in  both  instances  identical  results. 
In  angina,  which  is  both  diphtheritic  and  streptococcal,  either  of  the  two 
microbes,  isolated  and  cultivated  separately,  is  rarely  virulent,  as  animal 
inoculation  shows.  The  two  microbes  together  reciprocally  increase  their 
virulence,  and  hence  the  exceptional  gravity  of  diphthero-streptococcal 
angina. 


582  TEXT-BOOK  OF  MEDICINE 

The  following  figures  indicate  the  gravity  of  these  cases  :  According  to 
Martin's  statistics,  8  deaths  in  10  cases  ;  Chaillou  and  Martin  give  13  deaths 
in  14  cases  ;  Tezenas  had  3  deaths  in  3  cases.  To  this  variety  of  mahgnant 
angina  belong  the  fulminating  cases  which  I  referred  to  at  the  commence- 
ment of  this  article.  Their  symptoms  have  been  admirably  described  by  our 
predecessors,  and  bacteriological  studies  have  in  part  explained  their  patho- 
genesis. At  the  onset  of  mahgnant  angina  the  face  is  pale,  leaden,  and 
bloated  ;  the  lips  are  cyanosed,  though  there  is  no  danger  of  suffocation. 
The  neck  is  enormous  and  "  proconsular  "  (Saint-Germain)  from  the  swell- 
ing of  the  glands  and  the  oedematous  infiltration  of  the  cellular  tissue. 
The  skin  of  the  face  and  neck  is  often  shiny  and  erysipelatous  in  appearance 
(Borsieri,  Trousseau).  The  breath  is  excessively  foetid,  especially  when 
the  exudates  are  invaded  by  the  bacilU  of  putrefaction.  Deglutition  is  very 
painful.  The  false  membranes  of  the  throat  have  often  a  gangrenous  appear- 
ance. The  temperature  is  usually  high,  and  the  pulse  is  rapid,  tliready,  and 
irregular.  Albuminuria  comes  on  early  and  is  persistent ;  diarrhoea  is  frequent ; 
haemorrhage  is  common  (epistaxis,  bleeding  gums,  purpura).  In  such  cases, 
the  nasal  fossse  being  often  invaded  by  both  microbes,  there  is  a  copious 
purulent  or  bloody  discharge,  with  rejection  of  false  membranes. 

Be  the  angina  rapid  or  slow,  its  gravity  is  considerable.  Extreme  rest- 
lessness with  or  without  delirium,  and  prostration  bordering  on  coma, 
are  present,  while  collapse  or  syncope  ends  the  scene.  Death  sometimes 
supervenes  from  certain  comphcations,  such  as  infective  croup,  purulent 
bronchitis,  or  streptococcal  broncho -pneumonia.  If  recovery  takes  place, 
convalescence  is  long,  and  at  times  accompanied  by  ulceration  of  the 
throat,  mouth,  or  nose,  and  by  suppurative  adenitis. 

This  description  differs,  as  will  be  seen,  from  that  of  purely  toxic  angina. 
In  the  latter  the  diphtheritic  poison  is  the  chief  factor  ;  in  diphthero- 
streptococcal  angina,  infection  by  the  streptococcus  claims  a  large  share. 
This  fact  is  made  quite  clear  in  Barbier's  paper,  in  which  he  shows  that  the 
streptococcus  enters  the  blood.  It  reaches  the  blood  of  the  pulmonary 
veins,  and  thence  affects  the  lungs,  the  bronchi,  the  mitral  valve,  the 
articulations,  the  pleurae  (purulent  pleurisy),  the  middle  ear  (purulent 
otitis),  the  tissues  of  the  neck  (adeno-phlegmon),  the  walls  of  the  pharynx 
(retropharyngeal  abscess),  the  spleen,  etc. 

What  I  have  just  said  of  the  streptococcus  is  in  part  apphcable  to  the 
staphylococcus.  Although  diphthero-staphylococcal  angina  is  not  so  grave 
as  diphthero-streptococcal  angina,  it  still  claims  a  place  in  the  group  of 
mahgnant  anginae.  The  truth  thereof  is  evident  on  consulting  the  statistics 
pubhshed  on  this  subject. 

Conclusions. — We  can  now  formulate  the  following  conclusions  as  to 
the  pathogenesis  of  diphtheritic  angina  : 


DISEASES  OF  THE  THROAT  AND  PHARYNX  583 

1.  Diphtheritic  angina  is  called  normal  or  benign  when  it  is  neither 
toxic  nor  infective.  Its  benign  nature  is  due  to  the  feeble  virulence  of 
the  diphtheria  bacilli,  or  to  the  feeble  receptivity  of  the  soil  in  which  they 
develop.  It  is  also  due  to  the  absence  of  other  microbes,  or  to  the  feeble 
power  possessed  by  the  associated  microbes  to  increase  in  virulence. 
Nevertheless,  normal  angina,  in  spite  of  its  benign  appearance,  is  not  always 
free  from  danger.  It  may  be  accompanied  by  asphyxia,  especially  in 
children  (croup),  or  be  followed  by  paralysis. 

2.  Diphtheritic  angina  is  called  malignant  when  it  is  toxic  and  in- 
fective. It  is  rather  toxic  than  infective  when  the  predominating  features 
can  be  ascribed  to  the  virulence  of  the  diphtheria  toxine  ;  it  is  rather 
infective  than  toxic  when  the  predominating  features  are  due  to  other 
microbes,  especially  the  streptococcus.  We  must  never  forget  the  part 
played  by  the  soil,  which  favours  more  or  less  the  development  of  the 
poison. 

3.  The  normal,  toxic,  and  infective  forms  of  diphtheritic  angina  occur 
with  their  distinctive  characteristics,  according  as  the  bacillus  limits  its 
action  to  the  production  of  membranes,  or  elaborates  the  poison  in 
every  degree  of  toxicity,  with  or  without  secondary  infections.  We 
find,  however,  mixed  cases  in  wliicli  these  varieties  are  associated,  and  it 
cannot  be  otherwise,  because  it  is  always  the  same  disease,  which  may 
present  different  aspects,  but  forms,  after  all,  only  one  species.  Diphtheritic 
angina,  therefore,  may  start  with  benign  symptoms,  and  then  assume  the 
characteristics  of  the  toxic  or  infective  form,  with  a  fatal  result. 

Polymorphism  of  Diphtheritic  Angina — Herpetic,  Lacunar,  and 
Pultaceous  Varieties. 

Diphtheritic  angina  is  not  always  characterized  by  the  formation  of 
false  membranes.  Eor  a  long  time,  until  bacteriological  examinations  were 
made,  writers  were  loath  to  admit  that  membranes  might  be  absent  in 
diphtheritic  angina.  Non-diplitheritic  membranous  angina  was  well  known, 
but  few  believed  that  membranes  were  ever  absent  in  diphtheritic  angina. 

For  some  years  past  bacteriological  researches  have  shed  light  on  the 
chaos  of  angina.  Thick  and  adherent  membranes  are  certainly  the  most 
common  clinical  feature  in  diphtheritic  angina,  but  in  a  large  number  of 
cases — more  numerous  than  we  think — membranes  are  absent.  It  resembles 
catarrhal,  erythematous,  pultaceous,  lacunar,  or  follicular  angina.  In  other 
cases  diphtheritic  angina  assumes  the  guise  of  herpetic  angina.  These 
herpetic,  erythematous,  pultaceous,  or  lacunar  varieties  are  more  frecjuent 
ia  adults  than  in  children.  Of  137  cases  of  diplitheritic  angina  in  adults, 
Roche  found  but  42  instances  of  the  membranous  variety.  I  shall  review, 
therefore,    these    various    kinds    of    diphtheritic    angina,    which,    as    will 


584  TEXT-BOOK  OF  MEDICINE 

be  seen,  is  essentially  polymorphous,  and  I  shall  first  describe  the  herpetic 
variety,  as  given  in  my  lectures  at  the  Faculte  de  Medecine  in  December^ 
1894. 

1.  Herpetic  Variety  of  Diphtheritic  Angina. 

I  will  begin  with  the  classical  description  of  simple  herpetic  angina. 
Whether  we  speak  of  herpetic  angina  (Gubler)  or  of  membranous  angina 
(Bretonneau  and  Trousseau),  or  whether  we  follow  other  authors,  and 
designate  it  "  herpes  of  the  pharynx,"  it  is  not  less  admitted  that  the 
characteristic  feature  of  herpetic  angina  is  the  presence  of  herpetic  vesicles 
on  the  mucous  membrane  of  the  throat. 

A  child  or  adult  is  taken  ill  with  symptoms  of  fever.  The  rigors  and  the 
fever  are  accompanied  by  lassitude  and  headache.  Dysphagia  appears. 
We  find  diffuse  redness  of  the  tliroat ;  the  tonsils  are  enlarged,  and  small 
swelUngs,  wliich  have  been  likened  to  sudamina,  appear  on  different  parts 
of  the  isthmus  of  the  gullet  or  the  pharynx.  This  condition  is  known  as 
herpetic  angina. 

In  some  cases  the  disease  has  the  appearance  of  an  erythematous  angina, 
and  the  exudate  is  shght.  In  other  cases  we  find  vesicles  on  the  mucous 
membrane  of  the  throat  and  also  a  whitish  pultaceous  exudate.  At  times, 
indeed,  we  find  not  simply  a  pultaceous  layer,  but  thick  and  extensive 
fibrinous  membranes,  simulating  diphtheria  so  closely  that  Trousseau 
called  this  variety  of  herpetic  angina  by  the  name  of  "  common  membranous 
angina,"  the  epithet  "common"  here  ehminating  all  idea  of  diphtheria. 

Every  medical  man  has  seen  more  or  less  frequently  these  erythematous, 
pultaceous,  or  membranous  forms  of  herpetic  angina.  When  we  are  able 
to  witness  the  actual,  but  sometimes  fugitive,  evolution  of  the  herpetic 
vesicles,  no  room  for  doubt  exists,  and  the  diagnosis  of  herpetic  angina  is 
clear.  The  diagnosis  often  receives  considerable  support  when  the  herpes, 
instead  of  remaining  confined  to  the  tliroat,  invades  other  regions,  such  as 
the  labial  commissure,  the  lips,  the  nostrils,  the  chin,  the  cheeks,  the  con- 
junctiva, etc.  If  a  patient  has  acute  painful  angina,  with  false  membranes, 
which  may  even  simulate  diphtheria,  and  if  at  the  same  time  herpes  is 
present  on  the  tonsils,  the  roof  of  the  palate,  the  pharynx,  and  the  face, 
we  may  diagnose  herpetic  angina,  but  we  cannot  exclude  diphtheria.  Tliis 
view  is  at  least  generally  admitted,  and  is  borne  out  by  experience.  The 
description  of  angina  with  herpes,  therefore,  must  be  revised.  Bacterio- 
logical research  in  the  last  few  years  has  shown,  and  is  showing  every  day 
that  angina,  whether  erythematous,  pultaceous,  or  membranous,  cannot 
be  diagnosed  for  certain,  except  by  bacteriological  examination. 

Herpetic  angina,  like  every  othei  variety,  cannot  escape  bacteriological 
control. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  585 

My  researches  on  this  subject,  communicated  to  the  Academie  de 
Medecine,*  have  enabled  me  to  place  the  matter  on  a  firm  basis.  I  have 
been  able  to  prove  that  so-called  herpetic  angina  is  fairly  often  of  a  diph- 
theritic nature.  I  found  it  easy  to  verify  the  inconstancy  and  the  insuffi- 
ciency of  the  symptoms  furnished  by  clinical  observation,  and  I  cannot  state 
too  forcibly  the  fact  that  the  eruption  of  herpes,  which  was  formerly  said 
to  ehminate  the  idea  of  diphtheria,  only  serves  to  deceive  us.  It  inspires 
us  with  false  security,  as  the  following  cases  show  : 

Case  I. — In  1895  a  man,  fifty-two  years  of  age,  admitted  for  severe  herpetic 
angina,  which  had  commenced  suddenly  four  days  before  with  rigors,  fever,  dysphagia, 
headache,  lassitude,  coryza,  and  slight  epistaxis.  Axillary  temperature,  103°  F.  Ex- 
amination of  the  throat  revealed  diffuse  redness  and  marked  swelling  of  the  tonsils, 
and  on  the  roof  of  the  palate  herpetic  vesicles  irregularly  disposed.  A  crop  of  herpetic 
vesicles  was  also  present  on  the  lips  and  on  the  right  labial  commissure.  The  maxillary 
glands  were  moderately  enlarged.     The  natural  diagnosis  was  herpetic  angina. 

Next  day  a  pultaceous  deposit  appeared  on  the  right  tonsil.  This  deposit  on  serum 
and  agar  showed  staphylococci  and  diphtheria  bacilli.  The  bacteriological  finding 
reversed  the  former  diagnosis.  Nasal  diphtheria,  clinically  suspected  a  few  days 
previously  from  slight  epistaxis  and  coryza,  now  appeared.  The  patient  had  nasal 
discharge  and  epistaxis,  and  voided  false  membranes  from  the  nose.  The  pillars 
of  the  fauces  and  the  uvula  were  also  covered  with  patches  of  membrane.  In  spite 
of  injections  of  serum,  which  were  given  too  late,  acute  paralysis  of  the  soft  palate 
appeared  a  few  days  later.  The  paralysis  invaded  in  turn  the  lower  and  upper 
limbs  and  the  bladder. 

This  case  of  angina  showed  all  the  cUnical  features  of  herpetic  angina,  and  it  was 
only  by  bacteriological  examination  that  we  discovered  the  diphtheria,  which  was 
confirmed  a  few  days  later  by  generalized  paralysis. 

Case  II. — A  girl,  eighteen  years  of  age,  was  admitted  under  Gouguenheim  for  sore 
throat,  accompanied  by  headache,  lassitude,  and  temperature  of  104°  F.  Generalized 
redness  of  the  pharynx  and  the  tonsils.  Herpetic  vesicles,  whitish  and  slightly  adherent 
membranes  on  both  tonsils  ;  herpetic  vesicles  also  present  on  the  lips  and  the  com- 
missures. No  glandular  enlargement.  The  clinical  diagnosis  pointed  to  herpetic 
angina.  Cultures  made  from  the  membranes  on  the  tonsils  yielded  diphtheria  bacilli, 
but  no  other  microbes.     An  injection  of  10  c.c.  of  serum  was  immediately  given. 

Case  III. — In  1892,  at  the  Necker  Hospital,  the  matron's  son  was  taken  ill  with 
angina.  The  throat  was  so  red  that  my  house-physicians,  Charrier  and  Renon,  took  it 
to  be  an  early  symptom  of  scarlatina.  Next  day  herpetic  vesicles  appeared  on  the 
tonsils,  and  the  diagnosis  was  herpetic  angina.  At  the  end  of  two  or  three  days  he  was 
admitted  to  the  hospital,  and  the  existence  of  the  herpetic  variety  of  diphtheria  was 
recognized.  I  also  discovered  diphtheritic  coryza,  which  had  commenced  with  epis- 
taxis. Very  severe  paralysis  followed.  The  velum  palati  was  first  affected,  and  then 
the  muscles  of  the  head  and  the  neck,  the  lower  limb.s,  and  finally  the  upper  limbs, 
were  attacked  in  turn.     He  recovered  two  months  later. 

Case  IV. — Kelsch  was  asked  to  make  a  bacteriological  examination  in  a  case  of 
angina  which  presented  aM  the  clinical  characteristics  of  herpetic  angina.  The  culture 
revealed  the  diphtheria  bacillus,  and  also  the  pneumococcua. 

Case  V. — Huchard  reported  the  following  case  to  me  :  He  was  called  upon  to  give 
bis  opinion  as  to  an  angina  in  a  child.     Relying  on  the  severity  of  the  fever,  the  sudden- 

*  Dieulafoy,  "  Angine  Diphtherique  a  Forme  Herpotirnio  "  (Academie  de  Medecine, 
Blanco  des  11  Juin,  2  et  3  Juillet,  1895). 


586  TEXT-BOOK  OF  MEDICINE 

ness  of  the  onset,  and  the  simultaneous  appearance  of  herpes,  he  diagnosed  herpetic 
angina,  which  was  confirmed  by  Brocq.  The  case,  which  had  every  appearance  ot 
herpetic  angina,  was  really  diphtheritic,  and  carried  off  the  child  in  a  few  days. 

Description. — We  are  in  possession  of  several  cases  which  prove  that 
the  herpetic  forms  of  diphtheritic  angina  are  fairly  common.  What,  then, 
becomes  of  the  classical  description  and  chnical  diagnosis  of  the  old  herpetic 
angina  ?  The  suddenness  of  its  onset,  the  severity  of  the  fever,  the  acute- 
ness  of  the  general  symptoms,  the  sharp  pain  in  the  throat,  and  the  appear- 
ance of  the  herpetic  vesicles  on  the  tonsils,  the  velum  palati,  and  the  Hps, 
formed  a  symptom-complex,  on  which  it  appeared  possible  to  base  the 
diagnosis  of  herpetic  angina.  And  in  the  differential  diagnosis  from 
diphtheritic  angina  great  care  was  taken  to  accentuate  the  difference 
between  the  acute  inflammation  of  herpetic  angina  and  the  more  insidious 
and  less  painful  onset  of  diphtheritic  angina. 

This  erroneous  idea  must  be  abandoned.  The  cases  abeady  quoted 
show  that  the  herpetic  variety  of  diphtheria  may  be  as  sudden  and  acute 
as  the  most  classical  so-called  herpetic  angina.  In  Huchard's  case  the 
angina  began  with  very  acute  fever.  The  tonsils  were  red  and  swollen ; 
herpes  was  present ;  and  a  most  toxic  diphtheria  was  masked  by  these  acute 
symptoms. 

My  httle  patient  in  the  Necker  Hospital  was  taken  ill  with  acute  fever 
and  severe  sore  throat.  Herpes  appeared,  but  here  again  the  acute  symp- 
toms masked  diphtheria,  wliich  was  followed  by  severe  paralysis.  In  a 
case  reported  by  Roux  and  Martin,  a  child  was  suddenly  taken  ill,  with 
a  temperature  of  104°  F.,  pulse  of  160,  and  delirium.'  The  sore  throat  was 
severe ;  the  tonsils  were  much  enlarged,  red,  and  pultaceous ;  herpes 
appeared  on  the  lips.  This  picture  is  typical  of  herpetic  angina,  and  yet 
it  is  quite  deceptive,  since  it  apphes  equally  to  diphtheritic  angina  with 
herpes, 

I  therefore  propose  to  abolish  the  so-called  herpetic  angina,  as  it 
has  been  bequeathed  to  us  by  our  predecessors.  It  can  no  longer  retain 
its  quasi-intangible  place  in  our  nosology.  If  we  retain  herpetic  angina 
in  the  old  sense  of  the  word,  we  must  remember  that  it  is  less  a  case  of 
herpetic  angina  than  of  angina  with  herpes. 

We  see  streptococcal,  staphylococcal,  or  pneumococcal  angina  with 
herpes,  and,  of  most  interest,  a  group  of  diphtheritic  anginse  with  herpes,* 
as  I  hope  I  have  clearly  proved. 

Nevertheless — and  tins  is  the  question  wliich  redoubles  the  interest- 
it  will  be  easy  for  us  to  connect  the  actual  state  of  science  with  the  tra- 
ditions handed  down  to  us  by  one  of  our  greatest  clinical  physicians.     For 

*  Jes  (of  Krakow)  has  found  the  diphtheria  bacillus  in  the  liquid  of  the  vesicles 
of  labial  herpes  in  a  patient  stricken  with  diphtheritic  angina  (1896). 


DISEASES  OF  THE  THROAT  AND  PHARYNX  587 

this  purpose  let  me  quote  from  Trousseau's  report,  wliich  was  presented 
by  him  to  the  Academie,  on  behalf  of  the  Conmiission  on  Epidemics,  on 
November  22,  1859. 

The  opinions  given  in  this  report  are  stated  some  years  later  in  his 
"  Chnical  Lectures  at  the  Hotel-Dieu  "  :  "  The  characteristic  of  the  epidemics 
of  the  year  1858,"  says  Trousseau,  "  was  the  concomitance  of  herpes  of  the 
pharynx  and  diphtheritic  angina.  The  former,  though  reduced  to  simple 
herpes  of  the  pharynx,  did  not  always  run  a  regular  course.  Some 
cases  were  very  prolonged ;  at  other  times  the  membranous  affection 
degenerated  in  situ.  The  physician  ought  anxiously  to  put  the  question 
to  himself  whether  he  is  justified  in  maintaining  a  favourable  prognosis. 
The  two  affections  not  only  occurred  one  after  the  other  (herpetic  angina 
and  diphtheritic  angina),  but  in  each  partial  epidemic  the  two  pathological 
forms  were  found  to  be  more  or  less  closely  associated." 

I  might  multiply  these  quotations,  which  prove  that  Trousseau  had 
seen  and  described  in  detail  the  relations  which  may  exist  between  diph- 
theria and  the  so-called  herpetic  angina.  The  bacteriological  researches 
wliich  I  have  already  mentioned  are  a  striking  confirmation  of  the  ideas 
of  the  greatest  chnical  physician  of  our  French  school.  Trousseau  not  only 
discovered  the  herpetic  variety  of  diphtheria,  but  also  formed  a  clear  idea 
of  the  gravity  of  the  prognosis.  We  should  be  wrong  to  imagine  that 
herpetic  diphtheria  is  always  benign.  The  cases  above  mentioned  are 
convincing  on  this  point.  The  child  at  the  Necker  Hospital  was  seized 
with  severe  diphtheritic  paralysis,  which  placed  its  life  in  danger.  Another 
of  my  patients  similarly  suffered  from  severe  paralysis,  lasting  four 
months.  Huchard's  patient  died  within  a  few  days.  Trousseau,  then,  was 
accurate  when  he  wrote  :  "  Fatal  diphtheria  often  commences  with  an 
eruption  of  herpes." 

Conclusions. — Diphtheritic  angina  may  assume  the  appearance  of  her- 
petic angina.  It  is  impossible  clinically  to  affirm  that  a  so-called  lierpetic 
angina  is  or  is  not  diphtheritic.  Bacteriological  examination  enables  us  to 
decide  the  nature  of  the  case. 

2.  Diphtheritic  Angina  of  a  Follicular  Appearance. 

Let  us  now  consider  diphtheritic  angina  that  simulates  follicular 
tonsillitis.  Here  again  the  clinical  picture;  of  the  disease  is  deceptive. 
Chnically,  a  case  appears  to  be  tonsillitis,  and  bacteriology  corrects  the  mis- 
take.    To  quote  the  proofs  : 

In  1891  Jacobi  showed  bacteriologically  that  follicular  tonsilUtis, 
especially  in  adults,  is  often  dii)htheritic.  During  an  epidemic  of  diphtherio 
in  a  boarding-school,  Mouillot  found  amongst  eiglaeen  })atients  eight  cases  of 
membranoua  angina  and  ten  cases  of  follicular  tonsillitis.     All  were  diph- 


588  TEXT-BOOK  OF  MEDICINE 

theritic.  One  of  the  latter  cases  was  followed  by  diphtheritic  paralysis. 
Escherich  has  found  the  bacillus  of  diphtheria  in  several  cases  of  so-called 
follicular  tonsillitis.  Koplik,  in  1892,  reported  numerous  cases  of  follicular 
diphtheritic  angina. 

Chaillou  and  Martin  have  quoted  eight  cases  of  diphtheritic  angina, 
presenting  white  points  on  the  tonsils,  and  simulating  follicular  tonsilhtis. 
Gouguenheim  says  that  in  eighty-three  cases  of  adults  suffering  from 
diphtheritic  angina  at  the  Lariboisiere  Hospital,  he  found  forty  cases  of 
follicular  diphtheria. 

Diphtheritic  angina,  therefore,  assumes,  especially  in  the  adult,  the  guise 
of  folhcular  tonsillitis,  and  bacteriological  examination  alone  can  decide 
the  diagnosis.  This  follicular  diphtheritic  angina,  although  generally 
benign,  may  in  exceptional  cases  be  toxic  and  dangerous,  as  the  cases  of 
Chaillou  and  Martin  show,  as  weU  as  Case  CXII.  in  Martin's  monograph. 

3.  Diphtheritic  Angina  of  the  Pultaceous  Variety. 

This  form  is  the  rarest  and  most  benign  of  all.  The  patient  has  angina 
presenting  all  the  appearances  of  catarrhal,  erythematous,  pultaceous  angina, 
and  bacteriology  reveals  the  bacillus  of  diphtheria. 

Feer  reports  three  cases.  One  child  showed  at  first  moderate  rednees  of  the  throat, 
with  a  temperature  of  103°  F.  The  next  day  the  thermometer  registered  105"  F.  The 
tonsils  were  swollen  and  red,  with  some  pultaceous  deposit.  Glandular  enlargement 
was  present  on  one  side.  The  child  was  cured  in  a  few  days.  The  cultiire  revealed  the 
presence  of  diphtheria  bacilli.  Inoculation  with  a  pure  culture  of  these  diphtheria  bacilli 
killed  a  guinea-pig  in  ten  hours.  Concetti,  in  1894,  reported  two  cases  of  pultaceous 
diphtheritic  angina,  arising  by  contagion  from  children  suffering  with  fatal  pharyngeal 
and  nasal  diphtheria.  The  tonsils  were  enlarged,  and  covered  with  a  layer  which  in 
nowise  resembled  diphtheria,  but  had  rather  the  coarse  appearance  of  a  pultaceous 
exudate.     The  condition  was  diphtheritic. 

Clinical  Diagnosis. — In  a  case  of  acute  angina  two  mistakes  may  be 
made.  The  first  error  consists  in  diagnosing  diphtheritic  angina  when  it 
is  not  present.  The  converse  mistake  consists  in  mistaking  a  case  of  diph- 
theria for  a  non-diphtheritic  angina.  In  the  latter  case  we  fail  to  recognize 
an  existing  diphtheria.  The  result  is  that  the  patient  is  not  isolated  and 
spreads  the  disease.  Moreover,  a  patient  who  has  not  been  treated  early 
with  serum  Avill  be  more  exposed  to  the  immediate  or  remote  consequences 
of  diphtheria,  including  croup,  early  or  late  poisoning,  and  paralysis. 

These  cases,  wliich  are  too  numerous,  prove  that  it  is  imperative  to 
recognize  diphtheritic  angina  from  the  first,  under  the  penalty  of  the  gravest 
mishaps.  CHnical  resources,  however,  are  very  often  insufficient.  What 
signs  and  symptoms  are  to  be  looked  for  ?  Can  we  rely  upon  the  manner 
in  which  the  angina  commences  ?  It  has  been  truly  said  that  diphtheritic 
angina  at  its  commencement  is  more  insidious  and  accompanied  by  less 


DISEASES  OF  THE  THROAT  AND  PHARYNX  589 

fever  than  other  forms  of  angina,  which  are  more  clearly  inflammatory.  If 
the  reader  \\all  refer  to  the  cases  quoted  in  the  preceding  section,  he  will 
see  that  the  herpetic  form  has  often  a  most  sudden  onset,  with  marked 
sjTnptoms  of  fever. 

Can  the  severity  of  the  dysphagia  be  rehed  on  ?  It  has  been  said  and 
repeated— not  without  some  truth — that  deglutition  is  rektively  easy  in 
diphtheria,  whilst  it  is,  as  a  rule,  very  painful  in  non-diphtheritic  angina. 
Tliis  statement  is  often  true,  but  yet  we  find  many  exceptions.  The  cas3S 
of  herpetic  diphtheria  enumerated  above  showed  early  and  severe  dys- 
phagia. 

Can  the  character  and  the  growth  of  the  false  membrane  be  relied  on  ? 
Here  again  the  clinical  characteristics  of  the  diphtheritic  membranes  which 
were  classical  before  bacteriological  examination — viz.,  colour,  thickness, 
adherence,  elasticity,  and  reaction  to  chemical  agents — are  common  both  to 
diphtheritic  and  non-diphtheritic  membranes.  Is  not  the  ready  reproduc- 
tion of  false  membranes  at  least  a  characteristic  inherent  in  diphtheria  ? 
It  was  formerly  beheved  to  be  so,  but  since  bacteriological  examinations 
have  been  made,  we  know  that  membranes  caused  by  Brisou's  cocci, 
streptococci,  staphylococci,  or  pneumococci,  may  be  reproduced  with  the 
same  readiness  as  the  diphtheritic  membrane. 

Is  not  the  tendency  which  the  membranes  possess  of  invading  the 
nasal  cavities  and  the  larynx  at ,  least  in  favour  of  diphtheria  ?  In  the 
section  on  Pseudo-diphtheritic  Membranes  we  shall  see  that  many  of  them, 
though  due  to  streptococci  or  to  Brisou's  coccus,  may  invade  the  nose  and 
the  larynx.  Cannot  the  glandular  enlargement,  which  has  been  looked  upon 
as  a  valuable  sign,  be  of  some  help  to  us  ?  On  the  one  hand,  enlargement 
of  the  submaxillary  glands  may  be  almost  wanting  in  pure  diphtheria,  and 
very  marked  in  pseudo-diphtheritic  angina.  Baginski  has  reported  sub- 
maxillary adenitis  in  five  out  of  six  cases  of  streptococcal  angina.  Tezenas 
speaks  of  similar  swelling  four  times  in  four  cases  of  streptococcal  and 
staphylococcal  angina.  Jaccoud  found  adenitis  in  a  case  of  pneumococcal 
angina.  Martin  has  repeatedly  noted  marked  adenitis  in  membranous 
angina  due  to  Brisou's  coccus.  I  have  often  made  the  same  observation. 
Submaxillary  adenitis  is,  therefore,  of  little  assistance  in  diagnosis. 

Is  albuminuria  a  sign  of  diphtheritic  angina  ?  Pseudo-diphtheritic 
angina,  caused  by  various  microbes — notably  streptococci — is  frequently 
accompanied  by  albuminuria. 

This  critical  study  of  the  signs  and  symptoms  of  diphtheritic  angina  sliows 
thatcHnical  signs  alone  are  insufficient  for  diagnosis.  Several  cases  regarded 
by  eminent  physicians  as  diphtheria  have  been  proved  by  bacteriology  to  be 
not  so.  I  need  only  refer  to  pseudo-diphtheritic  angina  due  to  the  strepto- 
cocci, Brisou's  coccus,  the  pncuniococcus,  or  the  staphylococci,  which  we 


590  TEXT-BOOK  OF  MEDICINE 

shall  discuss  in  the  next  section.  Per  contra,  several  cases  considered  as 
being  non-diphtheritic  have  been  proved  by  bacteriology  to  be  diphtheria. 
I  need  only  refer  to  the  numerous  cases  of  polymorphous  diphtheria  (her- 
petic, lacunar,  and  pultaceous  forms). 

I  am  well  aware  that  even  at  the  present  day  many  practitioners  make 
their  diagnosis  in  the  case  of  angina  solely  by  the  chnical  signs,  and  reserve 
bacteriological  examination  for  doubtful  cases.  Bacteriological  examina- 
tion, carried  out  systematically,  is,  in  their  oj^inion,  unnecessary.  After 
my  communication  to  the  Academic  de  Medecine,  I  was  taken  to  task  in  the 
Premier-Paris  of  one  of  our  medical  journals,  where  I  read  the  following 
sentence  :  "  According  to  Dieulafoy  and  all  bacteriologists,  it  is  no  longer 
permissible  to  make  a  diagnosis  of  angina  without  bacteriological  examina- 
tion. Is  there  not  some  exaggeration  in  this  proposition  ?"  That  is  the 
very  word  :  we  are  taxed  with  exaggeration.  We  are  given  to  understand 
that  bacteriological  examination  is  only  useful  in  a  case  where  chnical 
examination  may  be  at  fault.  I  cannot  too  strongly  contradict  such  assertions. 

We  are  told  that  great  clinical  physicians  in  the  past  did  not  await  the 
aid  of  bacteriology  in  order  to  diagnose  cases  of  angina.  I  apologize  to 
those  who  speak  thus,  but  we  must  speak  the  whole  truth.  No  one  respects 
tradition  more  than  I  do,  and  I  place  great  reUance  on  chiiical  investiga- 
tion, but  evidence  must  be  accepted.  I  would  refer  my  critics  to  the 
diagnosis  made  in  his  own  case  by  Gillette,  physician  to  the  Children's 
Hospital,  and  one  well  versed  in  the  diagnosis  of  diphtheria.  Gillette 
thought  he  was  suffering  from  herpetic  angina.  He  congratulated  himself 
on  the  severity  of  the  inflammatory  symptoms,  the  whiteness  of  the  mem- 
branes, the  bright  redness  of  his  throat,  and  the  pain  which  he  felt ;  and  yet 
the  angina  was  diphtheritic,  and  proved  fatal  in  a  few  days.  I  would  ask 
my  critics  what  they  think  of  the  diagnosis  of  Gubler,  who  was  a  man  well 
versed  in  the  study  of  angina.  He  taught  that  herpetic  angina  causes 
general  paralysis,  as  diphtheria  does,  thus  committing  an  error  which  he 
would  never  have  made  if  bacteriology  had  enhghtened  his  diagnosis. 

I  would  refer  my  critics  to  the  classification  of  Lasegue,  who  did  not  know 
exactly  where  the  group  of  diphtheritic  anginse  began  or  ended,  and  in- 
vented the  name  diphtheroid  angina.  This  name  created  the  greatest 
confusion,  wliich  only  bacteriology  has  been  able  to  dissipate. 

In  the  subject  under  discussion  chnical  observation  must  give  way  to 
bacteriology.  I  know  that  it  is  hard  to  give  up  deeply-rooted  convictions, 
but,  at  the  risk  of  repetition,  evidence  must  be  accepted.  A  knowledge  of 
the  bacteriological  work  of  the  last  few  years  shows  the  innumerable  errors 
committed  when  the  diagnosis  of  angina  rested  on  chnical  observation 
alone.  In  order  to  convince  my  readers,  I  think  it  useful  tc  point  out  the 
errors  corrected  by  bacteriology. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  591 

In  the  third  report  of  the  Pasteur  Institute,  Roux  and  Yersin  state  that 
out  of  52  cases  of  membranous  angina  of  diphtheritic  appearance  19  were 
not  diphtheritic.  Morel,  in  his  thesis  on  diphtheria,  states  that  in  86  cases 
of  membranous  angina  simulating  diphtheria  20  were  not  diphtheritic. 

The  most  important  paper  pubKshed  in  France  on  this  subject  is  that  of 
Martin,  who  says  :  "  Of  112  patients  admitted  to  the  Hospital  for  Sick  Chil- 
dren for  diphtheritic  angina  36  had  not  diphtheria  at  all."  He  takes  care 
to  add  :  "  CUnical  study  gave  no  information  as  to  the  nature  of  these  36 
cases.  Physicians  had  taken  them  for  diphtheria,  and  yet  bacteriological 
examination  proved  the  absence  of  the  diphtheria  bacillus.  They  gave 
rise,  therefore,  to  36  diagnostic  errors  which  it  was  cKnically  impossible  to 
avoid,  and  which,  consequently,  exposed  to  contagion  36  children  who  were 
in  a  state  of  receptivity." 

Baginsky,  in  1891,  published  a  series  of  93  cases  of  membranous 
angina  of  diphtheritic  appearance ;  bacteriological  examination  proved 
that  25  of  these  cases  were  not  diphtheria.  In  1892  Baginsky  published 
a  second  series  of  154  cases  of  angina  of  diphtheritic  appearance,  in 
which  bacteriology  revealed  36  errors  in  diagnosis.  WiUiam  Hallock  Park 
says :  "  In  159  cases  of  membranous  angina  of  diphtheritic  appearance, 
89  cases — that  is  to  say,  more  than  half — were  not  diphtheritic." 

In  1892  Kophk  reported  33  cases  of  membranous  angina  of 
diphtheritic  appearance ;  Loffler's.  bacillus  could  not  be  found  in  16  of 
them. 

Errors  are  more  numerous  in  the  case  of  secondary  anginse  supervening 
in  the  course  of  the  infectious  fevers,  and  notably  in  scarlatina. 

We  have,  therefore,  a  series  of  cases  in  which  hundreds  of  errors  have 
been  made,  because  certain  microbes — namely,  Brisou's  little  coccus, 
streptococcus,  staphylococcus,  etc. — gave  to  these  cases  of  angina  the 
clinical  appearance  of  diphtheria. 

Another  series  of  errors  consists,  as  we  have  said,  in  mistaking  diph- 
theria for  simple,  lacunar,  pultaceous,  or  herpetic  angina.  As  this  question 
has  been  fully  discussed  in  the  previous  section,  I  shall  not  reopen  the 
discussion.  This  polymorphism  was  a  very  frequent  cause  of  error  before 
bacteriology  established  the  facts.  Practitioners  were  too  much  accus- 
tomed to  the  idea  of  membranous  diphtheria.  We  know  to-day  that 
herpetic,  lacunar,  and  pultaceous  forms  of  diphtheria  exist.  We  must  there- 
lore  eliminate  a  partially  correct  diagnosis.  In  the  case  of  angina  the  only 
way  to  arrive  at  an  absolute  diagnosis  is  by  bacteriological  examination. 
Jaccoud  expressed  this  opinion  in  1891,  and  Landouzy  made  an  important 
communication  to  the  Academie  de  Medecine  on  the  same  subject 
in  1895. 

The  above  discussion  apphes  equally  to  syphilitic  angina.     Chancre  of 


592  TEXT-BOOK  OF  MEDICINE 

the  tonsil,  whicli  is  covered  with  greyish  false  membranes  and  accompanied 
by  dysphagia  and  glandular  enlargement,  somewhat  resembles  diphtheria ; 
but  in  the  case  of  the  chancre  the  lesion  is  unilateral,  the  tonsil  is  indurated, 
the  disease  runs  a  slow  course,  the  ulcerated  surface  is  readily  cleaned,  and 
the  detritus  is  pultaceous  rather  than  membranous.  Mucous  patches  of 
the  throat  and  of  the  tonsils  are  sometimes  covered  with  false  membranes, 
which  simulate  diphtheria.  These  membranes  are  whitish  or  greyish,  of 
a  gangrenous  appearance,  adherent  to  the  mucous  membrane,  and  accom- 
panied by  submaxillary  adenitis.  These  forms  of  syphilitic  angina  closely 
resemble  diphtheria.  These  two  lesions  may,  indeed,  appear  simultaneously, 
and  are  so  much  alike  that  the  diagnosis  can  only  be  made  by  bacteriological 
examination. 

Ulcero-membranous  angina,  described  in  Section  2,  is  accompanied 
by  diphtheroid  membranes,  and  may  simulate  diphtheria.  The  absence  of 
diphtheria  bacilli  and  the  presence  of  fusiform  bacilH  and  spirilla  (Vincent) 
prove  the  diagnosis. 

Phlegmonous  tonsillitis  itself  may  present  difficulties  in  diagnosis  from 
certain  forms  of  diphtheritic  angina.  In  both  cases  the  pain  is  very  severe, 
deglutition  is  difficult,  the  swelhng  of  the  neck  may  be  considerable,  and  the 
pulpy,  sanious,  diffluent  coating  sometimes  present  in  malignant  angina 
closely  resembles  the  diphthero-streptococcal  coating  which  covers  the  throat 
in  phlegmonous  tonsilhtis.  Albuminuria  may  exist  in  either  cask  On 
what  symptoms  can  the  clinical  diagnosis  be  based  ?  In  phlegmonous 
amygdalitis  the  pain  is  more  acute  and  more  general,  the  dysphagia  is 
excessive,  and  the  patient  can  scarcely  turn  his  head,  which  is  rendered 
immovable  by  the  contraction  of  the  muscles  of  the  neck ;  he  cannot  open 
his  mouth  without  acute  pain,  and  can  scarcely  move  his  tongue.  These 
symptoms  are  not  so  severe  in  diphtheria.  In  both  cases  the  neck  is  puffy 
and  swollen,  but  the  swelUng  appears  earlier  and  is  more  marked  in  the 
glands  than  in  diphtheria.  In  both  cases  respiration  may  be  interfered 
with  on  account  of  the  contraction  of  the  isthmus  of  the  gullet,  but  this 
symptom  is  much  more  prominent  in  phlegmonous  tonsillitis,  and  gave  to 
it  the  name  of  quinsey.  In  both  cases  examination  of  the  throat  may 
be  difficult,  but  the  patient  suffering  from  diphtheria  is  the  better  subject, 
because  he  feels  less  pain.  One  essential  feature  is  absent  in  diphtheria — 
viz.,  the  tonsil  and  the  velum  palati  are  not  pushed  back  and  depressed  by 
the  peritonsillar  phlegmon.  Certain  cases  of  suppurative  tonsilhtis,  how- 
ever, may  be  associated  with  the  diphtheria  bacillus  and  other  microbes. 
I  saw  a  case  of  diphthero-streptococcal  angina  which  simulated  suppurative 
tonsillitis.     Bacteriological  examination  is  therefore  indisiDensable. 

Bacteriological  Examination. — In  a  case  of  angina,  what  is  the  correct 
technique  in  a  bacteriological  examination  ?     A  piece  of  membrane  may  be 


DISEASES  OF  THE  THROAT  AND  PHARYNX  593 

stained  and  examined  under  the  microscope ;  this  method,  however,  is  not 
trustworthy,  and  I  therefore  prefer  to  make  cultures.  A  small  piece  of 
membrane  is  placed  in  a  tube  of  gelatinized  serum,  as  described  in  the  pre- 
ceding section. 

Diphtheritic  Angina. — In  the  case  of  diphtheria,  either  pure  or  asso- 
ciated with  ocher  microbes,  it  is  possible,  after  an  incubation  of  eighteen 
hours,  to  make  out  diphtheria  colonies,  which  are  the  more  characteristic 
the  more  spaced  they  are.  The  rapidity  with  which  the  first  colonies 
appear  is  almost  pathognomonic  of  diphtheria  ;  it  is  only  in  membranous 
angina  due  to  Brisou's  coccus  that  we  find  equally  rapid  growth.  Typical 
colonies  of  the  diphtheria  bacilh  are  rounded,  whitish,  and  more  opaque  at 
the  centre  than  at  the  periphery.  They  project  shghtly  above  the  surface 
of  the  serum,  and  I  have  therefore  called  them  papular.  A  fragment 
stained  with  Roux's  blue  shows  the  Klebs-LofHer  bacillus  (Section  V.). 

Membranous  Angina  due  to  Brisou's  Coccus.— A  patient  is  sufiering 
from  membranous  angina  which  might  easily  be  considered  diphtheritic  ; 
it  has  all  the  characteristics  of  a  case  of  normal  diphtheritic  angina.  I  have 
seen  such  a  case  at  the  Necker  Hospital,  and  the  resemblance  to  diphtheria 
was  such  that  bacteriology  alone  could  decide  the  diagnosis.  On  making  a 
culture,  after  eighteen  hours  colonies  appear  in  the  gelatinized  serum  ;  they 
closely  simulate  diphtheria  colonies.  They  appear  early ;  they  are  rounded 
and  whitish,  but  their  centre  is  not  opaque.  They  are  transparent  through- 
out their  whole  extent,  and  have  a  humid  appearance  ;  moreover,  they  are 
flat,  and  I  have  therefore  called  them  macular,  to  distinguish  them  from 
the  diphtheria  colonies  which  are  papular.  On  examining  a  stained  fragment 
under  the  microscope  we  find  no  diphtheria  bacilli,  but  only  a  small  coccus, 
which  is  often  paired  hke  a  diplococcus.  We  know,  therefore,  the  nature 
of  the  angina  which  at  first  sight  so  closely  simulates  diphtheria.  We 
know  that  it  is  neither  toxic  nor  infective,  that  it  will  not  be  followed 
by  paralysis,  and  that  even  if  croup  is  present,  tracheotomy  will  not  be 
required. 

Membranous  Angina  due  to  Streptococci.— These  cases  simulate  diph- 
theria so  exactly  that  in  Martin's  report  we  find  an  account  of  eight  patients 
who  were  sent  to  the  diphtheria  ward  when  they  had  streptococcal  angina. 
This  angina  will  be  studied  in  the  next  section.  I  will  here  content  myself 
with  giving  the  distinctive  bacteriological  signs.  When  membrane  from 
the  pharynx  is  placed  on  the  culture  medium,  the  colonies  of  streptococci 
make  their  appearaiic(>.  somewhat  later  than  those  of  diphtheria.  We  find 
immerous  small  punctiform  colonies,  which  I  call  powdery ;  they  show  but 
little  tendency  to  grow  larger,  and  the  microscope  reveals  the  streptococcus 
in  straight  or  bent  chains  of  three,  four,  five,  or  six  elements.  Primary  or 
secondary  streptococcal  angina  is  frequent  in  the  early  stages  of  scarlatina, 

38 


594  TEXT-BOOK  OF  MEDICINE 

whilst  the  angina  which  appears  during  the  dechne  of  scarlatina  may  be 
diphtheritic. 

Membranous  Angina  due  to  Staphylococci. — Membranous  angina  due 
to  staphylococci  has  been  taken  for  diphtheria.  The  colonies  {Staphylo- 
coccus alhus  and  aureus)  usually  develop  in  twenty-four  hours,  and  the 
bacteriological  examination  is  so  characteristic  that  a  mistake  is  impossible. 

Membranous  Angina  due  to  Pneumococcus. — This  variety  of  angina 
(see  Section  VII.)  has  been  described  by  Jaccoud.  The  diagnosis  from  diph- 
theritic angina  is  absolutely  impossible  without  bacteriological  examination. 
This  variety  of  angina,  wliich  is  due  to  the  pneumococcus,  is  not  toxic,  and 
does  not  spread  to  the  larynx. 

Prognosis. — The  prognosis  of  diphtheritic  angina  depends  upon  the 
chnical  and  bacteriological  examination.  Clinically,  we  must  beware  of 
cases  of  angina  preceded  or  accompanied  by  nasal  diphtheria.  The  nasal 
cavities  are  an  excellent  soil  for  the  growth  of  the  diphtheria  bacillus  ;  it 
elaborates  its  toxine  under  the  most  favourable  conditions,  for  it  finds 
an  even  temperature  and  an  incessant  renewal  of  air  by  nasal  respiration, 
just  as  in  the  method  devised  by  Roux  for  the  manufacture  of  the  toxine. 
In  mild  diphtheria,  early  and  grave  comphcations  need  not  be  feared,  but 
yet  the  poison  is  made  on  such  a  surface  that  sufficient  toxine  to  cause 
diphtheritic  paralysis  may  penetrate  it.  In  mahgnant  diphtheritic  angina 
the  presence  of  nasal  diphtheria  is  of  evil  omen,  as  Trousseau  rightly  in- 
sisted. Early  pallor,  leaden  and  puffy  face,  abundant  albuminuria,  and 
tendency  to  prostration  are  bad  symptoms.  When  thQ  submaxillary  glands 
are  much  enlarged  from  the  first,  the  prognosis  is  usually  grave.  In  some 
cases  the  inflamed  glands  behave  like  buboes — "  they  reek  of  the  pest " — 
and  form  abscesses.  The  glandular  suppuration  may  not  be  discovered, 
because  the  patient  succumbs  before  the  formation  of  an  abscess.  Early 
suppuration  is  a  fatal  sign  :  this  statement  does  not  hold  in  late  suppuration. 
If  the  adenitis  commences  to  suppurate  when  the  angina  is  at  an  end,  recovery 
may  follow.  These  cases  of  adenitis  are  due  to  the  association  of  the  strepto- 
coccus with  the  diphtheria  bacillus. 

Bacteriological  examination  furnishes  valuable  information  as  to  the 
prognosis.  A  culture  which  shows  discrete  colonies  of  medium  bacilli 
indicates  less  grave  diphtheria  than  if  the  culture  produce  confluent  colonies 
with  long  curved  bacilH.  As  regards  the  prognosis,  it  is  very  important  to 
know  whether  the  bacillus  of  diphtheria  is  associated  with  other  microbes. 
Bacteriological  examination  is,  as  we  shall  see,  an  indispensable  element 
in  the  prognosis.  Angina  in  wliich  the  bacillus  of  diphtheria  is  present 
alone  is  generally  normal,  with  firm  and  elastic  fibrinous  membranes.  It  may 
be  followed  by  croup,  especially  in  children,  and  by  paralysis,  but  it  rarely 
assumes  the  maUgnant  form.     Diphtheritic  angina  which  is  associated  with 


DISEASES  OF  THE  THROAT  AND  PHARYNX  595 

Brisou's  coccus,  is  generally  benign.  Diphtheritic  angina  with  which  the 
staphylococcus  is  associated,  is  far  more  serious  than  the  preceding  forms. 

In  the  most  serious  or  malignant  form  the  streptococcus  is  also  present. 
It  is  in  such  cases  that  the  membranes  may  have  a  putrilaginous  aspect  and 
foetid  odour,  while  the  enlarged  glands  lead  to  the  condition  known  as  "  the 
proconsular  neck."  MaUgnant  angina  is  fairly  frequently  met  with  as  a 
secondary  affection  in  the  dechne  of  scarlatina  or  during  the  course  of 
measles  and  whooping-cough. 

etiology. — Diphtheritic  angina  is  especially  common  in  young  subjects. 
It  is  endemic  in  certain  countries,  and  when  it  rages  in  an  epidemic  form,  the 
epidemic  is  often  relatively  benign  or  mahgn  in  a  family,  a  town,  or  a 
district.  In  countries  visited  for  the  first  time  by  diphtheria  the  angina 
and  the  other  manifestations  of  the  disease  are  generally  severe.  For 
example,  in  Bessarabia,  where  the  scourge  made  its  appearance  for  the  first 
time  in  1872,  it  carried  o£E  more  than  12,000  victims  in  eight  years. 
"  In  1875  it  appeared  in  the  Province  of  Kerson,  where  the  mortality 
varied  from  27  to  62  per  cent." 

Diphtheria  is  contagious,  and  the  contagion  may  be  direct  or  indirect. 
Inoculation  of  diphtheria,  tried  by  Trousseau  and  Peter  upon  themselves, 
did  not  succeed ;  it  was  a  lucky  failure,  which  only  proves  that  the  subjects 
were  not  in  a  state  of  receptivity.  Direct  contagion  is  only  too  well  proved 
by  the  numerous  examples  of  parents  and  physicians  who  have  contracted 
the  disease  from  a  patient.  I  need  only  cite  the  case  of  Walleix,  already 
mentioned,  and  of  Herpin,  who  from  a  piece  of  membrane  which  entered 
his  nostril,  contracted  coryza,  angina,  and  paralysis.  The  cases  of  Blanche, 
Clozel  de  Boyer,  Armango,  and  many  others,  whose  memory  we  revere,  will 
suffice. 

The  contamination  may  be  contracted  from  patients  who  have  recovered 
from  the  attack  because  virulent  bacilli  are  present  for  weeks  in  their  oral  and 
nasal  cavities.  After  the  disappearance  of  the  membranes,  virulent  bacilli 
may  exist  for  a  fairly  long  time,  although  the  mucous  membrane  appears  quite 
healthy  (Roux).  Tezenas,  who  studied  the  duration  of  the  contagious 
period  in  convalescent  patients,  furnishes  us  with  the  following  information  : 
He  made  cultivations  daily  in  sixty  cases  after  the  disappearance  of  the 
membrane  from  the  throat.  In  five  cases  bacilli  were  present  for  a  variable 
period.  In  eleven  cases  the  bacillus  was  present  in  the  nose,  while  it  was 
absent  from  the  mouth  and  pharyjix.  It  was  found  in  the  nose  for  fifty- 
five  days,  and  while  it  was  present,  it  gave  rise  to  a  clear  nasal  discharge, 
that  was  generally  unilateral.     Centres  of  contagion  may  thus  result. 

In  other  cases  the  contagion  is  indirect,  and  spreads  through  the  interme- 
diary of  the  membranes,  or  of  the  dried  sputum  which  has  fallen  on  l)e(l(ling, 
clothing,  toyy,  or  toilet  articles.    Cases  of  diphtheria  occurring  si.x  months  or 

38—2 


596  TEXT-BOOK  OF  MEDICINE 

a  year  later  in  previously  infected  surroundings  are  thus  explained.  These 
chnical  cases  agree  with  experimental  researches,  Roux  having  found  that  a 
particle  of  diphtheritic  membrane,  wrapped  in  a  piece  of  Hnen  and  placed 
in  a  wardrobe,  kept  its  virulence  for  more  than  five  months. 

In  other  cases  the  diphtheria  bacillus  exists  in  the  naso-pharyngeal 
cavity  without  causing  the  shghtest  comphcation  (Loffler).  If,  however, 
the  virulence  of  the  bacillus  is  increased,  diphtheria  occurs,  and  appears 
to  be  spontaneous. 

A  first  attack  does  not  confer  immunity  ;  diphtheritic  angina  may  occur 
a  second  time. 

In  some  cases  the  angina  is  secondary — that  is  to  say,  it  supervenes 
in  the  course  of  some  other  disease  (scarlatina,  measles,  typhoid  fever). 
These  cases  will  be  described  under  the  primary  disease. 

Do  fowls  suffer  from  diphtheria,  and  can  they  transmit  it  to  human 
beings  ?  Saint- Yves  Menard  denies,  with  good  reason,  the  identity  of 
human  and  avian  diphtheria.  The  latter  is  a  pseudo-diphtheria  which  is 
not  transmissible  to  man. 

Pathological  Anatomy. — I  described  under  Diphtheritic  Angina  the  ap- 
pearance of  the  false  membranes.  These  fibrinous  membranes  adhere  more  to 
the  chorion  when  the  mucous  membrane  is  covered  with  stratified  epithehum 
than  when  it  is  covered  with  simple  epithelium,  as  in  the  air- passages.  The 
membranes  may  acquire  great  thickness  (^  millimetre  to  2  milhmetres)  from 
the  stratified  layers  which  are  formed  on  the  deep  surface  in  contact  with  the 
mucous  membrane.  The  younger  the  layers  the  more  resistant  they  are,  whilst 
the  older  ones  are  pushed  towards  the  surface  and  became  friable.  Each 
layer  of  the  false  membrane  is  developed  at  the  expense  of  the  corresponding 
layer  of  the  epithelium,  and  becomes  more  superficial  as  a  new  layer  is  pro- 
duced beneath.  "  A  discussion  has  been  raised  as  to  whether  the  false  mem- 
brane is  situated  above  or  below  the  epithelium.  From  what  has  gone  before, 
we  see  that  it  is  formed  in  the  epithelial  lining,  and  partially  at  the  expense 
thereof."  The  false  membrane  replaces  the  epithehum.  On  post-mortem 
examination  the  diphtheritic  membranes  have  in  part  disappeared,  but 
examination  during  hfe  shows  that  they  are  composed  of  a  more  or  less 
dense  network  of  fibrin,  that  encloses  in  its  meshes  altered  epithelial 
cells,  lymphocytes,  red  corpuscles,  and  micro-organisms.  Many  of  the 
cells  are  dead,  and  their  nuclei  do  not  stain  with  picro-carmine. 

The  epithelial  cells  are  infiltrated  with  colloid  substance,  lose  their 
nucleus,  and  are  converted  into  homogeneous  refracting  blocks  with  pro- 
longations which  branch  like  a  stag's  horns  (Wagner) — Weigert's  coagula- 
tion necrosis.  A  haemorrhagic  exudate  is  sometimes  found  under  the 
false  membranes,  and  gives  rise  to  ecchymoses.  The  structure  of  the  false 
membrane  changes  somewhat  at  different  periods  of  its  growth.     At  first 


DISEASES  OF  THE  THROAT  AND  PHARYNX  597 

fclie  epithelial  changes  are  most  marked  and  the  fibrinous  network  is  less 
important.  Later  the  membrane  becomes  epithelial,  fibrinous,  and  purulent, 
and  in  the  last  stage  the  fibrin  is  in  excess  (Leloir).  The  behaviour  of  the 
diphtheria  bacilli  was  described  in  the  previous  section. 

The  mucosa  on  which  the  membranes  are  about  to  develop  is  intiamed 
and  swollen.  After  the  membranes  have  disappeared,  the  mucosa  has  a 
dull  look  from  the  absence  of  epitheUum.  Ecchymoses  may  be  seen,  but 
ulcers  are  rare.  Ulceration,  haemorrhage,  and  gangrene  are  chiefly  seen  in 
malignant  diphtheria. 

When  attacked  by  diphtheria,  the  tonsil  undergoes  changes,  the 
description  of  which  I  borrow  from  Cornil.  In  a  section  we  see  the 
following  features  from  the  surface  to  the  deep  tissue  :  The  false  membrane 
which  has  replaced  the  epithehum  burrows  into  the  tonsillar  crypts.  In 
its  deepest  part  it  seems  to  blend  mth  the  mucous  chorion.  The  connective 
tissue  of  the  mucous  membrane  is  infiltrated  with  red  and  white  corpuscles, 
its  capillary  vessels  are  filled  with  white  corpuscles,  and  the  inflammation 
which  affects  the  reticular  tissue  and  the  folhcles  of  the  tonsils  explains 
the  marked  swelhng  of  these  organs.  The  pharynx  is  the  seat  of  similar 
lesions  ;  inflammatory  hypertrophy  of  the  lymphatic  follicles  is  seen.  The 
lymphatic  glands  of  the  neck  are  swollen  and  infiltrated  with  a  turbid, 
"»erous,  or  purulent  fluid. 

The  membranes  on  the  skin  closely  resemble  those  on  the  mucous  mem- 
brane. They  are  in  part  formed  at  the  expense  of  the  modified  epidermal 
layers,  and  are  adherent  to  the  papillae.  Gangrene  of  the  derma  is  some- 
times found.  Ecchymoses  have  been  found  in  the  sulci  of  the  cerebral 
convolutions.  Pulmonary  lesions  (bronchitis,  broncho-pneumonia)  are 
very  common,  especially  when  croup  complicates  angina.  They  are  gener- 
ally the  result  of  secondary  infections,  the  staphylococcus  and  streptococcus 
being  responsible  in  many  instances.  The  kidneys  are  almost  always 
affected  in  severe  diphtheria.  We  find  hypera?niia  and  haemorrhage  in  the 
cortical  layer,  with  cloudy  swelUng  of  the  epithelium  of  the  tubules.  The 
changes  in  the  kidneys,  hke  those  in  the  liver  (fatty  degeneration  of  the  cells), 
are  due  to  the  diphtheritic  toxine. 

The  heart  muscle  is  affected,  and  the  papillary  muscles  in  particular 
show  granular  degeneration.  Interstitial  myocarditis  is  at  times  fairly 
well  marked.  The  valvular  endocardium  shows  changes  described  by 
Labadie-Lagrave  as  endocarditis.  They  are  rare,  and  result  from 
secondary  infections.  In  malignant  angina  the  blood  is  fluid  and  sepia- 
coloured  (Millard),  and  the  number  of  rod  corpuscles  is  diminished.  This 
condition  of  dissolution  is  met  with  in  certain  infectious  diseases. 

Treatment. — Since  Roux's  communication  at  the  Buda-Pesth  Congress, 
the  treatment  of  diphtheria  by  serotherapy  has  replaced  otlier  methods. 


598  TEXT-BOOK  OF  MEDICINE 

Behring  first  thought  of  applying  serotherapy  to  the  treatment  of  diphtheria, 
but  it  was  Roux  who,  by  discovering  the  toxine,  rendered  the  discovery  of 
the  antitoxine  possible.  Roux  selected  the  horse  as  the  animal  to  produce 
the  serum,  and,  while  the  labours  of  Behring  gained  few  adherents  in  Germany, 
Roux's  reports  and  results  of  his  labours  and  those  of  his  collaborators  were 
sufficient  to  insure  universal  employment  of  the  new  method. 

The  method  consists  in  making  horses  immune  against  diphtheria, 
and  in  making  use  of  the  serum  from  an  immune  horse  as  a  preventive  and 
curative  agent  in  diphtheria. 

The  animal  is  inoculated  under  the  skin  of  the  neck  and  shoulders  with 
progressively  increasing  doses  of  diphtheritic  toxine.  We  start  with  very 
weak  doses — less  than  1  c.c,  with  or  without  the  addition  of  iodine — and 
in  a  few  weeks  it  is  possible  to  inject  at  one  sitting  doses  which  are 
200  and  300  times  as  large.  In  less  than  three  months  the  horse  is 
immune.  As  suggested  by  M.  Nocard,  some  10  pints  of  blood  are  taken 
from  the  jugular  vein,  yielding  about  5  pints  of  serum.  The  same  horse, 
if  he  continues  immune,  can  supply  the  above  quantity  of  antidiphtheritic 
serum  every  three  weeks.  Antidiphtheritic  serum  does  not  quite  deserve  the 
name  antitoxine.  The  serum  is  not  antitoxic  in  the  true  sense  of  the  word, 
as  it  does  not  destroy  the  toxine.  It  does  not  affect  the  toxine,  but  acts 
on  the  cells  of  the  organism,  making  them,  for  the  time  being,  insensible  to 
the  poison.  The  toxine  destroys  the  activity  of  the  cell,  while  the  anti- 
toxine revives  and  stimulates  it  (Roux).  The  serum  restores  to  the  cells 
of  the  organism  a  part  of  the  phagocytic  activity  which  they  have  lost 
through  the  action  of  the  poison  (Metchnikoff). 

Experiments. — The  following  method  is  used  in  studying  the  action  of 
the  serum  on  infected  animals  : 

Vulvar  diphtheria  is  induced  in  a  female  guinea-pig.  A  few  hours  after 
inoculation  we  find,  first,  redness  of  the  vulva,  with  swelhng  and  oedema  of 
the  mucous  membrane,  and  later  the  appearance  of  diphtheritic  membranes, 
vaginal  discharge,  fever,  and  loss  of  appetite.  Some  animals  die  in  a  few  days 
from  diphtheritic  poisoning,  some  recover,  and  others  suffer  from  paralysis. 

If,  however,  these  animals  receive  a  prophylactic  dose  of  serum  equal 
to  one  ten-thousandth  part  of  their  weight,  the  diphtheritic  membranes 
disappear  by  the  second  day ;  fever  is  less  severe,  and  recovery  always 
follows. 

If,  instead  of  giving  the  antitoxine  as  a  prophylactic,  we  inject  it  twelve 
hours  after  inoculation  with  diphtheria,  curative  results  are  obtained.  The 
diphtheritic  membranes  disappear  on  the  second  day,  and  do  not  reform ; 
the  bacilh  disappear,  and  the  animals  recover.  In  any  case,  the  curative 
dose  of  antitoxine  used  (after  inoculation  of  diphtheria)  must  be  very  much 
larger  than  the  prophylactic  dose. 


DISEASES  OF  THE  THROAT  AND  PHARNYX  599 

Curative  experiments  give  similar  results  in  croup.  If  croup  is  pro- 
duced in  rabbits,  these  animals  die  in  a  few  days,  the  respiratory  troubles 
and  laryngo-tracheal  lesions  resembhng  those  found  in  croup  in  children. 

Rabbits  which  have  been  inoculated  in  the  trachea  after  injection  of 
serum.  "  do  not  take  diphtheria,  or,  at  least,  it  does  not  show  itself  by  any 
apparent  malaise."  If  the  serum  is  injected  into  animals  after  tracheal 
inoculation,  it  may  arrest  well-marked  diphtheria. 

These  experiments,  then,  are  very  conclusive,  and  prove  the  eflS.cacy  of 
antitoxic  serum,  provided  the  injection  is  not  given  too  late. 

The  serum,  however,  does  not  produce  the  same  benefit  in  diphtheria 
associated  with  the  streptococcus.  "  The  association  of  the  two  microbes 
(diphtheria  bacillus  and  streptococcus)  produces  in  the  rabbit  rapid  diph- 
theria, such  as  we  see  in  young  children.  The  pathological  picture  is  the 
same."  These  two  microbes  reciprocally  increase  their  virulence,  and 
injections  of  antidiphtheritic  serum  have  not  the  same  efficacy. 

Let  us  now  consider  the  treatment  in  a  case  of  diphtheria.  A  sterilized 
syringe  of  a  capacity  of  20  c.c.  is  used,  and  the  serum  is  injected  under  the 
subcutaneous  tissue  of  the  flank,  the  skin  being  first  rendered  aseptic. 
To  a  child  under  fifteen  years  of  age  10  to  15  c.c.  of  serum  are  given;  above 
fifteen  years  of  age  20  to  25  c.c.  are  injected  at  one  sitting.  In  some  cases 
it  is  necessary  to  repeat  the  injection  on  one  or  more  occasions. 

Let  us  analyze  the  results — (1)  in  pure  diphtheria  ;  (2)  in  diphtheria 
with  other  micro-organisms. 

Pure  Diphtheritic  Angina. — Recovery  is  the  rule  after  the  serum  has 
been  injected.  Fresh  membranes  do  not  appear  twenty-four  hours  after 
the  injection,  and  those  already  present  become  detached  in  two  days. 
The  temperature  falls  abruptly  (Martin)  and  the  general  condition  speedily 
improves.  Furthermore  (tliis  point  is  very  important),  complications  and 
croup  are  very  rare,  or,  at  least,  if  croup  appears,  it  is  very  mild.  The  follow- 
ing quotation  deserves  consideration :  "  In  169  children  admitted  into 
hospital  with,  diphtheritic  angina,  36  showed  laryngeal  troubles,  31  had 
croupy  cough,  and  25  had  lost  their  voice  and  showed  marked  sucking-in, 
80  that  tracheotomy  appeared  advisable.  Under  the  influence  of  the  serum 
(and  an  injection  may  be  given  every  twelve  hours)  the  sucldng-in  diminished, 
and  only  returned  at  intervals.  The  child  coughed  up  the  false  membranes, 
and  at  the  end  of  two  or  three  days  the  respiration  was  normal,  to  the  great 
surprise  of  the  house-physicians  and  the  nurses,  who,  from  their  experience 
of  croup,  were  convinced  that  operation  could  not  be  avoided- 

Let  us  now  see  the  action  of  serum  in  a  case  of  diphtheritic  angina  when 
other  microbes  are  present. 

The  association  of  the  diphtheria  bacillus  with  Brisou's  coccus  is  benign, 
and  recovery  is  the  rule  after  injections  of  serum. 


600  TEXT-BOOK  OF  MEDICINE 

The  association  of  the  bacillus  with  the  staphylococcus  causes  more 
severe  angina  ;  nevertheless,  recovery  almost  always  follows  after  injections 
of  serum,  and  this  association  is  not  as  serious  in  the  case  of  angina  as  it  is 
in  the  case  of  croup  after  tracheotomy. 

The  presence  of  the  streptococcus  gives  rise  to  grave  angina,  in  which 
injections  of  serum  are  not  so  effectual.  The  mortaUty  has  been  25  per 
cent. 

In  diphthero-streptococcal  angina,  antidiphtheritic  serum  and  Marmorek's 
antistreptococcic  serum  have  been  used  together,  but  the  results  so  far 
obtained  with  the  latter  serum  have  not  been  encouraging  :  "  There  is  no 
reason  to  expect  a  positive  action.  We  can  only  look  for  a  modification  of 
the  condition  of  the  throat  and  of  the  glands ;  we  cannot  rely  on  any  anti- 
toxic action  "  (Sevestre). 

I  need  not  refer  here  to  the  treatment  of  croup  by  injections  of  serum 
{vide  Croup),  but,  taking  all  the  cases  of  diphtheria  (angina  or  croup)  as  a 
whole  treated  with  antitoxic  serum,  we  obtain  the  following  figures  : 

The  statistics  of  Roux,  Martin,  and  Chaillou  refer  to  446  cases.  Death- 
rate,  24*5  per  cent. 

The  statistics  of  Moizard  refer  to  231  cases.  Death-rate,  14'7  per 
cent. 

The  statistics  of  Le  Gendre  refer  to  16  cases.  Death-rate,  12' 5  per 
cent. 

The  statistics  of  Lebreton  refer  to  242  children.  Death-rate,  12  per 
cent. 

The  statistics  of  Variot  for  the  year  1895  give  a  total  death-rate  of 
14"  5  per  cent. 

"  The  year  1894,"  says  Bayeux,  "  divides  the  therapeutics  of  diph- 
theria into  two  distinct  epochs  :  the  first,  in  which  55  per  cent,  of  the  cases 
died,  and  the  second,  when  the  mortality  fell  to  16  per  cent.,  thanks  to  the 
use  of  antitoxine.  This  figure  (16  per  cent.)  is  supported  by  my  own  returns 
of  more  than  200,000  cases." 

The  rate  of  mortaUty  is  diminishing  continually,  and  will  diminish  still 
further,  in  proportion  as  cases  of  broncho-pneumonia  are  isolated,  and 
tracheotomy  is  replaced,  as  far  as  possible,  by  intubation,  and  serum  is  in- 
jected without  a  moment's  loss  of  time.  We  have  Uved  to  see  a  thing  hitherto 
unknown — that  is,  a  week  passing  in  Paris  without  a  single  case  of  diphtheria 
being  notified  ! 

A  condition  of  success  is  to  make  the  injection  as  soon  as  possible  after 
the  outbreak  of  the  disease.  Diphtheritic  paralysis  only  supervenes,  as  a 
rule,  when  injection  of  serum  has  been  delayed.  I  hold,  therefore,  that  in 
a  suspicious  case  of  membranous  angina,  before  bacteriological  examination 
has  decided  the  nature  of  the  disease,  we  should  begin  by  giving  an  injection. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  601 

No  one  will  ever  repent  having  done  so,  even  though  the  angina  is  not 
diphtheritic,  whilst  delay  till  the  next,  day  may  cause  regret. 

As  for  local  treatment  in  diphtheria,  we  must  be  satisfied  with  irrigations 
containing  chlorinated  soda  (Roux).  Painting  with  poisonous  or  caustic 
substances,  such  as  carbohc  acid  and  subhmate,  must  not  be  prescribed. 

I  asked  myself  whether  local  painting  of  the  throat  with  serum  might 
not  be  beneficial.  I  therefore  conducted  some  experiments  with  my  house- 
physician,  Marion.  Female  guinea-pigs  were  inoculated  with  vulvar 
diphtheria,  and,  when  the  disease  appeared,  the  parts  were  painted  several 
times  a  day  with  serum.  No  result  was  obtained.  This  conclusion,  how- 
ever, refers  only  to  ordinary  serum  obtained  by  the  injection  of  toxine  into 
animals.  Martin,  by  injecting  the  bodies  of  the  bacilli  themselves  into 
animals,  obtained  a  serum  which  was  no  longer  antitoxic,  but  anti-infective. 
Rist  has  shown  that  the  bodies  contain  a  poison  differing  from  the  soluble 
toxine.  Martin's  anti-infective  serum  can  be  made  up  in  pastilles,  which 
dissolve  in  the  mouth  and  seem  to  have  an  action  in  situ  on  the  diphtheria 
bacillus. 

Injections  of  antidiphtheritic  serum  sometimes  cause  cutaneous  erup- 
tions, urticaria,  and  articular  pains,  which  are  less  frequent  in  proportion  as 
the  technique  has  been  perfected.  Other  complications  for  which  the  serum 
has  been  blamed  (albuminuria,  tachycardia,  arrhythmia,  muscular  pains) 
must  be  set  down  to  diphtheria  or  to  streptococcal  infections.  It  is  important 
however,  to  make  use  of  properly  prepared  serum  ;  bad  serum  might  lead 
to  trouble. 

Prophylactic  Treatment. — As  serum  injections  have  a  prophylactic 
action,  it  may  be  beneficial  to  inoculate  the  contacts,  especially  children 
and  nurses.  This  prophylactic  application  of  serum  has  given  most  satis- 
factory results  (Mewim,  Schiiler),  and  is  a  means  of  stamping  out  epidemics 
or  of  preventing  their  spread. 

Netter  and  Guinon  have  made  systematic  use  of  this  prophylactic 
power.  Every  child  admitted  into  the  Trousseau  Hospital  receives  5  c.c. 
of  antidiphtheritic  serum,  subject  to  reinoculation  every  three  w^eks. 
Internal  cases  of  diphtheria  in  the  wards  have  become  unknown. 

Patients  must  be  closely  watched,  even  after  complete  disappearance 
of  the  membranes,  because  the  bacilU  may  remain  for  weeks  in  the  throat 
or  nose.  Tezenas  has  published  a  very  interesting  work  on  this  sul)ject. 
In  sixty  cases  of  diphtheria  he  found  diphtheria  bacilli  in  the  Jiasal  cavity, 
although  the  angina  was  completely  cured  and  the  bucco-pharyngeal  cavity 
was  free  from  them.  This  persistence  of  the  bacillus  in  the  nasal  cavity  is 
always  associated  with  a  limpid  nasal  discharge,  whi(;h  generally  comes 
from  one  nostril.  "  As  long  as  this  discharge  lasts,  Loffler's  bacilli  arc 
found  in  the  nasal  cavity.     The  bacillus  disappears  with  the  discharge." 


602  TEXT-BOOK  OF  MEDICINE 

The  most  minute  precautions  must  be  taken  with  regard  to  things  that 
have  been  in  contact  with  a  diphtheritic  patient.  Linen  or  bedding  must 
be  baked  in  a  steam-oven  under  pressure,  for  the  diphtheria  bacillus  is  very 
resistant,  and  persons  have  contracted  diphtheria  in  a  bed  which  a  patient 
suffering  from  diphtheria  had  used  several  months,  or  even  a  year,  previously, 
no  antiseptic  precautions  having  been  taken. 


VII.  PSEUDO-DIPHTHERITIC  MEMBRANOUS  ANGINA. 

Before  the  discovery  of  bacteriology  it  was  well  known  that  certain  cases  of  mem- 
branous angina  simulated  diphtheria,  though  they  were  not  diphtheritic.  Bretonneau 
had  expressed  this  view,  and  Trousseau  wrote  a  most  remarkable  chapter  on  this  subject. 
Returning  to  the  familiar  question  of  specificity,  Trousseau  reviews  the  forms  of  mem- 
branous angina  which  are  not  diphtheritic  :  membranous  angina  following  cauteriza- 
tion of  the  pharynx  with  nitrate  of  silver  and  ammonia,  and  membranous  angina  due 
to  the  abuse  of  mercury.  He  teaches  us  that  in  scarlatina  membranous  angina  is 
rarely  diphtheritic  (and  bacteriology  has  proved  that  he  is  correct),  and  quotes  cases 
of  angina  in  the  course  of  enteric  fever  which  have  been  wrongly  taken  for  diphtheria. 
Finally,  following  Bretonneau,  he  separates  diphtheria  from  herpetic  membranous 
angina,  which  he  calls  common  membranous  angina. 

The  distinction  made  by  these  great  masters,  as  a  result  of  clinical  observation, 
between  diphtheritic  and  pseudo-diphtheritic  membranous  angina,  has  been  clearly 
established  by  bacteriological  researches.  Bacteriology  is  responsible  for  this  section, 
which  is  only  the  continuation  and  the  complement  of  the  two  preceding  sections. 
Bacteriology  has  enabled  us  to  classify  and  to  enumerate  the  nature  and  the  character- 
istics of  pseudo-diphtheritic  membranous  angina. 

The  different  microbes  which  will  be  referred  to  in  the  description  of  pseudo-diph- 
theritic  angina,  include  Brisou's  coccus,  the  streptococcus,  the  pneumococcus,  the 
staphylococcus,  and  the  Bacillus  coli  ;  they  may  be  associated  in  all  the  varieties  of 
angina,  whether  catarrhal,  pultaceous,  herpetic,  or  suppurative.  In  some  cases,  however, 
they  are  associated  with  the  formation  of  membranes,  and  the  angina  then  simulates 
diphtheria,  and  merits  the  name  "  pseudo -diphtheritic." 

Pseudo-Diphtheritic  Angina  due  to  Coccus.— A  child  four  or  five 
years  of  age  has,  two  days  before,  been  taken  ill  with  moderate  fever, 
headache,  loss  of  appetite,  and  sore  throat.  The  temperature  has  been 
about  103°  F.  On  examining  the  throat  the  mucous  membrane  is  found  to 
be  red  and  covered  with  patches  of  membranous  exudate.  If  the  angina 
be  of  two  or  three  days'  duration,  the  tonsils,  the  uvula,  and  the  pharynx 
may  be  covered  with  false  membranes  which  simulate  diphtheria.  No 
distinction  is  possible  between  these  membranes  and  those  seen  in  certain 
cases  of  diphtheritic  angina,  as  they  are  similar  in  appearance  and  structure. 
In  each  case  they  show  the  same  power  of  adhesion,  mode  of  invasion,  and 
reproduction  after  removal.  In  addition,  glandular  enlargement  is  often 
found,  though  in  a  moderate  degree. 

These  signs  and  symptoms,  therefore,  are  those  of  normal  diphtheria. 
They  were  complete  in  a  case  at  the  Necker  Hospital.   My  diagnosis  of  normal 


DISEASES  OF  THE  THROAT  AND  PHARYNX  603 

diphtheria,  which  seemed  obvious,  was  proved  to  be  incorrect  by  bacterio- 
logical examination. 

This  variety  of  angina  wliich  simulates  diphtheria  so  closely  is  due  to 
Brisou's  coccus,  and  was  thus  named  from  the  child  in  whom  Roux  and 
Martin  first  observed  this  kind  of  angina. 

As  it  is  absolutely  impossible  to  make  a  diagnosis  between  this  false 
and  true  diphtheritic  angina  by  clinical  observation  alone,  bacteriological 
examination  is  necessary.  For  tliis  purpose  we  make  a  culture.  A  particle 
of  the  membrane  is  removed  on  a  platinum  loop  and  sown  on  a  tube  of 
gelatinized  serum,  which  is  placed  in  the  oven  at  a  temperature  of  36°  to 
37°  0.  Colonies  appear  on  the  surface  of  the  serum  after  about  eighteen 
hours  ;  they  have,  when  well  developed,  the  greatest  analogy  to  those  of 
diphtheria.  In  the  first  place  they  appear  early — in  fact,  almost  as  early  as 
those  of  diphtheria  ;  they  are  also  rounded  and  whitish.  They  differ,  how- 
ever, in  some  points.  Their  centre  is  not  opaque  ;  they  are  transparent 
throughout  their  whole  extent,  and  present  a  humid  appearance.  In 
addition,  they  are  flat,  for  which  reason  I  have  named  them  macular, 
in  order  to  distinguish  them  from  the  diphtheritic  colonies  wliich  are 
papular. 

A  stained  fragment  of  the  culture  under  the  microscope  shows  no  diph- 
theria bacilU,  but  only  Brisou's  coccus,  the  elements  of  which  are  often 
paired.  We  know,  therefore,  the  nature  of  this  angina,  which  at  first 
sight  closely  simulates  diphtheria,  and  we  may  be  satisfied  as  to  the  prog- 
nosis, because  angina  due  to  Brisou's  coccus  does  not  give  rise  to  toxaemia 
and  is  not  followed  by  paralysis.  In  some  cases  it  has  been  followed  by 
croup,  but  in  a  very  mild  form. 

This  pseudo-diphtheritic  angina  most  often  simulates  diphtheria.  It  is 
liable  to  recur.  It  has  been  met  with  three  times  by  Roux  and  Yersin. 
Martin's  returns  give  twenty-five  times  in  200  cases  of  membranous  angina  ; 
Chaillou  and  Martin's  figures  give  eleven  times  in  ninety  cases. 

Streptococcal  Pseudo-Diphtheritic  Angina.— The  streptococcus  may 
be  found  in  every  variety  of  angina.  We  are  here  concerned  with  mem- 
branous angina  simulating  diphtheria,  for  in  the  throat,  as  elsewhere,  the 
streptococcus  readily  produces  membranes  (Widal). 

This  angina,  though  generally  benign,  may  be  in  some  cases  of  excep- 
tional gravity.  The  disease  sets  in  with  rigors,  fever,  headache,  and  lassi- 
tude. The  dysphagia  is  acute,  and,  on  inspection  of  the  throat,  the  mucous 
membrane  is  found  to  be  red  and  inflamed,  and  the  tonsils  are  sometimes 
enlarged.  In  some  cases  the  exudate  is  pultaceous,  but  in  otliers  we  find 
thick  adherent  membranes  on  the  tonsils,  the  posterior  wall  of  the  i)liarynx 
and  the  velum  palati ;  they  may  even  extend  to  the  tongue  and  the  lips. 
It  has  been  rightly  said  that  the  streptococcal  membranes  are  less  elastic  and 


604  TEXT-BOOK  OF  MEDICINE 

more  friable,  yellowish,  and  cedematous  than  the  diphtheritic  membranes, 
which  are  whiter  and  more  nacreous,  as  well  as  more  firm  and  dry.  These 
differences  are  more  easy  of  description  than  recognition.  As  a  matter  of 
fact,  some  streptococcal  membranes  so  closely  resemble  diphtheritic  mem- 
branes that  we  cannot  tell  the  difference.  Inflammation  of  the  submaxillary 
glands  is  said  to  appear  earUer  in  streptococcal  than  in  diphtheritic  angina. 
Here  again  there  are  constant  exceptions. 

As  a  clinical  resemblance  between  streptococcal  pseudo-diphtheria  and 
true  diphtheria,  let  me  add  that  we  often  find  rhinitis  and  laryngitis  in  both 
cases.  The  nasal  discharge  in  each  disease  may  be  mucous,  blood-stained, 
or  puriform,  with  rejection  of  membranous  shreds.  In  both  cases  the  cough 
and  the  hoarseness  indicate  the  invasion  of  the  larynx  by  the  streptococcus 
or  by  the  diphtheria  bacillus. 

In  some  cases  streptococcal  angina  brings  about  such  grave  infection 
that  erythema,  polymorphous  eruptions,  albuminuria,  and  rheumatic  pains 
may  be  noticed,  just  as  in  diphtheria,  and  such  a  grave  general  condition 
that  death  may  result.  Streptococcal  angina  is  often  secondary  (grippe, 
measles,  typhoid  fever)  ;  it  is  most  common  at  the  commencement  of  scarlet 
fever.  These  secondary  forms  may  be  grave.  We  see,  however,  primary 
cases  which  prove  fatal. 

The  above  description  shows  that  the  clinical  diagnosis  between  tliis 
pseudo-diphtheria  and  true  diphtheria  is  quite  impossible.  Streptococcal 
angina  simulates  diphtheria  so  closely,  that  in  Martin's  monograph  we  read 
that  eight  patients  who  were  sent  to  the  diphtheria  ward  were  really  suffering 
from  streptococcal  angina.  Chaillou  and  Martin  mention  eight  cases  of 
streptococcal  angina  simulating  diphtheria. 

I  had  quite  recently  at  the  Necker  Hospital  a  case  of  streptococcal 
mebranous  angina  which  simulated  diphtheria  so  closely  that  a  diagnosis 
would  have  been  impossible  without  bacteriological  examination.  This 
xanaination  is  carried  out  in  the  manner  already  described.  The  strepto- 
coccus colonies  appear  rather  later  than  those  of  diphtheria  and  of  Brisou's 
coccus.  After  some  twenty-four  hours  they  appear  in  the  form  of  a  whitish 
stipphng,  wliich  never  shows  much  increase  in  size.  I  have,  therefore, 
thought  it  advisable  to  call  these  colonies  dusty,  and  thus  distinguish  them 
at  first  sight  from  the  macular  colonies  of  Brisou's  coccus  and  the  papular 
colonies  of  the  diphtheria  bacillus.  Even  after  fourteen  to  fifteen  hours, 
stained  fragments  of  the  colonies  on  the  surface  of  the  serum  show  under 
the  microscope  little  chains  of  mature  streptococci.  The  cocci  are  arranged 
in  chaplets,  and  in  straight  or  wavy  chains.  Four  or  more  cocci  may  be 
seen  in  each  fragment  of  the  chain. 

The  streptococcus  may  be  found  in  the  mouth  in  the  normal  or  patho- 
logical state  under  different  conditions.       Widal  and  Bezanfon  have  found 


DISP:ASES  of  the  throat  and  pharynx  605 

it  in  pseudo-membranous,  diphtheritic,  pultaceous,  phlegmonous,  and 
tubercular  angina. 

Staphylococcal  Pseudo-Diphtheritic  Angina. — Staphylococci  also  may- 
be present  in  every  variety  of  angina.  I  shall  here  discuss  only  the  pseudo- 
diphtheritic  variety.  Tliis  form  is  very  much  rarer  than  those  previously 
described.  I  have,  however,  found  four  cases  in  Martin's  paper,  and  four 
in  that  of  Chaillou  and  Martin.     I  have  seen  three  cases  in  adults. 

The  patient  shows  the  symptoms  common  to  acute  angina  :  febrile 
onset,  dysphagia,  inflammatory  redness  of  the  palato -pharyngeal  mucous 
membrane,  and  sweUing  of  the  submaxillary  glands.  The  membranes  then 
appear,  but  they  are  not  as  thick,  adherent,  and  extensive  as  in  diphtheria. 
It  is,  however,  quite  impossible  to  diagnose  the  condition  from  true  diph- 
theria by  chnical  methods  alone. 

Recourse  must  therefore  be  had  to  bacteriological  examination.  The 
staphylococcus  forms,  in  less  than  twenty-four  hours,  wide,  flattened,  and 
irregular  colonies  on  the  serum,  which  at  once  indicate  the  diagnosis.  The 
same  culture,  if  allowed  to  remain  in  the  oven,  will  soon  give  rise  to  much 
larger  colonies,  and  after  suitable  staining  the  Staphylococcus  alhus  and 
aureus  are  readily  found.  The  slide  shows  a  heap  of  grains  which  do  not 
form  Uttle  chains  like  the  streptococcus,  but  are  collected  in  grapehke 
bunches. 

Pneumococcal  Pseudo-Diphtiveritic  Angina. — This  variety  has  been 
described  by  Jaccoud.  It  is  very  rare  in  children,  and  Chaillou  and  Martin 
have  only  seen  one  case.  This  disease  has  a  sudden  onset,  with  rigors, 
general  malaise,  and  rapid  rise  of  temperature  to  103°  or  104°  F.  On  the  first 
day  the  dysphagia  is  acute  ;  the  mucous  membrane  of  the  throat  is  red  and 
shiny  ;  the  tonsils  are  swollen  and  purple.  On  the  next  day  false  membranes 
are  seen  in  the  throat.  They  commence  in  the  form  of  white  points,  become 
confluent,  and  then  spread  and  thicken  hke  diphtheritic  membranes.  The 
angina  is  usually  accompanied  by  marked  swelhng  of  the  glands.  If  to 
these  symptoms  we  add  albuminuria,  it  is  evident  that  this  chnical  picture 
closely  resembles  diphtheria.  In  the  few  cases  which  have  so  far  been  pub- 
hshed,  the  disease  has  not  the  shghtest  tendency  to  invade  the  nasal  fossae 
and  the  larynx.  In  such  a  case  it  is  impossible  for  clinical  observation 
alone  to  decide  whether  the  angina  is  diphtheritic  or  not.  Bacteriological 
examination  is  necessary,  and  reveals  the  presence  of  the  pneuraococcus. 

Membranous  Angina  due  to  the  Coli  Bacillus. — This  variety  of  pseudo- 
diphtheritic  angina  is  very  rare.  The  pathological  agent  is  the  coh  bacillus, 
which  has  been  found  as  an  accessory  organism  in  several  cases  of  angina  ; 
in  some  cases,  however,  pseud()-dij)hthoritic  angina  is  due  to  the  coli 
i)acillus  alone.  Martin  and  Chaillou  mention  two  cases,  while  Lemioycz  has 
pubhshed  a  most  conclusive  case. 


600  TEXT-BOOK  OF  MEDICINE 

Herpetic  Angina. — Herpetic  angina  (common  membranous  angina, 
Trousseau)  will  form  the  subject  of  a  special  section. 

Angina  due  to  the  Micrococcus  Tetragenus. — In  some  cases  tliia 
organism  gives  rise  to  an  angina  which  somewhat  resembles  diphtheria. 
I  give  three  cases  which  I  have  observed  : 

Case  I. — A  healthy  man  was  taken  with  fever,  malaise,  and  pain  in  the  right  side. 
Pleural  effusion  was  found  on  the  right  side.  When  I  saw  him  some  days  later  the  effu- 
sion had  almost  disappeared,  but  the  throat  was  covered  with  a  pecuUar  white  layer, 
Avhich  extended  over  the  back  of  the  pharynx,  the  velum  palati,  the  jDillars,  and  the 
uvula.  In  places  there  appeared  a  multitude  of  prominent  isolated  granules,  which 
gave  the  throat  the  appearance  of  having  been  sprinkled  with  sand.  I  have  therefore 
proposed  the  name  "  sandy  angina  "  for  this  variety.  Tonsils  not  swollen  ;  no  hyper- 
trophy of  the  submaxillary  glands. 

Apert  sowed  two  tubes  of  coagulated  ox  serum  and  two  tubes  of  peptonized  agar 
with  the  exudate  ;  he  also  made  preparations  by  crushing  one  of  the  granules  between 
two  shdes,  on  which  he  found  present,  almost  exclusively,  encapsuled  cocci,  arranged 
in  groups  of  four  or  in  pairs.  The  serum  culture  showed  no  growth  till  the  fourth  day, 
but  the  tubes  of  agar  from  the  first  day  showed  a  large  number  of  prominent  whitish 
colonies,  which  were  glue-like,  and  formed  threads  when  a  fragment  was  lifted  with 
the  platinum  wire.  On  microscopic  examination,  they  were  composed  of  tetrads, 
having  all  the  characteristics  of  the  Micrococcus  tetragenus. 

Case  II.  — The  patient  had  been  under  my  charge  for  a  fortnight  with  pleurisy,  and 
the  effusion  had  dried  up,  when  he  was  seized  with  angina.  On  each  tonsil  five  or  six 
lenticular  points  of  a  clear  white  ;  it  had  the  appearance  of  a  folUcular  angina,  but 
resembled  the  form  which  diphtheria  also  assumes.  The  serum  culture  gave  within 
twenty-four  hours  streptococci  and  some  colonies  of  staphylococci.  The  tubes  of  agar 
gave  an  almost  equal  number  of  tetrads  and  staphylococci.  The  Micrococcus  tetra- 
genus, on  being  isolated,  was  cultivated  in  broth.  A  few  di-ops  of  this  broth,  injected 
into  a  mouse,  killed  it  in  twenty-four  hours  ;  the  encapsuled  tetrad  was  found  in  the 
blood. 

Case  III. — A  man  was  admitted  to  the  Hotel-Dieu  with  symptoms  of  influenza, 
accompanied  by  rales,  due  to  pulmonary  congestion  and  pleural  friction  sounds  ;  some 
whitish  exudate  on  the  throat.  The  serum  culture  gave  a  negative  result  as  regards 
diphtheria,  but  on  agar  there  were  mysterious  colonies,  including  streptococci,  small 
cocci,  alone  or  in  pairs  and  heaps,  and  about  a  dozen  colonies  of  the  Micrococcus 
tetragenus.  This  coccus,  cultivated  on  broth,  proved  harmless  on  injection  of  a  mouse 
with  doses  of  J  c.c. 

In  these  three  cases  "  the  tetragenic  angina  was  accompanied  or  preceded  by 
pleurisy.  In  the  cases  of  tetragenic  septicaemia  hitherto  observed  (Chauffard  and 
Ramond,  Castaigne)  pleurisy  was  present.  Netter,  Faisans,  and  Le  Danamy  have 
found  the  tetragenus  in  the  fluid  from  sero-fibrinous  pleurisy.  The  Micrococcus  tetra- 
gemis  shows  a  liking  for  the  pleura." 

Syphilitic  Membranous  Angina. — In  the  previous  section  I  said  that 
the  mucous  patches  on  the  throat  and  tonsils  are  at  times  covered  with 
adherent  greyish  membranes  which  simulate  diphtheria,  the  more  as  the 
glands  at  the  angle  of  the  jaw  are  generally  enlarged.  The  diagnosis  is  easy 
if  specific  lesions  are  present  in  the  mouth  and  pharynx,  or  if  cutaneous  or 
mucous  syphihdes  have  been  found.  In  cases  of  doubt,  or  even  in  cases 
where  the  two  infections  are  superposed,  bacteriological  examination  can 
alone  confirm  the  diagnosis.     The  absence  of  Loffler's  bacillus  excludes  the 


DIPHTHERIA. 


Plate  I. 


Fig.  23 


Fig.  24. 


\/ 


n/\ 


/\ 


•v^- 


\\V, 


Fig,  2  3. 


Fig.  23.  —  Culture  ok  Diphtheria  on  Gelatinized  Serum. 
Discrete  Colonies. 

When  the  colonics  of  diphtheria  are  well  developed,  they  are 
characterized  by  round  whitish  snots,  more  opaque  in  the  centre 
than  at  the  circumference.  I  call  these  colonies  papular,  because 
they  project  from  the  surface  of  the  serum.  Some  resemble  little 
grains  or  semolina. 

Fig.  24.  —  Colonies  of  Diphtheria. 
Fig.  25.  —  Bacilli  ok  Diphtheria. 

They  are  as  long  as,  hut  thicker  than,  the  bacilli  of  tuberculosis. 
They  are  swollen  at  their  extremities,  and  are  straight  or  slightly 
curved  inwards.  They  are  often  disposed  in  groups  of  three  or 
four,  arranged  in  parallel  lines,  imitating  the  letters  V,  X,  L,  or 
simulating  the  acute  (')  or  the  circumllex  ("i  accent.  They  are 
never  placed  end-(jn.  They  look  sometimes  like  short  square 
needles  which  have  been  allowed  to  fall  on  a  table  in  little  heaps 
(Martini. 


To  face  p.  6or> 


SMALL  COCCUS,  BRISOU'S  COCCUS. 


Plate  II. 


^*eL^, 


Fig.  27. 


^ 


Sb 


cP 


CO 


<Sb 


Fig.  26. 


00 

^ 

cb 
0 

5b 
S9 

Qd 

00 

0 

0 

d& 

0 

^ 

0 

d6 

Fig 

.  28. 

Fig.  26.  —  Cultures  of  Brisou's  Coccus  on  Gelatinized 
Serum.  Discrete  Colonies. 
The  colonies  are  characterized  by  rounded  and  whitish  spots, 
simulating  at  first  sight  colonies  of  diphtheria;  but  they  are 
smaller,  more  humid,  and  more  transparent  than  those  of  diph- 
theria. Their  centre  is  not  transparent,  and  they  arc  Jlat,  ter- 
ming no  prominence.  I  therefore  propose  to  call  them  macular, 
in  contradiction  to  the  papular  colonies  of  diphtheria. 

P'iG.  27.  —  Colonies  ok  Brisou's  Small  Coccus. 
Fig.  28.  —  Elements  of  Brisou's  Coccus. 
Isolated   micrococci  are  seen,  as  well  as  numerous  diplococci 
and  some  little  heaps  of  micrococci. 


To  face  p.  606 


Plate  III. 


THE  STREPTOCOCCUS. 


■m 


Fig.  29. 


Fig.  3i, 


Fig.  29.  —  Cultures  of  the   Streptococcus 
ON  Gelatinizki)  Serum. 
Colonies  of  streptococci,  so  small  that  they  look  like  a  whitish 
stippling.  1  therefore  propose  to  call  them  dusty. 

Fig.  3o.  —  Colonies  of  Streptococci. 

Fig.  3 1.  —  Little  Chains  of  Streptococci. 

These  chains  vary  in   length,  being  straight,  wavy,  or  curved 

inwards;    they  are  formed   of  rounded  granules,  placed    like   a 

chaplet,  containing  three,  four,  five,   ten,  or  fifteen  elements,  as 

the  case  may  be. 


To  face  p.  606 


STAPHYLOCOCCUS  ALBUS. 


Plate  IV. 


M 


Fig.  33. 


Fig.  32. 


F"iG.  34. 


Fig.  32.  —  Cultures  of  the  Staphylococcus 
ON  Gelatinized  Serum. 
Colonies    of    white,    flattened,    and    irregular    staphylococci. 
These  colonies   are   yellowish    in    the  case    of    Slapnylococcus 
aureus. 

F'iG.  33.  —  Colonies  of  Staphylococcus  Albus. 
P^ig.  34.  —  Clusters  of  Staphylococci. 
The  elements  (jf  the  staphylococcus  do  not  form  chains,  like 
the  streptococcus,  but  are  united  in  clusters  or  masses. 


To  face  p.  606 


DISEASES  OF  THE  THROAT  AND  PHARYNX  G07 

hypothesis  of  diphtheria.  Other  microbes,  either  cocci  or  streptococci, 
may  be  present. 

Summary. — I  think  that  the  reader  will  agree  that  cHnical  observation 
alone  is  often  incapable  of  formulating  a  diagnosis.  We  are,  however,  armed 
with  means  which  no  longer  admit  of  mistakes.  In  angina  with  whitish 
deposits,  and  especially  with  membranes,  bacteriological  examination  must 
always  be  made,  even  though  we  feel  certain  of  our  diagnosis.  The  diagnosis 
and  prognosis  depend  on  this  examination. 

It  is  as  easy  and  as  simple  to  make  a  bacteriological  examination  in  a 
case  of  angina  as  to  make  an  examination  of  urine.  The  physician  only 
requires  some  tubes  of  gelatinized  serum.  As  soon  as  the  tube  has  been  sown, 
it  is  sent  to  a  laboratory.  The  diagnosis  and  prognosis  of  the  angina  are 
verified,  and  we  are  not  exposed  to  the  uncertainty  and  the  errors  which 
I  have  already  pointed  out  in  this  study. 

Plates  I.,  II.,  III.,  and  IV.,  give  an  idea  of  the  cultures  and  the 
morphology  of  the  diphtheria  bacillus,  of  Brisou's  small  coccus,  of  the 
streptococcus,  and  the  staphylococcus,  which  may  all  be  found  in  mem- 
branous angina. 


VIII.  DIPHTHERITIC  PARALYSIS. 

Description. — Paralytic  troubles  may  supervene  in  diphtheria  which 
involves  the  skin  or  the  mucous  membranes,  but  they  are  chiefly  seen  in 
faucial  or  nasal  diphtheria.  Some  days  or  weeks  after  recovery  from  the 
angina,  or  even  in  some  cases  while  the  angina  is  at  its  worst,  paralysis 
affects  the  velum  palati,  which  hangs  motionless ;  the  mucous  membrane 
has  lost  all  tonicity  ;  the  voice  is  nasal,  the  articulation  of  sounds  is  defec- 
tive, and  deglutition  difficult,  while  food  and  drink  regurgitate  through  the 
nose.  When  the  pharynx  is  also  paralyzed,  the  dysphagia  is  so  great  that, 
in  spite  of  every  effort,  the  bolus  cannot  be  properly  swallowed,  and  food 
mc.y  lodge  in  the  larynx,  causing  fits  of  suffocation,  which  may  prove  fatal. 

An  exact  idea  of  the  hindrances  to  the  act  of  deglutition  retpiires  a  brief 
description  of  the  physiological  mechanism  of  this  function.  During  the 
first  act  of  deglutition  the  bolus  is  collected  into  a  mass  on  tlie  surface  of 
tlie  tongue,  which  is  a[)plicd  to  the  roof  of  the  palate.  The  bolus,  pushed 
from  before  backwards,  passes  the  isthmus  of  the  gullet,  and  enters  into  the 
pharynx.  During  this  act  the  palat()-])luiryng(H  contract  and  obliterate  the 
posterior  narcs.  "  Tlie  pharynx  is  raised,  so  that  it  meets  and  seizes  the  bolus 
of  food  ;  the  lary-ix  is  also  raised,  because  the  middle  and  lower  constrictor 
muscles  and  the  siylo-pharyngcus  are  elevators  of  the  pharynx  and  larynx. 
The  larynx,  therefore,  follows  the  upward  movement  of  the  pharviix,  and  is 
carried  forward  under  the  base  of  the  tongue,  which  is  retracted.     This 


608  TEXT-BOOK  OF  MEDICINE 

mechanism,  which  protects  the  orifice  of  the  larynx,  is  completed  by  the 
movement  of  the  epiglottis  over  the  upper  opening  of  the  larynx  "  (Mathias- 
Duval).  This  mechanism  prevents  the  entrance  of  food  and  drink  into  the 
nose  or  the  larynx  during  deglutition.  When,  however,  diphtheritic  para- 
lysis attacks  the  palato-pharyngei,  the  food  passes  into  the  nose  ;  when  the 
paralysis  involves  the  muscles  of  the  pharynx,  the  food  passes  into  the 
larynx. 

When  the  paralysis  extends  to  the  tongue  and  the  lips,  the  symptoms 
at  first  sight  simulate  labio-glosso-laryngeal  paralysis ;  the  difficulty  in 
pronunciation  is  very  marked,  and  the  saliva  drools  from  the  mouth. 

The  paralysis  may  be  limited  to  the  velum  palati  or  be  general,  and  affect 
in  an  irregular  manner  the  hmbs,  the  muscles  of  the  neck  and  trunk,  the 
sensory  nerves  and  sense  organs,  as  well  as  the  sphincters,  the  oesophagus, 
the  larynx,  the  muscles  of  respiration,  and  the  heart.  The  paralysis  almost 
always  commences  in  the  velum  palati,  but  it  may  appear  simultaneously 
at  several  points— viz.,  the  hmbs  or  the  face.  In  rare  cases  the  hmbs  are 
paralyzed  before  the  palate,  which  may  remain  quite  free.  A  paraplegic 
form  that  is  independent  of  any  other  paralytic  trouble  has  been  seen. 
The  paraplegia  may  be  shght  or  severe  ;  sphincter  troubles  and  Babinski's 
sign  are  absent.  The  reflexes  of  the  patella  and  tendo  Achillis  are  abohshed. 
Early  paralysis  of  the  muscles  of  the  trunk  and  nape  of  the  neck  has  been 
noticed.  In  the  face  the  paralysis  may  affect  one  or  both  sides.  When  it 
is  double,  the  physiognomy  loses  all  expression  and  looks  hke  a  mask 
(Duchenne). 

The  patient  may  be  almost  unable  to  move  his  legs  and  arms.  He  has 
not  the  strength  to  sit  down  or  turn  in  his  bed  ;  the  head  may  be  inchned 
to  the  right  or  the  left,  or  may  fall  upon  his  chest.  The  muscular  weakness 
is  sometimes  so  pronounced  that  the  paralysis  is  complete.  These  symptoms 
sometimes  show  variations ;  paralysis  which  was  present  in  one  Hmb  may 
improve  and  show  itself  in  another  one.  We  may  find  neither  muscular 
atrophy  nor  altered  electrical  reactions  (Duchenne),  but  in  other  cases 
atrophy  may  be  present  and  the  reactions  disturbed.  In  a  few  rare  cases  the 
paralysis  is  persistent.  The  sensory  troubles  consist  of  tinghng,  pricking, 
and  pains,  which  generally  accompany  the  muscular  paralysis  from  the 
first ;  the  pain  may  be  very  pronounced.  Anaesthesia  is  frequent  in  the  hands 
and  feet ;  it  affects  all  forms  of  sensibility  and  may  involve  one  part  of  the 
body. 

All  the  sense  organs,  but  especially  the  eyes,  may  be  affected  by  the 
paralysis.  Ptosis,  strabismus,  mydriasis,  myopia,  amblyopia,  and  complete 
blindness  have  been  observed.  These  troubles  are  transient,  and  the  oph- 
thalmoscope reveals  no  lesion  of  the  fundus  oculi.  The  sense  of  taste  is 
often  blunted,  and  the  sense  of  hearing  is  sometimes  affected. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  609 

The  bladder  does  not  escape,  and  retention  or  incontinence  of  urine  may 
result,  according  as  the  paralysis  affects  the  body  of  the  bladder  or  the 
sphincter.     Similar  troubles  are  seen  in  the  rectum. 

Vomiting  is  common.  Sexual  debihty  or  impotence  may  be  present.  The 
most  serious  complication  of  those  just  enumerated  is  the  entrance  of  food 
into  the  respiratory  passages,  because  death  may  result  from  asphyxia.  In 
other  cases,  however,  the  paralysis  may  become  dangerous,  because  it  affects 
the  organs  of  respiration  and  the  heart.  The  bulbar  form  (Duchenne) 
causes  troubles,  which  vary  in  severity,  I  shall  merely  sketch  the  principal 
varieties. 

The  muscles  of  the  larynx  may  be  paralyzed.  If  the  paralysis  attacks 
the  muscles  of  phonation,  dysjahonia  or  aphonia  results.  If  it  attacks  the 
posterior  crico-ar\i;enoidei  muscles,  the  breathing  is  seriously  compromised. 
When  the  diaphragm  and  the  intercostal  muscles  are  affected,  the  patient 
becomes  breathless,  because  he  cannot  properly  renew  the  air  in  his  lungs. 
He  may  suffer  from  terrible  fits  of  dyspnoea.  Suffocation  may  also  arise  from 
paralysis  of  the  bronchial  muscles  of  Reissessen,  which  are  intrinsic  muscles 
of  expiration  (Duchenne).  In  addition  to  dyspnoea,  cardiac  troubles  are 
sometimes  seen  :  the  pulse  is  irregular  and  slow,  or  more  often  quickened ; 
angina,  intermittence  of  the  heart-beats,  and  fatal  syncope  may  occur. 
The  asphyxia  and  tlie  syncope  must  be  set  down  fx)  central  or  peripheral 
poisoning  of  the  pneumogastric'  nerve,  and  perhaps  also  to  cardiac  lesions 
(myocarditis). 

In  some  cases  the  symptoms  are  so  severe  from  the  outset  as  to  simulate 
angina  pectoris ;  terrible  precordial  pain  radiating  into  the  arms  and 
shoulders,  cutis  anserina,  cold  sweats,  acute  mental  distress,  and  syncope 
characterize  the  cardio-aortic  form.  In  other  cases  the  abdominal  symp- 
toms are  very  marked.  Gulat  speaks  of  a  patient  who  had  paralysis  of  the 
velum  palati  and  ocular  troubles,  when  he  was  suddenly  seized  with  ab- 
dominal pain,  cardialgia,  vomiting,  restlessness,  extreme  dyspnoea,  delirium 
cordis,  and  fatal  syncope. 

Duration. — The  duration  of  the  paralysis  is  variable.  Wlien  the  mischief 
is  limited  t(j  the  throat,  the  velum  palati,  and  the  pharynx,  it  usually  lasts 
only  a  few  weeks  ;  wlien  it  becomes  general,  and  affects  the  face,  the  limbs, 
the  bladder,  and  the  eyes,  it  may  last  several  months.  The  i)araplegic 
form  may  be  of  unlimited  duration.  In  certain  cases  the  paralytic  com- 
plications are  very  rapid.  During  an  epidemic,  of  which  I  shall  speak 
shortly,  some  patients  were  carried  off  in  a  few  hours,  the  diphtlicria  having 
from  the  outset  attacked  the  organs  of  respiration  and  the  heart. 

^Etiology. — Paralysis  is  most  common  in  faucial  diphtheria.  The 
angina  may  have  been  slight  and  apparently  quite  benign,  but  yet  the 
paralysis  may  be  so  grave  as  to  cause  death.     I  am,  however,  of  the  opinion 


610  TEXT-BOOK  OF  MEDICINE 

that  nasal  diphtheria  plays  a  large  part  in  causing  paralysis.  The  diphtheria 
bacillus  finds  a  vast  culture  field  in  the  nasal  cavities,  where  it  can  elaborate 
its  toxine.  The  proper  temperature  and  the  incessant  renewal  of  air  at 
each  nasal  inspiration  are  both  present.  Roux  elaborated  the  diphtheritic 
toxine  in  a  model  of  this  apparatus.  If  we  examine  the  cases  of  diph- 
theritic paralysis,  we  find  that  nasal  diphtheria  is  the  most  frequent  cause. 
The  patients,  whom  I  have  had  under  my  care  during  several  years  past 
with  paralysis,  have  almost  all  had  nasal  diphtheria.  Still,  cases  are  known 
of  unilateral  paralysis  of  the  soft  palate  following  unilateral  angina,  and, 
moreover,  similar  results  have  been  obtained  experimentally. 

Paralysis  may  follow  diphtheria  affecting  any  part  of  the  body.  Grave 
paralysis  has  been  known  to  follow  diphtheria  which  developed  on  the  raw 
surface  of  a  blister,  whilst  the  mucous  membranes  were  not  affected.  Para- 
lysis may,  indeed,  appear  in  the  aberrant  forms  of  the  disease  in  which  the 
eruption  is  absent,  though  the  other  symptoms  are  severe. 

Boissarie,  in  an  interesting  paper,  describes  an  epidemic  of  diphtheria 
in  which  several  people  were  carried  off  by  acute  paralysis  without  previous 
angina  or  other  signs  of  diphtheria.  In  this  epidemic  some  patients  were 
attacked  by  membranous  angina,  wliich  followed  the  paralytic  troubles, 
instead  of  preceding  it,  as  is  usually  the  case.  Other  patients,  again,  had 
angina  only,  and  were  not  troubled  "svith  paralysis.  These  facts  are  of 
extreme  importance.,  since  tney  prove  that  in  diphtheria  the  membrane 
has  only  a  relative  importance.  The  poisoning  may  appear  when  the 
membranes  are  sUght,  or  when  a  mucous  coating  without  membranes  is  the 
only  local  manifestation  of  the  disease. 

Paralysis  is  far  more  common  in  adults  than  in  children.  Paralysis 
Hinited  to  the  palato- pharyngeal  region  has  been  noticed  in  one  out  of  every 
six  persons  with  diphtheritic  angina  (Roger) ;  general  paralysis  only  occurs 
in  about  5  per  cent,  of  cases. 

Pathogeny. — Many  opinions  have  been  expressed  as  to  the  nature  of 
the  paralysis.  The  most  natural  view  is  that  the  paralysis  is  due  to  tOXic 
poisoning.  This  theory  was  upheld  by  Trousseau,  and,  although  it  was 
opposed  for  a  bng  time,  it  has  received  abundant  confirmation  from  the 
experiments  of  Roux  and  Yersin.  As  we  have  seen  in  a  previous  section, 
the  microbe  of  diphtheria  elaborates  a  toxine  which  is  the  cause  of  the 
paralysis.  Roux  and  Yersin  have  reproduced  paralysis  in  animals  by  the 
injection  of  filtered  culture  Hquid  which  is  free  from  micro-organisms. 

This  toxic  poisoning  having  been  proved,  how  is  the  paralysis  produced  ? 
Is  it  the  result  of  a  nervous  lesion,  and  what  is  this  lesion  ?  In  1862  Vulpian 
and  Charcot  published  a  case  of  diphtheritic  paralysis  of  the  soft  palate, 
with  changes  in  the  muscular  fibres  and  the  palatine  nerves.  Pierret  later 
described  changes  in  the  nerves,  patches  of  spinal  meningitis,  and  perineuritis 


DISEASES  OF  THE  THROAT  AND  PHARYNX  611 

of  the  nerve  roots.  Dejerine  has  found  atrophy  of  the  sheaths  of  the 
nerves  and  parenchymatous  neuritis  of  the  anterior  roots,  consecutive  to 
interstitial  and  parenchymatous  myeUtis. 

The  question  has  advanced  a  step  farther.  For  several  years  past 
writers  have  described  cases  of  peripheral  neuritis  which  seem  to  run  their 
course  without  affecting  the  nerve  centres.  This  peripheral  neuritis,  which 
has  been  described  under  tuberculosis,  diabetes,  alcohohsm,  lead-poisoning, 
etc.,  has  also  been  met  with  in  diphtheria. 

In  a  case  of  cutaneous  diphtheria  with  subsequent  paralysis,  Pitres 
and  Vaillard  found  peripheral  neuritis  of  the  radial,  ulnar,  median,  external 
and  internal  saphenous  nerves,  etc.,  while  the  spinal  cord  was  absolutely 
healthy.  The  lesions  were  very  slight  in  the  anterior  and  posterior  roots. 
It  is  true  that  the  patient  had  tuberculosis,  which  predisposes  to  peripheral 
neuritis.  The  progress  and  nature  of  the  paralysis  in  this  patient,  its  com- 
mencement in  the  soft  palate,  and  its  gradual  extension  to  the  limbs  and  the 
diaphragm,  were  certainly  the  result  of  diphtheria.  It  seems  certain, 
therefore,  that  the  diphtheria  toxine  can  produce  paralysis  by  acting  on 
the  peripheral  nerves;  but,  in  view  of  the  cases  of  sudden  death  from  affec- 
tions of  the  lungs  and  heart,  it  is  probable  that  the  poison  also  acts  on  the 
cells  of  the  nerve  centres'  and  paralyzes  them. 

Diagnosis — Prognosis— ^Treatment. — The  diagnosis  is  simple  and  easy 
when  the  course  of  the  angina  has  been  followed,  but  it  sometimes  happens 
that  a  patient  presents  himself  with  general  muscular  weakness,  incomplete 
paraplegia,  incontinence  of  urine,  facial  paralysis,  amblyopia,  amaurosis, 
or  dyspnoea,  which  may  at  first  sight  point  to  some  affection  of  the  spinal 
cord,  the  brain,  and  the  nerves.  If  the  paralysis  has  commenced  in  the 
soft  palate,  the  nasal  voice  and  the  difficulty  in  swallowing  at  once  indicate 
the  correct  diagnosis ;  but  this  guide  is  sometimes  at  fault,  and  we  must  then 
examme  for  sore  throat  with  membranes  and  enlarged  glands.  We  must 
remember  that  any  form  of  diphtheria  may  be  followed  by  paralysis, 
and  that  in  some  cases  paralytic  troubles  may  precede  the  formation  of 
membranes,  or  may  even  be  jjresent  in  epidemics  without  any  apparent 
membrane. 

The  prognosis,  which  is  benign  when  the  paralysis  is  Umited,  and  very 
grave  when  the  paralysis  attacks  the  muscles  of  respiration  and  the  heart, 
is  always  a  matter  of  uncertainty,  because  we  can  never  foretell  what  the 
course  of  the  paralysis  will  be. 

The  treatment  is  difficult.  As  soon  as  deglutition  becomes  difficult, 
bougies  must  be  employed.  Preparations  of  nux  vomica,  liniments,  hydro- 
therapy, and  electrical  treatment,  should  be  employed,  in  addition  to  tonics, 
such  as  quinine  and  iron.  Sulphate  of  strychnine  gives  good  results.  In- 
jections of  serum,  given  during  the  onset  of  diphtheria,  diminish  the  risk  of 

39—2 


612  TEXT-BOOK  OF  MEDICINE 

paralysis,  but  seem  to  have  little  effect  when  once  paralysis  is  present.  This 
proves  that  injections  of  serum  must  be  given  without  delay,  for  early  in- 
jections prevent  complications,  while  later  they  have  not  the  same  effect. 

IX.  HERPETIC  ANGINA. 

Erythematous,  lacunar,  pultaceous,  or  diphtheritic  angina  may  be 
accompanied  by  an  eruption  of  herpes.  When  membranes  appear,  we  re- 
serve for  it,  with  Trousseau,  the  name  of  common  membranous  angina,  the 
epithet  "  common  "  removing  all  idea  of  diphtheria. 

Herpetic  angina  does  hot,  however,  represent  a  morbid  entity,  and  the 
disease,  as  our  predecessors  understood  it,  must,  in  my  opinion,  be  spHt  up. 
It  is  rather  an  angina  with  herpes  than  herpetic  angina.  In  these  cases  we 
may  find  any  of  the  following  organisms — viz.,  micrococci,  streptococci, 
staphylococci,  pneumococci,  and  diphtheria  bacilli.  The  vesicles,  although 
analogous  to  those  on  the  skin,  run  a  slightly  different  course,  because  the 
morbid  process  which  produces  crusts  on  the  skin  may  produce  false  mem- 
branes on  the  mucosa  (Gubler). 

Description. — Though  herpetic  angina  may  occur  at  any  age,  it  is  most 
common  in  children  from  three  years  onwards.  It  has  a  latent  incubation 
period,  which  lasts  from  a  few  hours  to  two  days,  and  it  then  bursts  forth 
with  violent  rigor,  high  fever,  and  intense  headache,  which  is  sometimes  as 
severe  as  in  meningitis  (Lasegue).  This  febrile  condition  is  often  accom- 
panied by  dyspepsia,  and  the  patient  has  a  burning- feehng  in  the  throat. 
The  pain  is  generally  hmited  to  one  side  of  the  pharynx,  and  the  submaxillary 
glands  are  but  little  swollen. 

If  the  throat  be  examined  at  the  outset,  we  may  see  the  eruption  of  the 
vesicles.  The  mucous  membrane  is  red,  and  the  tonsils  are  swollen. 
Vesicles  then  develop  on  the  tonsils,  the  pillars  of  the  fauces,  the  uvula,  and 
the  soft  palate.  When  they  are  discrete,  they  resemble  sudamina ;  when 
confluent,  they  form  more  or  less  extensive- and  irregular  groups. 

These  vesicles  become  opalescent,  excoriated,  and  then  covered  with 
a  whitish  membrane.  This  process  is  often  so  rapid  that  the  vesicular 
stage  may  pass  unnoticed,  and  the  false  membrane  only  be  seen.  In  other 
cases,  on  the  contrary,  the  vesicles  disappear  without  the  formation  of 
membranes.  The  false  membranes  may  be  found  on  the  pharynx,  the 
tonsils,  the  uvula,  and  the  pillars  of  the  fauces.  When  the  membranes  are 
clearly  Hmited,  they  are  generally  surrounded  by  a  reddish  areola ;  when 
they  extend  beyond  the  hmits  of  the  erosion,  they  blend  with  the  neigh- 
bouring exudates,  and  large  membranous  patches  are  formed.  Another 
factor  assists  in  tlie  growth  of  the  membranes.  The  inflammation  is  not 
solely  confined  to  the  vesicles,  but  attacks  the  neighbouring  mucous  mem- 


DISEASES  OF  THE  THROAT  AND  PHARYNX  613 

brane  also,  and  "  though  it  is  not  ulcerative,  it  none  the  less  gives  rise  to 
the  exudation  of  plastic  products  hke  those  which  are  formed  by  an  ulcerated 
surface "  (Trousseau).  The  membranes  are  frequently  adherent  to  the 
subjacent  niucous  membrane.  They  may,  however,  become  detached, 
and  expose  the  mucous  membrane,  which  may  be  ulcerated  or  completely 
cicatrized.  These  false  membranes  have  almost  the  same  structure  as 
those  of  diphtheria.  The  fever  and  the  dysphagia  last  for  some  days,  and 
restoration  to  health  takes  place  suddenly.  Second  attacks  are  not  rare. 
Herpetic  angina  is  sometimes  accompanied  by  an  eruption  of  vesicles  on 
the  nostrils,  the  lips,  the  mouth,  the  prepuce,  the  vulva,  or  the  cervix  uteri. 
These  eruptions  are  of  help  in  diagnosis  and  indicate  tlie  nature  of  the 
angina.  Vesicles  may  be  found  in  the  larynx ;  herpetic  croup  is  the  result, 
but  it  has  neither  the  character  nor  the  gravity  of  diphtheritic  croup. 

We  have  seen  in  a  previous  section  that  the  diagnosis  is  made  by  bacterio- 
logical examination. 

Herpetic  angina  may  be  epidemic.  It  is  hable  to  occur  a  second  time 
in  menstruating  women.  Cold  is  the  chief  determining  cause.  The  prog- 
nosis is  benign.  The  treatment  is  very  simple — viz.,  soothing  and  anti- 
septic gargles. 


X.  GANGRENOUS  ANGINA. 

etiology. — Gangrene  of  the  pharynx  is  more  common  in  children 
than  in  adults  ;  it  may  be  primary  or  secondary.  The  secondary  form  is 
by  far  the  more  frequent,  and  is  caused  by  diphtheria,  measles,  scarlatina, 
dysentery,  smallpox,  or  typhoid  fever — in  short,  by  any  morbid  condition 
which  lowers  the  vitahty  and  favours  secondary  infection  and  death  of  the 
tissues,  not  only  of  the  pharynx,  but  also  of  other  regions.  Other  causes, 
such  a.s  inflammatioai  of  the  throat,  and  especially  phlegmonous  angina, 
are  much  less  common.  Diphtheritic  angina  may  sometimes  apparently 
become  gangrenous  in  adults,  but  we  must  not  mistake  the  appearance 
for  the  reaUty.  On  the  other  hand,  the  opposite  error  must  be  avoided, 
for  diphtheria  may  cause  gangrene  of  the  throat,  the  vulva,  and  the  vagina, 
in  this  event  the  condition  is  grave,  and  the  diphtheria  is  associated  with 
other  organisms.  Primary  gangrenous  angina  may  be  seen  in  adults. 
Its  chief  feature  is  early  mortification  of  the  pharyngeal  mucous  membrane, 
comparable  with  gangrene  of  the  mouth. 

Many  organisms  arc  present  in  gangrene  of  the  pliarynx.  Pyogenic 
micro-organisms  and  saprophytes  are  associated  with  the  specific  germs. 

Description. — The  invasion  is  generally  insidious  in  the  secondary 
form.  Th(^  primary  disease  boj^'iiis  witli  fever  and  pain.  On  examining 
the  throat,  greyish  or  blackish  patches  of  gangrene  are  seen  on  the  tonsils 


614  TEXT-BOOK  OF  MEDICINE 

and  other  parts  of  the  pharynx,  varying  in  size  from  a  lentil  to  a  shilHng. 
The  edges  of  the  patch  are  prominent,  irregular,  and  surrounded  by  hvid 
red  mucous  membrane.  If  the  gangrene  is  circumscribed,  the  scab  becomes 
detached,  and  leaves  in  its  stead  an  ulcer,  which  attacks  the  subjacent 
muscular  layer,  and  may  terminate  by  cicatrization.  If  the  gangrene  is 
diffuse,  the  gangrenous  patches  unite,  invade  the  soft  palate  and  the  uvula, 
and  in  some  cases  extend  forward  as  far  as  the  Ups,  or  backwards  as  far  as 
the  aryteno- epiglottic  folds. 

Gangrene  of  the  pharynx  is  generally  accompanied  by  marked  glandular 
enlargement.  The  breath  is  foetid,  saUvation  is  abundant,  and  the  voice 
is  nasal.  Difficulty  in  swallowing  varies.  There  is  a  foul  discharge  from 
the  nose.  Prostration  and  adynamia  are  always  present.  The  pulse  is 
feeble  and  slow ;  the  skin  is  pale ;  delirium  and  restlessness  are  sometimes 
present.  The  prognosis  is  often  fatal.  The  patient  may  survive  two  to 
six  days  in  the  secondary  form,  and  eight  days  to  a  fortnight  in  the  primary 
form,  when  death  occurs  from  coma  or  sudden  syncope. 

Two  patients  of  Eichardiere  recovered.  "  The  first  patient,  who  had  diffuse 
gangrene,  recovered,  with  much  loss  of  substance,  due  to  sloughing  of  the  soft  palate, 
the  tonsils,  and  the  pillars  of  the  fauces.  This  loss  of  substance  interfered  considerably 
with  deglutition  and  phonation  ;  food  and  drink  regurgitated  through  the  nose  ;  the 
voice  was  nasal.  Tlie  child  was  fed  for  several  weeks  with  the  oesophageal  tube.  After 
four  to  five  weeks  the  loss  of  substance  was  limited,  as  it  were,  by  regeneration  of  the 
velum  ;  deglutition  became  easier,  and  the  child  could  take  nourishment  by  the  mouth 
without  regurgitation  through  the  nose.  The  second  child,  who  suffered  from  gangrene 
limited  to  the  tonsils,  recovered  without  other  deformity  than  the  loss  of  the  tonsils." 

The  treatment  consists  in  cauterization  of  the  sloughing  surfaces  (hydro- 
chloric acid,  thermo-cautery),  and  frequent  cleansing  by  means  of  disin- 
fectants (hyposulpliite  of  soda,  eucalyptus).  The  patient's  strength  must 
be  supported  by  tonics  (quinine,  wine,  etc.). 


XL  CHANCRE  OF  THE  TONSIL. 

Description. — Chancre  of  the  tonsil  is  very  common.  Every  year  I 
see  four  or  five  cases  at  the  Hotel-Dieu.  If  mistakes  are  frequent,  it  is 
because  we  are  not  familiar  with  its  various  symptoms  and  forms.  This 
point  is  well  worthy  of  recognition.  Due  attention  has  not  been  directed 
to  the  fact  that  this  chancre  often  commences  with  pain,  fever,  and  sore 
throat.  We  are  so  accustomed  to  consider  chancres  in  general  as  indolent 
and  apyretic  lesions,  that  symptoms  of  acute  angina,  with  fever,  lead  us 
wrongly  to  reject  the  idea  of  chancre.  I  have  consulted  the  recorded  cases  as 
well  as  my  personal  observations,  and  I  maintain  that  in  half,  or  even  more, 
of  the  cases  this  chancre  commences,  like  tonsillitis,  with  fever,  headache,  and 
malaise.     In  a  clinical  lecture  on  chancre  of  the  tonsil,  I  have  recorded 


DISEASES  OF  THE  THROAT  AND  PHARYNX  615 

several  cases  which  began  like  acute  tonsilUtis,  but  were  really  chancres 
of  the  tonsil. 

I  do  not  say,  of  course,  that  every  chancre  of  the  tonsils  has  such  an 
acute  onset,  with  fever  and  pain,  but  this  feature  is  so  common  that  it 
deserves  mention.  We  find  at  this  period  diffuse  redness  and  swelhng  of 
the  tonsil,  which  may  be  covered  by  a  pultaceous  coating.  The  chancrous 
erosion  may  be  apparent  or  hidden.  Later,  when  the  chancre  is  developed, 
it  may  present  the  following  varieties  : 

First  Variety. — The  chancre  resembles  an  acute  tonsiUitis ;  pain,  fever, 
dysphagia,  headache,  and  lassitude  are  present.  The  patient  thinks  of 
simple  tonsillitis,  and  employs  soothing  gargles,  and  hot  compresses  to  the 
neck.  As  he  begins  to  feel  worse  he  seeks  advice,  telUng  the  physician  : 
*'  There  is  hardly  anything  wrong  with  me,  but  a  sore  throat  has  been 
causing  me  some  trouble  for  the  last  three  or  four  days."  The  physician 
examines  the  tliroat,  finds  it  red  or  covered  with  a  pultaceous  coating,  while 
the  tonsils  are  swollen.  It  looks  like  an  ordinary  tonsilhtis,  "  without 
special  characteristics,  at  any  rate,  for  the  time  being."  The  diagnosis  is 
clearly  difficult  at  this  period.  The  chancre  develops  in  the  sulci  of  the 
enlarged  tonsil,  which  may  be  covered  by  a  pultaceous  coating,  so  that 
even  an  experienced  eye  may  not  always  distinguish  it.  We  can  only  make 
a  diagnosis  by  means  of  the  signs,  which  we  shall  study  later. 

Second  Variety. — In  this  case  the  chancre  is  visible  on  the  tonsil,  as 
an  erosion  which  may  be  red  and  glossy,  or  grey  and  opaline,  varying  in 
size  from  a  lentil  to  a  sliilling.  The  following  case  is  typical  of  this  erosive 
chancre  : 

A  patient  came  to  the  hospital  to  consult  me  for  painful  angina,  which  had 
begun  a  fortnight  before  with  high  fever.  He  had  been  obUged  to  take  to  his  bed. 
Multiple  painless  glands  had  made  their  appearance  in  the  submaxillary  and  retro- 
maxillary  regions  on  the  riglit  side.  The  symptoms  were  quite  in  accordance  with 
tlie  diagnosis  of  infectious  angina.  The  fever  and  general  malaise  did  not  cause  the 
least  suspicion  of  chancre  of  the  tonsil.  On  examination  of  the  pharynx,  however, 
I  saw  that  the  right  tonsil  was  alone  affected.  It  was  prominent,  and  on  its  surface 
there  was  seen  a  glossy  red  patch,  with  a  curly  border.  The  left  tonsil  was  healthy  ; 
no  false  membranes  were  present.  As  the  erosion  and  the  induration  of  the  right 
tonsil,  together  with  the  presence  of  painless  swollen  glands,  were  unilateral,  I  diagnosed 
chancre  ;  my  diagnosis  was  soon  confirmed  by  the  appearance  of  the  roseola. 

Third  Variety.— The  chancre  is  ulcerated  and  the  tonsil,  which  is  more 
or  less  enlarged,  is  hollowed  by  an  ulcer,  which  may  be  as  large  as  a  florin. 
The  ulcer  may  be  situated  on  any  part  of  the  tonsil.  The  colour  is  brownish 
or  greyish,  and  the  raised  edges,  formed  by  the  projection  of  the  tonsils, 
cause  it  to  look  deeper  than  it  really  is.  The  following  case  (Le  Gendre) 
gives  an  idea  of  it : 

A  man  was  admitted  for  sore  throat,  pain,  fever,  malaise,  and  hoadaolie.  An  ulcer 
of  the  size  of  a  sixpence  was  visil)lo  on  the  right  tonsil.      The  edges  were  clean-cut ; 


616  TEXT-BOOK  OF  MEDICINE 

the  floor  was  greyish,  sanious,  and  anfractuous.  The  ulcerated  tonsil  was  a  third  larger 
than  the  other  one.  Palpation  showed  tliat  the  ulcer  rested  on  an  indurated  base, 
while  the  corresponding  maxillary  glands  formed  a  mass  as  big  as  a  pigeon's  egg.  The 
pain  radiated  from  the  throat  to  the  ear.  The  patient  complained  of  insomnia,  caused 
by  headaclie,  which  was  worse  at  night.  Fournier  diagnosed  chancre  of  the  tonsil, 
and  the  subsequent  roseola  confirmed  his  diagnosis. 

Fourth  Variety. — The  chancre  is  diphtheroid.  The  ulcerated  surface 
of  the  chancre  is  covered  with  a  greyish  or  yellowish  adherent  membranous 
exudate,  which  at  first  sight  looks  hke  diphtheria.  Whether  the  membrane 
is  due  to  the  tendency  which  every  chancre  of  the  mucous  membrane  has 
to  become  covered  with  a  more  or  less  thick  pseudo-membrane,  or  whether 
it  is  due  to  secondary  infection  by  the  streptococcus,  Brisou's  coccus,  etc., 
it  is  none  the  less  true  that  in  certain  cases  the  chancre  is  hidden  under  a 
more  or  less  adherent  membrane  of  a  greyish  colour,  which  may  give  rise 
to  errors  in  diagnosis.  This  mistake  consists  in  not  recognizing  an  existing 
chancre,  or  in  diagnosing  diphtheria  which  does  not  exist.  The  next  case 
is  taken  from  my  chnical  lectures  : 

In  February,  1898,  I  saw  a  patient  who  had  been  taken  ill  in  January  with  mem- 
branous sore  throat  and  enlarged  glands  on  the  left  side.  The  glands  were  hard,  pain- 
less, and  quite  separate  from  one  another.  On  examining  the  throat,  an  ulcer,  covered 
by  a  thick,  greyish,  adherent  membrane,  was  seen  on  the  left  tonsil.  I  was  in  doubt 
between  chancre  and  diphtheria.  Bacteriological  examination  of  the  exudate  revealed 
short  diphtheria  bacilli.  Next  day  numerous  colonies  of  the  same  bacillus  were  found 
in  the  serum.  Was  tliis  a  case  of  only  pseudo -diphtheria — for  the  short  bacilli  are  not 
considered  by  most  authors  as  true  virulent  diphtheria — or  was  it  one  of  diphtheria  ? 

An  injection  of  serum  was  given,  but  led  to  no  improvement  in  the  local  conditions. 

A  guinea-pig  was  inoculated  with  2  c.c.  of  a  broth  culture, of  the  same  bacillus  ; 
neither  fever  nor  oedema  at  the  point  of  inoculation.  Further  injections  of  serum  were 
therefore  considered  useless,  as  the  diagnosis  of  chancre  was  clear,  and  specific  treat- 
ment was  promptly  commenced.  On  February  8,  thirty-five  days  after  the  appearance 
of  the  chancre,  the  roseola  appeared.  When  I  saw  the  patient,  the  tonsil  was  still  in- 
durated and  of  large  size,  the  adenitis  was  still  present,  and  the  roseola  was  in  course 
of  evolution. 

Fifth  Variety. — The  chancre  is  gangrenous.  The  appearance  of  the 
lesion,  its  blackish  colour,  and  the  foetor  of  the  breath,  give  the  impression 
of  gangrene  of  the  tonsil.  This  gangrenous  chancre  was  well  marked  in 
the  following  case  : 

A  young  man  admitted  into  the  Charite  had  suffered  for  a  month  from  difficulty 
of  swallowing,  headache,  and  a  painful  swelling  in  the  neck.  In  the  right  cervical 
region  there  was  a  mass  formed  of  large  tender  glands.  The  isthmus  of  the  gullet  was 
red  ;  the  right  tonsil  was  swollen,  and  on  its  upper  portion  was  a  gangrenous  patch 
^  inch  in  diameter.  The  eschar  was  separated  from  the  rest  of  the  tonsil  by  a  demarca- 
tion sulcus  filled  with  pus.  The  breath  was  foetid  and  the  dysphagia  marked.  No 
diagnosis  was  made,  and  tonsillectomy  was  performed.  The  cause  of  the  lesions  in  tlie 
tonsil  was  soon  explained  by  the  appearance  of  the  secondary  rash. 

Sixth  Variety. — By  slightly  straining  the  analogy,  a  chancre  of  the 
epithelioma  tons  kind  has  been  described. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  617 

These  difEerent  cases  prove  that  chancre  of  the  tonsil  is  polymorphous. 
Whatever  its  morphology  may  be — whether  it  resembles  hypertrophic  tonsil- 
htis,  or  whether  it  is  erosive,  ulcerative,  diphtheroid,  or  gangrenous — its 
onset  is  often  painful,  and  accompanied  by  fever  and  general  symptoms.  It 
is  well  known  how  painless  chancres  of  the  genital  organs  are ;  chancre  of 
the  tonsil,  on  the  other  hand,  often  causes  pain  and  fever.  In  one  of 
my  cases  the  chancre  began  with  sore  throat,  rigors,  weakness,  severe 
dysphagia,  and  pains  which  radiated  to  the  ear,  neck,  and  face.  In  another 
patient  an  erosive  chancre  also  began  with  intense  dysphagia,  rigors,  fever, 
and  lassitude.  Le  Gendre's  case  of  a  diphtheroidal  chancre  started 
w?th  rigors,  dysphagia,  malaise,  and  attacks  of  vertigo.  In  other  cases 
quoted  by  Le  Gendre  the  disease  began  with  fever  and  acute  pain  on 
swallowing. 

Diagnosis. — Chancre  of  the  tonsil  begins  in  many  cases  Uke  an  acute 
tonsillitis,  so  that  the  diagnosis  is  obscured  when  the  characters  of  chancre 
of  the  tonsil  are  not  faniihar.  This  fact  so  impressed  me,  that  some  years 
ago,  in  my  lectures  at  the  Faculte,*  I  pointed  it  out  at  some  length.  Fournier 
states  the  same  opinion,  and  describes  this  form  under  the  name  of  chancre 
of  the  anginoid  type. 

At  first  the  diagnosis  is  naturally  doubtful.  The  patient  is  examined, 
and  tonsilhtis  or  peritoiwillar  abscess  is  discussed,  and  even  if  the  idea  of  a 
chancre  has  occurred  to  the  mind,  the  means  of  confirming  the  diagnosis 
are  not  yet  at  hand.  The  variety  of  chancre  soon  becomes  clear  :  the  tonsil, 
in  which  the  chancre  is  more  or  less  hidden,  is  red,  swollen,  and  furrowed. 
In  other  cases  an  erosive,  ulcerative,  diphtheroidal  or  gangrenous  chancre 
appears.  The  aspect  of  the  chancre  may  vary  ;  pain  and  fever  may  or  may 
not  be  present ;  but  yet  in  a  few  days  we  find  the  triad  of  symptoms,  which 
makes  diagnosis  possible — unilateral  lesion,  induration  of  the  tonsil,  and 
develoi^ment  of  a  glandular  mass. 

The  chancre  is  unilateral,  which  means  that  only  one  tonsil  is  affected, 
and  this  unilateral  character  is  of  great  value.  In  every  other  variety  of 
tonsilhtis  botli  tonsils  are  attacked,  though  possibly  to  an  unequal  degree ; 
they  are  more  or  less  swollen,  red,  and  painful.  In  chancre,  on  the  other 
liand,  only  one  tonsil  is  affected.  There  are,  however,  exceptions  to  this 
rule.  JuUen  has  recorded  the  case  of  a  young  girl  suffering  from  general 
roseola,  with  an  ulcerative  chancre  on  each  tonsil,  and  enlarffed  jilands  on 
both  sides  of  the  neck. 

Cases  of  this  kind  are,  however,  exceedingly  rare,  and  Fournier,  who 

quotes  those  of  Duncan  lUilkloy,  has  never  seen  an  instance.     I  have  seen 

several  chancres  of  the  tonsil,  but  I  have  never  seen  a  case  in  which  the  lesion 

was  bilateral.      The  chancre  may  not  be  absolutely  confined  to  the  tonsil. 

*  "  Le  Chancre  de  T  Amygdivle  "  (La  Scmaine  Medicule,  3  Avril,  1895). 


618  TEXT-BOOK  OF  MEDICINE 

It  may  encroach  on  the  anterior  pillar  or  on  the  base  of  the  tongue,  but  it 
still  preserves  its  unilateral  character. 

Induration  of  the  tonsil  is  a  sign  of  the  utmost  importance.  If  both  tonsils 
are  palpated,  the  healthy  organ  feels  supple,  while  the  other  is  indurated, 
especially  around  the  base  of  the  suspected  lesion.  This  induration  of  the 
chancre,  though  not  so  readily  made  out  as  on  the  genitals,  is  none  the  less 
a  valuable  sign,  which  is  present  in  at  least  eight  cases  out  of  ten. 

"  Some  chancres  of  the  tonsil  are  as  indurated  as  those  on  the  prepuce 
or  the  vulva,  and  it  is  not  impossible  that  a  chancre  of  the  tonsil  may 
form  a  cartilage-like  meniscus,  which  is  as  hard  as  wood."  The  induration, 
just  as  in  genital  chancres,  persists  for  a  long  time  after  the  disappearance 
of  the  chancre,  and  allows  a  retrospective  diagnosis  to  be  made.  In  palpating 
the  tonsil  we  may  place  one  hand  on  the  side  of  the  neck  and  push  the  tonsil 
against  the  examining  finger  inside  the  mouth. 

The  tliird  sign — viz.,  glandular  bubo  in  the  neck — must  be  carefully 
sought  for,  as  its  absence  practically  excludes  chancre,  while  its  presence 
confirms  the  diagnosis.  The  satellite  bubo  appears  a  few  days  after  the 
chancre,  and  is  situated  in  the  neck  on  the  same  side,  and  not  far  from  the 
thyroid  cartilage.  We  often  find,  in  addition  to  the  bubo,  a  chain  of  smaller 
glands,  which  are  mobile,  hard,  and  painless.  It  is  by  "  hunting  after 
glands  "  that  we  may  sometimes  assert  the  previous  existence  of  a  chancre 
after  it  has  disappeared.  The  chain  may  extend  from  the  angle  of  the  jaw 
to  the  supraclavicular  region.  In  exceptional  cases  some  of  the  glands  on 
the  opposite  side  may  be  enlarged,  as  in  a  case  Avhjch  I  have  reported. 
Although  this  sign  has  not  previously  been  described  in  unilateral  chancre 
of  the  tonsil,  I  point  it  out,  because  the  presence  of  a  bubo  on  both  sides  of 
the  neck  must  not  lead  to  mistakes.  With  chancre  of  the  genital  organs 
the  inguinal  bubo  is  usually  bilateral ;  with  chancre  of  the  tonsil  it  is  quite 
the  exception.  In  order  to  explain  the  presence  of  enlarged  glands  on  the 
side  opposite  to  the  chancre,  we  must  admit  that  the  infection  has  been 
spread  by  the  lymphatics  of  the  tonsillar  and  palatine  mucous  membrane, 
which  anastomose  with  those  of  the  opposite  side  at  the  base  of  the  tongue. 
To  sum  up :  the  unilateral  position  of  the  lesion,  the  induration  of  the  tonsil, 
and  the  presence  of  the  satellite  bubo,  with  its  shotty  glands,  form  a  triad 
of  symptoms  which  proves  chancre  of  the  tonsil.  In  making  this  diagnosis, 
however,  we  must  remember  that  chancre  of  the  tonsil  often  resembles  an 
acute  angina. 

The  diphtheroid  chancre  may  simulate  diphtheria,  but  the  limitation  of 
the  membranes  to  the  tonsil  and  the  chancrous  ulceration,  exposed  after 
the  removal  of  the  membranous  layer,  are  signs  which,  with  the  triad  of 
symptoms,  will  give  the  correct  diagnosis.  However,  in  cases  of  doubt 
bacteriological  examination  and  cultures  must  be  made. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  619 

A  chancre  must  not  be  mistaken  for  ulcerative  tonsillitis,  due  to  fusiform 
bacilK  and  spirilla  (Vincent).     See  section  on  Tonsillitis. 

There  remains,  then,  the  differential  diagnosis  between  chancre  and 
epithehoma  of  the  tonsil.  Some  analogy  exists  between  these  lesions  as 
regards  appearance.  Enlarged  glands  and  pain  are  present  in  each  case. 
There  are,  however,  certain  differential  characteristics.  In  chancre  the 
adenitis  appears  much  earher  than  in  cancer.  In  cancer  it  is  a  question  of 
weeks,  in  chancre  of  days.  In  doubtful  cases  the  progress  of  the  affection 
decides  the  question,  for  chancre  shows  a  tendency  to  recovery  after  tliree 
weeks,  whilst  cancer  is  of  slow  growth,  and  does  not  recede,  but  extends 
and  bleeds.  Finally,  cancer  is  not  accompanied  by  roseola  and  mucous 
patches,  which  closely  follow  the  appearance  of  the  chancre.  Doubt,  there- 
fore, cannot  last  long. 

I  have  still  to  mention  the  diagnosis  of  chancre  from  gumma  and  tertiary 
ulceration  of  the  tonsil.  Tertiary  syphilides  of  the  tonsil  are  not  accom- 
panied by  the  satelhte  bubo,  unless  secondary  infection  is  present.  Further- 
more, the  chancre  occurs  as  the  primary  lesion  in  an  individual  so  far  free 
from  signs  of  syphiUs,  whilst  gummata  occur  in  persons  who  have  previously 
shown  such  signs. 

The  diagnosis  of  chancre  of  the  tonsil  is  confirmed  by  the  appearance 
of  the  roseola  and  mucous  syphihdes,  which  must  be  carefully  looked  for 
five  to  eight  weeks  after  the  appearance  of  the  chancre. 

Before  closing  this  section  I  should  like  to  say  a  few  words  on  herpes, 
which  sometimes  accompanies  chancre,  and  may  lead  to  the  erroneous 
diagnosis  of  herpetic  angina.  One  of  my  patients  had  a  chancre  of  the 
tonsil,  and  also  an  eruption  of  herpes  on  the  left  pillar  of  the  fauces,  the 
right  tonsil,  the  lower  Up,  and  the  tongue.  Had  the  herpes  supervened 
fortuitously,  or  was  it  connected  with  the  attack  of  syphilis  ?  In  IHGfi 
Diday  and  Doyon  published  a  work  on  genital  herpes,  and  later,  in  1868, 
Doyon  described  recurrent  herpes  of  the  genitaUa  in  syphihtic  patients. 
In  1879  Julien  discussed  the  question  fully.  "  A  fact,"  says  he,  "  that 
deserves  notice  in  connection  with  uterine  chancres  is  the  frequent  coinci- 
dence of  genital  herpes  :  the  perineum,  the  vulva,  and  the  cervix  uteri  are 
often  the  seat  of  herpetic  eruptions.  A  syphilitic  lesion  of  the  cervix  must 
also  be  thought  of  when  a  woman  presents  herself  without  other  apparent 
lesions  than  a  crop  of  herpes." 

Fournier  has  also  discussed  the  question  of  recurrent  herpes  of  the 
tongue  in  sypliilitic  patients.  "  You  see  people,"  says  Fournier,  "  who, 
after  an  attack  of  syphilis  one  or  more  years  previously,  consult  you,  because 
they  fancy  that  they  have  bucco-hngual  mucous  patches,  which  recur  in 
spite  of  treatment.  If  you  examine  carefully,  you  will  find  that  those 
so-called  mucous  patches  are  polycycUcal  or  microcyclical  erosions— that  is 


620  TEXT-BOOK  OF  MEDICINE 

to  say,  herpes."  Syphilis,  therefore,  favours  the  eruption  of  "  parasypbiUtic 
herpes."  Sometimes  the  herpes  supervenes  at  a  period  more  or  less  distant 
from  the  chancre,  and  reappears  more  or  less  often  in  the  recurrent  form. 
The  eruption  of  herpes  is  sometimes  contemporary  with  the  chancre.  In 
my  patient,  herpes  suj)ervened  during  the  active  stage  of  a  tonsillar  chancre, 
and  in  Le  Gendre's  monograph  I  find  that  one  of  his  patients  had  a  chancre 
on  one  tonsil  and  a  crop  of  herpes  on  the  other. 


XII.  SYPHILIS  OF  THE  SOFT  PALATE,  THROAT,  AND 

PHARYNX. 

While  chancre  of  the  isthmus  of  the  gullet  and  of  the  pharynx  is  rare, 
secondary  and  tertiary  lesions  are  common  in  these  regions. 

Secondary  Lesions. — I  must  first  mention  the  erythematous  angina, 
characterized  by  erythema,  which  is  diffuse  or  limited  to  the  soft  palate, 
pillars,  and  tonsils.  The  erythema  often  has  a  red  coloiir.  Sometimes  the 
anterior  pillars  of  the  soft  palate  and  the  uvula  appear  to  have  been  painted 
with  a  brush.  The  erythema,  which  coexists  with  mucous  patches,  causes 
some  dysphagia,  and  is  often  accompanied  by  cold  and  hoarseness,  because 
erythema  of  the  larynx  is  also  present  in  many  cases.  The  condition 
deserves  mention,  because  it  has  a  certain  value  in  diagnosis,  as  I  have  often 
proved. 

Mucous  patches  in  the  throat  may  present  various  appearances.  They 
include  erosions,  papules,  hypertrophied  papules,  and  ulcerations  (Fournier). 
The  patches  are  usually  situated  on  the  tonsils,  the  pillars,  and  the  soft 
palate.  They  are  extremely  rare  in  the  pharynx,  no  doubt  because  the 
mucous  membrane  is  almost  wanting  in  papillae.  The  tonsillar  region 
is  a  "  very  nest  for  syphihdes."  The  patches  are  flat,  opahne,  and  some- 
times so  confluent  that  they  cover  the  tonsils  and  the  pillars  of  the  fauces. 
In  some  patients  the  mucous  patches  in  the  throat  and  on  the  tonsils  are 
covered  with  greyish  adherent  false  membranes,  which  simulate  diph- 
theritic angina,  the  more  in  that  the  submaxillary  glands  are  swollen. 

The  forms  of  syphilis  just  described  cause  discomfort  and  even  pain. 
They  interfere  with  mastication  and  render  deglutition  painful.  They  make 
their  appearance  about  two  to  three  months  after  infection,  and  are  prone  to 
recur  for  two  or  three  years.  They  are  moist  and  essentially  contagious. 
Syphilis  of  the  throat  affects  the  corresponding  glands  and  determines 
adenitis  at  the  angle  of  the  jaw. 

As  regards  secondary  syphilides,  a  point  in  diagnosis,  which  I  have  not 
seen  mentioned  elsewhere,  was  suggested  to  me  by  the  history  of  a  case 
in  the  Necker  Hospital. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  621 

A  woman  had  a  red  and  painful  swelling  of  the  vault  of  the  palate.  I  found  on 
the  swelling  and  in  the  neighbourhood  superficial  polycyclical  ulcers  and  some  rounded 
opalescent  granules,  which  looked  like  yellow  tubercles ;  the  granules  were  also 
visible  on  the  left  tonsil.  The  diagnosis  had  been  either  syphihs  or  tuberculosis,  but 
I  accepted  neither  view.  A  few  days  before,  she  had  been  taken  ill  with  pain,  which 
interfered  with  mastication  and  deglutition.  The  polycychcal  aspect  of  the  ulcers  did 
not  in  the  least  resemble  those  of  syphiUs.  The  so-called  tubercles  proved  on  close 
examination  to  be  vesicles  of  herpes.  The  groups  of  vesicles  on  the  roof  of  the  palate 
and  the  tonsil,  the  surrounding  erythema,  and  the  excessive  pain,  led  me  to  diagnose 
zona  palato-pharyngea.  As  a  matter  of  fact,  new  groups  of  vesicles  developed  in  a 
few  days  on  the  roof  of  the  palate,  soft  palate,  and  tonsil.  The  patient  stated  that 
she  had  often  had  similar  troubles  at  the  menstrual  period.  She  recovered  in  a  fort- 
night.    This  case  is  not  an  isolated  one,  and  others  have  been  published. 

Tertiary  Lesions. — Gummata  of  the  throat  and  of  the  pharynx  deserve 
careful  attention,  because  they  are  common,  not  only  in  acquired,  but  also 
in  hereditary  syphilis.  In  acquired  syphihs  the  gummata  do  not  appear, 
as  a  rule,  until  some  years  after  infection.  In  the  hereditary  disease  lesions 
of  the  throat  are  met  with  at  all  ages  between  five  and  twenty-five,  and  the 
proof  that  these  lesions  are  common  is  that  they  were  found  forty-six 
times  in  212  cases  of  hereditary  syphihs,  which  make  up  the  returns  of 
Fournier.  The  description  refers,  therefore,  both  to  the  gummatous  lesions 
of  acquired  and  of  hereditary  syphilis. 

The  lesions  are  of  different  kinds  ;  the  infiltration  is  sometimes  circum- 
scribed and  forms  a  tumour,  but  In  other  cases  the  infiltration  is  spread  out, 
and  we  see  but  Uttle  tumour  formation.  The  gumma  commences  with 
infiltration.  At  this  stage,  though  the  soft  palate  is  deformed,  thickened, 
violet  in  colour,  and  indurated,  the  patient  may  experience  no  functional 
troubb,  no  pain,  and  only  shght  dysphagia.  The  gumma  projects  as  a 
little  tumour.  We  find  next  a  period  of  softening,  characterized  by  pain, 
which  may  be  so  slight  that  patients  do  not  trouble  about  it,  and  are  quite 
surprised  when  symptoms  of  perforation  appear. 

The  ulcerated  gumma  varies  in  appearance,  according  as  it  is  followed 
by  perforation  or  not.  In  the  latter  event  the  ulcer  forms  a  deeply  excavated 
cavity,  large  enough  to  contain  a  lentil  or  a  hazel-nut.  The  floor  is  covered 
with  a  greyish  sloughy  layer  ;  the  edges  are  clean-cut,  adherent,  and  often 
perpendicular,  while  the  surrounding  tissues  are  smooth,  or  red,  hard,  and 
infiltrated.  At  this  period  the  pain  is  very  great,  and  if  the  ulcers  run 
together  at  the  isthmus  of  the  fauces,  the  dysphagia  is  extreme. 

Gummata  of  the  soft  palate  often  end  in  perforation,  which  estabhshes 
communication  between  the  throat  and  the  posterior  cavity  of  the  nasal 
fossa).  The  progress  may  be  so  rapid  that  the  opening  may  become  as  large 
as  a  lentil  in  twenty-four  hours,  and  in  three  weeks  as  large  as  a  penny. 
The  perforation  may  be  median  or  lateral ;  and  rounded  or  elongated  in  a 
transverse  direction.     The  ulcerative  process  continues  its  ravages,  so  that 


622  TEXT-BOOK  OF  MEDICINE 

the  soft  palate  is  sometimes  split  in  two,  or  almost  entirely  destroyed.  In 
some  cases  several  perforations  have  been  found.  The  perforation  at  once 
causes  alteration  in  the  voice,  which  becomes  nasal,  and  regurgitation  of 
food  and  drink  into  the  nasal  cavity.  In  some  cases  the  sudden  appearance 
of  these  symptoms  greatly  surprises  the  patient,  because  he  has  had  no  idea 
of  the  nature  or  the  gravity  of  "  his  sore  throat." 

Tertiary  ulceration  often  occurs  in  the  triangular  space  formed  by  the 
junction  of  the  two  pillars  of  the  fauces  and  the  tonsil.  The  ulcerations 
extend  from  this  space  and  "  destroy  the  upper  half  of  the  tonsil  and  the 
pillars,  and  in  some  cases  the  free  portion  of  the  soft  palate,  the  lateral  wall 
of  the  pharynx,  and  the  Eustachian  tube.  This  fact  explains  the  presence 
of  deafness  and  acute  pains  in  the  ear. 

When  the  syphiloma  is  diffuse,  it  does  not  stand  out  in  rehef ,  but  gives 
rise  to  spreading  ulcers,  which  are  extremely  painful.  They  are  phagedsenic, 
serpiginous  in  outline,  and  are  frequently  found  on  the  soft  palate.  The 
ulcerative  process  may  be  so  rapid  'that  the  tissue  seems  to  melt  away. 
The  soft  palate  may  be  partly  or  entirely  destroyed,  though  it  may  be 
impossible  to  see  a  single  slough  separate.  The  condition  is  one  of  rapid 
necrobiosis,  presenting  here,  as  on  the  skin,  the  characteristics  of  phage- 
daena.  The  ulcer  is  bathed  in  ichorous  pus,  the  floor  is  pale,  and  the  edges 
are  loose  and  jagged.  Haemorrhage  is  frequent.  The  pain  is  so  acute  that 
deglutition  and  alimentation  become  most  difficult. 

The  tertiary  lesions  which  we  have  just  described  in  the  soft  palate  and 
throat  are  Hkewise  common  in  the  pharynx.  The  posterior  wall  of  the 
pharynx  is  a  favourite  seat  for  gummata.  They  are  generally  painless, 
causing  only  slight  dysphagia,  as  long  as  ulceration  is  absent.  Patients, 
therefore,  do  not  trouble  about  them,  and  "  gummatous  syphilides  are  only 
seen  in  practice  in  the  stage  of  ulceration.  At  this  period  they  may  be 
very  painful  and  have  definite  characteristics  :  circular  shape,  yellowish, 
sloughy  floor"  (Fournier).  When  the  gummata  are  seated  in  the  naso- 
pharynx, they  can  only  be  discovered  by  special  examination.  The  tertiary 
ulcers  of  th^  pharynx  present  special  pecuharities.  The  mucous  membrane  of 
the  posterior  wall  of  the  pharynx  is  swollen  and  reddish.  In  some  places  it  is 
covered  with  crusts,  and  in  others  a  greenish  pus  bathes  the  furrows  between 
the  projections  of  the  mucous  membrane.  The  ulcers  may  leave  deep  whitish 
scars,  which  cause  deformity,  and  favour  adhesion  to  the  neighbouring  parts. 
Out  of  150  cases  of  syphihtic  stenosis  of  the  pharynx,  Lubinski  found  sixteen 
cases  of  complete  atresia  of  the  isthmus  of  the  gullet.  When  the  soft  palate 
is  fixed  to  the  posterior  wall  of  the  pharynx,  nasal  respiration  is  impossible, 
and  the  senses  of  taste  and  smell  are  lost. 

Diffuse  syphiloma  of  the  sclerous  form  is  also  seen  in  this  region.  The 
pillars  of  the  soft  palate  may  be  so  infiltrated  that  they  become  three  or 


DISEASES  OF  THE  THKOAT  AND  PHARYNX  623 

four  umes  as  thick  as  normal.  The  parts  lose  their  suppleness  and  become 
indurated  and  deformed.  The  pillars  assume  a  furrowed  and  mammillated 
aspect;  the  isthmus  of  the  gullet  is  constricted;  the  uvula  is  thick  and 
indurated ;  and  the  tonsils  are  hypertrophied,  lardaceous,  and  cracked. 
These  lesions  interfere  with  phonation  and  deglutition  to  a  greater  or  lesser 
degree.  The  affection  begins  in  an  insidious  manner,  so  that  the  only 
symptoms  may  be  those  of  angina,  and  the  patient  does  not  worry  about 
the  disease,  wliich  slowly  pursues  its  course. 

Diagnosis. — The  tertiary  ulcers  of  the  throat  must  be  distinguished 
from  tubercular  ulcers.  Many  errors  were  made  until  late  hereditary 
syphiHs  became  known,  and  many  troubles  due  to  hereditary  syphihs  in 
children,  youths,  and  even  in  adults,  are  still  set  down  to  scrofula. 

This  question  has  been  ably  discussed  by  Fournier,  whose  writings  will 
serve  me  as  a  guide.  In  a  case  of  acquired  syphilis,  when  the  subject, 
who  is  attacked  by  gummatous  ulcers,  has  already  had  a  series  of  syphilitic 
lesions,  the  diagnosis  is  often  simple  ;  when,  however,  we  find  ulceration  of 
the  throat  in  a  young  subject  from  twelve  to  fifteen  years  of  age  who  never 
had  syphihs,  but  who  has  had  since  childhood  chronic  discharge  from  the 
ear,  persistent  eye  troubles,  or  chronic  coryza,  with  or  without  ozsena,  and 
thus  presents  "  the  old  picture  of  scrofula,  such  as  our  predecessors  be- 
queathed to  us,"  the  idea  of  syphihs  is  rejected.  An  error  then  occurs, 
because  this  old  picture  of  malign  scrofula  is  precisely  the  description  of 
heredo-syphihs. 

Let  us  see,  then,  what  are  the  local  differences  between  syphilitic  and 
tubercular  ulcers  of  the  throat.  The  former  have  often  been  confounded 
with  the  ulcerations  of  lupus  and  of  tuberculosis.  Lupus  and  tubercle  are 
varieties  of  the  same  morbid  species,  and,  "  in  any  case,  they  present,  in 
their  chronic  form,  characters  so  different  that  it  is  incorrect  to  unite  them 
in  one  description  "  (Fournier). 

Let  us  commence  with  lupus.  In  the  first  place,  lupus  of  the  throat 
is  extremely  rare — so  rare,  indeed,  that  out  of  100  cases  of  lupus 
Fournier  found  only  two  cases  of  lupus  of  the  throat.  Furthermore,  lupus 
of  the  throat  exists  almost  always  concurrently  with  lupus  of  the  face,  and 
the  ulceration  of  the  throat  only  occurs  as  a  late  phenomenon  of  tiie  in- 
filtration period,  wliich  is  very  long.  This  infiltration  of  the  tissues  is  shown 
by  a  granular  hypertrophy,  which  gives  to  the  soft  palate  and  the  affected 
puits  the  appearance  of  "  a  carpet  of  mulberry-like  granulations,"  and  has 
not  the  slightest  resemblance  to  the  sy[iliilitic  gumma.  The  phase  of 
ulceration  is  likewise  dissimilar.  In  the  gumma  the  ulceration  is  sudden, 
rapid,  and  invades  from  the  first  nearly  the  whole  of  the  infiltrated  zone  ; 
l)ut  in  lupus  the  ulceration  is  slow,  and  spreads  by  successive  outbursts, 
in  lupus  the  ulceration  is  only  a  part  of  the  lesion  ;  in  the  gumma  it  is  the 


624  TEXT-BOOK  OF  MEDICINE 

entire  lesion.  The  gummatous  ulcer  has  a  circumscribed  outline,  clean-cut 
adherent  edges,  and  an  excavated  floor,  which  is  greyish  and  sloughy.  In 
lupus  the  ulcer  has  no  defined  outline,  the  flat  edges  are  not  clean-cut,  the 
floor  is  but  slightly  depressed,  and  is  covered  with  fleshy  granulations. 
SyphiUs  perforates  the  velum  palati  and  "  makes  a  hole,"  but  does  not 
involve  the  surrounding  parts.  Lupus  eats  away  the  tissues,  and  the  sur- 
rounding parts  are  never  healthy.  Syphihs  takes  only  a  few  weeks,  or  at 
most  a  few  months,  to  produce  its  effects,  while  lupus  takes  years.  Tiieso 
local  characteristics  suffice  to  differentiate  the  lesions  in  acquired  or  heredi- 
tary syphilis  from  those  of  lupus.  In  a  suspicious  case  of  hereditary  syphilis 
the  inquiry  must  include  the  parents. 

Let  us  now  consider  the  diagnosis  between  gummatous  and  tubercular 
ulcerations  of  the  throat.  In  the  first  place,  a  patient  with  tubercular 
ulceration  of  the  throat  is  almost  always  suffering  from  pulmonary  phthisis 
or  from  intestinal  tuberculosis.  Ulceration  of  the  throat  is  hardly  ever 
the  first  manifestation  of  tuberculosis.  These  features,  however,  are  not 
sufficient  to  prove  the  diagnosis,  because  the  patient  may  have  both  tuber- 
culosis and  syphilis.  The  tubercular  ulcerations  are  less  extensive  and  not  so 
deep  as  those  of  syphilis  ;  they  have  neither  the  clearly-notched  edges  nor 
the  excavated  sloughy  floor.  The  tubercular  ulcerations  are  frequently  sur- 
rounded by  projecting  yellowish  granules ;  they  are  sometimes  accompanied 
by  swelling  of  the  cervical  glands,  whilst  the  "  gummatous  lesions  only  react 
in  exceptional  cases  on  the  neighbouring  glands."  Finally,  the  secretion 
or  the  scrapings  from  a  tubercular  ulcer  reveal  the  presence  of  the  bacillus. 

Treatment. — In  tertiary  lesions  mercury  is  the  best  drug.  Daily  injec- 
tions of  a  watery  solution  of  biniodide  of  mercury  are  given.  The  injections 
are  given  for  twelve  to  fourteen  days  ;  they  are  then  stopped  and  repeated  as 
required.  Prompt  action  is  imperative.  We  must  remember  that  gummata 
in  the  throat  or  the  soft  palate  terminate  rapidly  in  perforation  and  destruc- 
tion of  the  tissues.     Correct  treatment  prevents  these  complications. 

Tobacco,  alcohohc  drinks,  and  highly-spiced  foods  should  be  forbidden, 
because  they  favour  the  return  of  mucous  patches.  The  mouth  must  be 
kept  scrupulously  clean.  If  the  mercurial  treatment  produces  inflamma- 
tion of  the  gums,  chlorate  of  potash  should  be  given  daily  in  solution.  The 
following  remedies  may  be  employed  locally  : 

L  Soothing  gargles  of  decoction  of  mallow  and  poppy. 

2.  We  must  cleanse  the  ulcerated  surfaces  with  a  brush  soaked  in  the 
following  solution  : 

Water     . .  . .  . .  . .  . .         . .     100  parts. 

Tincture  of  iodine        . .  . .         . .  . .         5      ,, 

Iodide  of  potassium     . .  . .  . .         . .         5      ,, 

3.  We  must  hasten  healing  by  mild  applications  of  nitrate  of  silver. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  G25 


XIII.  TUBERCULOSIS  OF  THE  BACK  OF  THE  MOUTH  AND 
OF  THE  PHARYNX. 

Description. — The  disease  may  be  either  acute  or  chronic.  In  the 
acute  form  the  patient  complains  of  smarting  pain  in  the  throat  and  a  crop 
of  yellowdsh  granulations,  which  may  be  disseminated  or  confluent,  promptly 
appear  on  the  soft  palate,  the  pillars  of  the  fauces,  and  the  walls  of  the 
pharynx.  A  few  days  later  the  granulations  ulcerate,  and  give  place  to 
irregular  extensive  ulcers.  As  the  lesion  spreads,  the  mucous  membrane 
is  destroyed  in  places,  and  replaced  by  a  pulpy  surface  ;  the  uvula  is 
swollen  ;  the  pillars  of  the  fauces  are  deformed,  and  the  tonsils  are  destroyed 
by  the  ulceration. 

Acute  tubercular  angina  causes  such  intense  dysphagia  and  pain  that 
the  patient  finally  refuses  all  food.  The  angina  is  accompanied  by  saliva- 
tion, earache,  and  submaxillary  adenitis,  which  may  end  in  suppuration. 
The  disease  lasts  from  six  weeks  to  four  months ;  death  is  hastened  by  the 
lesions  in  the  lung. 

In  its  chronic  form  the  disease  differs  shghtly,  according  as  it  follows 
laryngeal  phthisis  or  not.  When  it  is  primary,  the  ulcerations  are  generally 
more  discrete,  hke  those  on  the  tongue  ;  they  develop  on  the  tonsils,  the 
pillars  of  the  fauces,  and  the  pharynx. 

When  it  is  secondary  to  lesions  in  the  larynx,  the  morbid  process  appears 
to  spread  from  the  larynx  to  the  throat ;  the  tubercular  lesions  invade  the 
epiglottis,  the  base  of  the  tongue,  and  finally  become  general.  The  dura- 
tion of  the  chronic  form  is  from  seven  to  nine  months,  unless  interrupted 
by  acute  attacks,  which  hasten  its  course.  Its  symptoms  are  at  times 
masked  by  the  concomitant  laryngeal  phthisis. 

Histologically  the  lesions  in  the  throat  resemble  those  in  the  mouth, 
but  changes  are  also  found  in  the  adenoid  tissue,  which  is  so  abundant  in 
this  region.  The  adenoid  follicles  of  the  pharynx,  the  tonsils,  and  the  tongue 
become  inflamed  and  ulcerated. 

The  tubercle  bacillus  is  present  in  the  lesions  just  described.  It  is  found 
in  the  small  vessels,  the  giant  cells,  the  granulation  tissue,  and  at  the  side, 
or  in  the  midst  of  the  tubercular  folhcles. 

During  life  it  is  often  easy  to  obtain  the  bacillus  by  collecting  the  secre- 
tion from  the  ulcers,  or  by  gently  scraping  the  surface. 

Tuberculosis  of  the  throat  is  generally  associated  with  ulcers  in  other 
parts  of  the  alimentary  canal,  and,  strange  to  say,  tubercular  uIcim's  of  tiie 
mouth  and  the  tongue  do  not  usually  accompany  those  of  the  throat,  for 
in  fortv-six  cases  buccal  tuberculosis  has  only  been  found  seven  times 
(Barth).     The  ulcers  are  generally  found  in  the  intestine.     In   nineteen 

40 


626  TEXT-BOOK  OF  MEDICINE 

autopsies  ulcers  of  the  intestine  have  been  met  with  fifteen  times  and  ulcera- 
tion of  the  anus  once  (Martineau). 

I  need  not  refer  to  the  diagnosis  of  tubercular  ulcers  of  the  throat,  as 
the  question  has  been  treated  in  the  previous  section. 

It  is  often  difficult  to  obtain  results  in  acute  tuberculosis  of  the  pharynx, 
but  in  all  other  cases  of  bucco-pharyngeal  tuberculosis,  treatment  may  be 
very  effective.  Applications  of  tinctm'e  of  iodine  and  iodoform  have  given 
good  results,  and  the  thermo-cautery  has  often  hmited  the  spread  of  the 
ulcer. 

Local  apphcations  of  cocauie  will  diminish  the  pain  caused  by  the 
taking  of  food. 


XIV.  MASKED  TUBERCULOSIS  OF  THE  THREE  TONSILS. 

Discussion. — ^When  we  read  the  classical  descriptions  of  tuberculosis  of  the  back  of 
the  mouth  and  pharynx,  we  see  that  the  authors  had  two  principal  forms  of  tuberculosis 
in  view — -the  one  acute  and  the  other  chronic — both  characterized  by  granulations, 
infiltration,  and  more  or  less  deep  and  extensive  ulceration. 

Acute  tuberculosis  of  the  back  of  the  mouth  and  pharynx  appears  in  the  course  of 
acute  phthisis,  or  during  the  decline  of  chronic  pulmonary  tuberculosis.  The  patient 
complains  of  smarting  pain  in  the  throat,  and  a  crop  of  discrete  or  confluent  granula- 
tions of  a  yellowish -white  colour  is  seen  on  the  soft  palate,  the  pillars  of  the  fauces, 
and  the  walls  of  the  pharynx.  These  granulations  soon  give  place  to  small  ulcers, 
which  in  turn  give  rise  to  more  extensive  and  irregular  ulcers.  The  lesion  spreads, 
and  the  mucous  membrane  is  in  part  replaced  by  a  pulpy  surface.  The  uvula,  the 
pillars  of  the  fauces,  and  the  tonsils  may  be  swollen  and  ulcerated.  The  disease  causes 
such  intense  dysphagia  and  pain  that  the  patient  at  last  refuses  all  food,  because  he  is 
afraid  of  swallowing.  Acute  tubercular  angina  is  accompanied  by  abundant  saliva- 
tion, earache,  and  submaxillary  adenitis,  which  in  some  cases  suppurates.  In  its 
chronic  form  the  disease  is  somewhat  different,  according  as  it  is  associated  or  not 
Avith  larjTigeal  phthisis.  We  find  soUtary  or  multiple  ulcers,  which  are  of  slow  growth, 
and  invade  the  pillars  of  the  fauces,  the  pharynx,  and  the  tonsils.  When  the  ulcer  forms, 
the  edges  are  festooned,  the  floor  is  sanious,  and  around  the  ulcer  a  crop  of  yellowish 
points  is  observed.  The  chronic  form  is  not  always  accompanied  by  submaxillary 
adenitis.  It  is  less  painful  than  the  acute  form,  and  its  symptoms  are  sometimes 
masked  by  those  of  the  concomitant  laryngeal  phthisis. 

This  brief  sketch  shows  the  varieties  of  pharyngeal  tuberculosis  described  in  the 
classical  treatises.  I  would  add  that  this  form  of  tuberculosis  is  relatively  rare,  because 
only  one  case  may  be  seen  during  a  year  of  hospital  practice. 

There  is  another  form  of  tuberculosis,  however,  which  I  consider  very  common 
It  has  not  been  previously  described,  because  it  is  quite  unlike  the  classical  forms 
We  find  neither  granulations  nor  ulcers  ;  as  pain  is  absent,  it  may  not  be  discovered 
until  it  causes  functional  disorders,  which  are  apparently  quite  benign  ;  and  yet  it  is  a 
grave  condition,  because  it  may  be  the  starting-point  of  extensive  tuberculosis. 

This  almost  latent  form  chiefly  affects  the  adenoid  tissue  of  the  naso-pharynx. 
Its  presence  is  sometimes  revealed  by  overgrowth  of  the  lymphatic  tissue  in  this  region — 
that  is  to  say,  by  the  hypertrophy  of  the  palatine  and  pharyngeal  tonsils.  As  regards 
the  pharjTigeal  tonsil,  the  lesion  is  sometimes  confounded  with  adenoid  vegetations ; 
and,  as  regards  the  palatine  tonsils,  the  lesion  may  be  taken  for  hypertrophy  of  these 


DISEASES  OF  THE  THEOAT  AND  PHARYNX  627 

organs.  In  many  cases  the  tonsils  present  a  normal  aspect  (Escomel).  At  first  sight, 
there  is  nothing  to  show  the  tubercular  nature  of  the  lesion  ;  we  do  not  find  granula- 
tions or  ulcers,  but  only  hypertrophy,  which  varies  in  degree,  and  causes  the  well- 
known  symptoms  of  adenoid  vegetations  and  enlarged  tonsils.  I  have  therefore  named 
this  form  masked  tuberculosis  ol  the  three  tonsils.  I  made  a  communication  con- 
cerning it  to  the  Academie  de  Medecine  in  1895,*  and  described  it  in  my  lectures  at  the 
Faculte  in  189-1.  In  the  same  year  Lermoyez  showed  at  the  Societe  Medicale  des 
Hopitaux  a  very  interesting  case  of  tubercular  adenoids  ;  he  discussed  the  question 
further  in  an  important  article  in  1895.  The  conclusions  which  I  stated  in  my  com- 
munication to  the  Academie  raised  some  surprise,  but  subsequent  researches  have  con- 
firmed these  conclusions,  which  have  become  classical.  Moure  and  Brindel  have  proved 
histologically  that  in  thirty  cases  of  adenoid  growths  tubercular  tissue  was  present 
in  eight.  Cornil  at  first  considered  this  tuberculosis  as  doubtful,  "  but  he  has  changed 
his  opinion  since  he  saw  the  slides  prepared  by  LetuUe  from  one  of  my  cases  " 
(Lermoyez). 

The  whole  question  was  taken  up  again  in  1902  by  Jankelevitch  ;  and  Escomel  of 
Lima,  who  carried  out  some  important  work  in  LetuUe's  laboratory,  states  as  his  chief 
conclusions  : 

"  Tuberculosis  of  the  tonsil  is  excessively  frequent,  and  the  macroscopical  diagnosis 
of  the  affection  bristles  with  difficulties.  The  tonsil  is  more  hable  to  tuberculosis 
than  any  other  organ  in  the  body.  Koch's  bacilli  may  be  met  with  in  every  part  of  the 
affected  tonsil ;  they  are,  indeed,  to  be  found  in  the  tonsillar  crypts  of  persons  who 
show  no  tubercular  lesion.  Tubercular  infection  of  the  tonsil  allows  the  bacillus  to 
penetrate  the  lymphatics  as  well  as  the  bloodvessels." 

I  do  not  say,  of  course,  that  every  adenoid  growth  and  every  enlarged  tonsil,  though 
simple  in  appearance,  is  tubercular  ;  but  I  do  say  thp.t  these  lesions,  which  are  benign  in 
appearance,  are  very  often  masked  forms  of  tuberculosis,  and  that  in  every  case  they 
form  a  field  most  favourable  for  the  growth  of  the  tubercle  bacillus.  I  shall  now  give 
the  experiments  on  which  I  base  the  above  facts. 

Experiments. — I  requested  several  of  my  colleagues  to  be  good  enough  to  place 
at  my  disposal  adenoid  growths  and  tonsils  affected  with  hypertrophy,  which,  while 
simple  in  appearance,  had  required  the  removal  of  these  organs  in  patients  of  various 
ages.  They  kindly  sent  me  100  tonsils  and  adenoid  growths,  accompanied  by 
their  clinical  notes.  With  the  valuable  help  of  Marion,  portions  of  the  tonsils  and 
of  the  adenoid  growths  were  inoculated,  with  every  precaution,  under  the  skin  of  the 
abdomen  in  several  series  of  guinea-pigs.  The  portion  was  taken  as  near  as  possible 
to  the  centre,  and  not  from  the  surface,  of  the  tonsil  or  adenoid  growth,  to  remove 
the  objection  that  my  experiments  dealt,  not  with  tubercular  tissue,  but  with  tissue 
serving  as  a  vehicle  for  the  tubercle  bacillus. 

ExPEKiMENT  1. — On  September  1  we  inoculated  a  guinea-pig  with  a  fragment 
from  the  centre  of  an  enlarged  tonsil  removed  from  a  child  five  years  of  age,  who 
was  healthy  in  other  respects,  and  had  no  enlarged  glands  in  the  neck.  Three  weeks 
later  a  tubercular  chancre  containing  Koch's  bacilU  appeared  at  the  point  of  inocula- 
tion. The  satellite  glands  in  the  groin  became  affected,  and  the  guinea-pig  succumbed 
on  October  28.  The  post-mortem  examination  showed  general  tuberculosis,  starting 
at  the  point  of  inoculation  with  a  tubercular  chancre  as  large  as  a  sixpence.  Tho 
following  lesions  were  also  found  :  tuberculosis  of  the  inguinal  glands  and  of  botli 
lungs,  with  cavities  at  the  apices,  as  well  as  caseous  tubercles  in  tho  spleen. 

Experiment  2. — On  October  20  wo  inoculated  a  guinea-pig  with  a  fragment  of 
adenoid  growth  removed  from  a  child  eleven  years  of  age.  She  was  in  good  health, 
but  had  aljundant  adonoid.s,  with  submaxillary  and  cervical  adenitis  on  both  sides  of 

*  Dieulafoy,  "Tuberculoso  Larv6o  des  Trois  Amygdalcs  "  {Amdemie  de  Medecine. 
seance  du  30  Avril,  1895). 

40—2 


628  TEXT-BOOK  OF  MEDICINE 

the  neck.  Three  weeks  afterwards  a  tubercular  chancre,  with  Koch's  bacilli,  appeared 
at  the  point  of  inoculation.  The  guinea-pig  died  on  November  28.  Post  mortem  we 
found  general  tuberculosis,  inguinal  adenitis,  pleuro-pulmonary  tuberculosis,  and 
effusion  into  the  left  pleura. 

Experiment  3. — On  January  16  we  inoculated  a  guinea-pig  with  a  fragment  of  an 
enlarged  tonsil  removed  from  a  child  six  years  of  age,  in  other  respects  quite  healthy, 
and  suffering  apparently  from  simple  hyjDertrophy  of  the  tonsils,  without  enlarged 
glands.  On  February  6,  after  an  incubation  of  three  weeks,  a  tubercular  chancre, 
with  Koch's  bacilli,  appeared  at  the  jjoint  of  inoculation.  The  guinea-pig  died  on 
February  26,  and  the  post-mortem  examination  revealed  general  tuberculosis.  On 
opening  the  thorax,  we  found  general  tuberculosis  of  the  lungs  ;  in  the  abdomen  we 
found  tuberculosis  of  the  liver  and  of  the  spleen. 

I  append  a  summary  of  our  experiments  : 

Ninety-six  guinea-pigs  were  inoculated — 61  with  fragments  of  tonsils,  and  35  with 
fragments  of  adenoid  growths. 

Out  of  the  61  guinea-pigs,  8  became  tubercular,  which  gives  an  average  of  12  jDer 
cent.     In  6  of  the  cases  the  tubercular  chancre  was  the  initial  lesion. 

Out  of  the  35  guinea-pigs,  6  became  tubercular,  which  gives  an  average  of  20  per 
cent.     In  3  of  these  cases  the  chancre  was  the  initial  lesion. 

Pathogenesis. — We  are  face  to  face  with  the  clearly-estabhshed 
experimental  fact  that  many  enlarged  tonsils  and  adenoid  growths  formerly 
considered  as  simple  are  really  a  latent  form  of  tuberculosis.  Chnically 
it  was  thought  that  these  lesions  were  brought  about  by  an  "  unknown 
cause."  I  feel  that  I  have  sufficiently  proved  that  they  are  only  too  often 
cases  of  latent  tuberculosis.  The  old  names  of  "  lymphatic  and  scrofulous 
temperament  "  are  thus  explained,  when  appHed  to  children  or  young  adults 
with  enlarged  tonsils  or  adenoids.  They  are,  after  all,  perfectly  justified, 
since  we  know  the  predilection  of  the  tubercle  bacillus  for  lymphatic 
tissues,  and  also  that  scrofular  and  tubercular  lymphatism  belong  to  the 
same  pathological  family. 

We  must  now  try  to  find  the  cause  of  the  tuberculosis  and  the  path  by 
which  the  bacillus  reaches  the  adenoid  tissue  of  the  three  tonsils.  It  is 
convenient  to  speak  here  of  German  investigations,  because  tuberculosis 
of  the  tonsil  is  considered  to  be  quite  common  in  Germany. 

In  1884  Cohnheim  and  Weigert  drew  attention  to  the  frequency  of 
tuberculosis  of  the  tonsils  in  phthisical  patients  :  the  lesion  is  scarcely  visible 
to  the  naked  eye,  and  presents  few  chnical  symptoms.  Orth  found  tuber- 
culosis of  the  tonsils  in  children  who  had  died  of  diphtheria,  the  lungs  being 
free  from  tuberculosis.  Schenkler,  in  1893,  found  tuberculosis  of  the  tonsils 
in  phthisical  patients,  and  reported  that  of  twenty-one  cadavera  on  which 
he  had  made  investigations  the  tonsils  were  tubercular  in  thirteen.  He 
asked  himself  what  were  the  relations  between  tuberculosis  of  the  tonsils 
or  the  glands  of  the  neck  and  the  same  disease  in  the  lungs,  and  concludes 
by  saying  :  "  My  opinion  is  that  the  glands  of  the  neck  become  infected 
through  the  tonsils,  which  receive  the  infection  from  the  lungs  by  means  of 


DISEASES  OF  THE  THROAT  AND  PHARYNX  629 

the  sputum."  Schenkler  therefore  thinks  that  tuberculosis  of  the  tonsils  is 
secondary  to  that  of  the  lung. 

In  1894  Krueckmann  (of  the  Pathological  Institute  of  Rostock)  produced 
an  excellent  work  on  the  relations  of  tuberculosis  in  the  glands  of  the  neck, 
the  tonsil,  and  the  lung.  He  says  :  "  In  the  half-year  from  January  1  to 
July  15,  1894,  I  examined  the  tonsils  microscopically  in  cases  where  tuber- 
culosis was  present  in  the  glands  of  the  neck.  In  each  case  I  found  tuber- 
culosis of  the  tonsils,  and,  seeing  the  great  importance  of  the  subject,  I 
thought  it  incumbent  to  publish  the  results."  Krueckmann,  like  Schenkler, 
concludes  that  tuberculosis  of  the  tonsils  follows  the  same  disease  in  the 
lungs,  and  is  produced  by  means  of  the  sputum.  He  quotes,  however,  two 
cases  of  primary  tuberculosis  of  the  tonsils  due  to  infected  food. 

The  German  writers,  therefore,  had  recognized  the  latent  existence  of 
tuberculosis  of  the  tonsils,  but  they  had  only  studied,  save  in  a  few  cases, 
the  secondary  form,  in  which  phthisical  patients  had  infected  their 
tonsils  by  their  own  sputum. 

]\Iy  experiments  were  undertaken  with  quite  another  object.  I  was 
anxious  to  prove  that  in  certain  patients  the  three  tonsils  are  frequently 
the  seat  of  primary  tuberculosis,  which  is  latent  in  character,  capable  of 
becoming  general,  and  analogous  to  the  latent  tuberculosis  of  the  lymphatic 
glands  so  clearly  proved  by  Pizzini.  We  must  consider  how  the  bacillus 
enters  the  economy  in  these  cases'. 

The  First  or  Tonsillar  Stage. 

A  child  or  a  youth  is  born  of  phthisical  stock  ;  he  has,  as  a  hereditary 
taint,  a  tendency  to  the  so-called  lymphatic  temperament,  and  it  is  almost 
certain  that  he  will  show  a  tendency  to  overgrowth  of  the  lymphatic  tissue 
in  the  naso-pharyngeal  cavities. 

Is  it  not  evident  that  these  regions  will  offer  a  favourable  retreat  for  the 
tubercle  bacillus  ? 

Tlie  bacillus  can  only  reach  them  by  the  acts  of  respiration  and  degluti- 
tion. In  nasal  respiration  the  bacillus  readily  enters  the  nasal  cavities. 
Strauss  has  shown  the  presence  of  active  tubercle  bacilli  in  tlie  nasal  cavities 
of  healthy  individuals  who  live  in  contact  with  phthisical  patients.  If  the 
inhaled  bacilli  reach  the  lymphatic  tissue  in  the  naso-pharynx  of  a  subject 
[)redisposed  by  heredity,  they  will  find  a  field  favourable  to  their  develop- 
ment, and  in  their  migration  it  is  the  adenoid  tissue  of  the  pharynx  with 
which  they  first  come  in  contact.  The  tissue  undergoes  defensive  hyper- 
trophy ;  if  the  bacillus  finds  a  footing,  we  have  the  growth  of  tubercular 
adenoids. 

I  think  that  infection  of  the  lymphatic  masses  in  the  naso-pharynx  occurs 
rather  from  nasal  respiration  than  from  the  swallowing  of  food-stuffs.     The 


630  TEXT-BOOK  OF  MEDICINE 

proof  rests  on  my  experiments,  which  show  that  the  pharyngeal  tonsil 
(adenoid  growth),  which  is  directly  concerned  with  nasal  respiration,  is 
invaded  almost  twice  as  often  as  the  faucial  tonsils,  which  are  directly  con- 
cerned with  deglutition.  In  other  words,  the  tubercle  bacillus  is  more  often 
inhaled  than  swallowed.  This  fact  need  cause  no  surprise,  for  people  fre- 
quently live  in  an  atmosphere  loaded  with  bacilH,  whilst  they  but  rarely 
swallow  active  tubercular  products. 

A  child  who  is  of  tubercular  stock,  and  therefore  predisposed  to 
lymphatism,  hves  in  close  contact  with  tubercular  parents  or  relatives. 
In  this  case  nasal  respiration  gives  the  tubercle  bacillus  many  chances  of 
fixing  itself  in  the  lymphatic  masses  of  the  pharnygeal  tonsil. 

Alimentation,  as  we  have  said,  may  to  some  extent  favour  infection 
of  the  tonsils  by  the  tubercle  bacillus.  The  question  is  settled  experimentally, 
since  Chauveau  caused  cows  to  swallow  tubercular  material,  and  then  found 
tuberculosis  of  the  pharyngeal  lymphatic  tissue.  Orth  fed  rabbits  on  tuber- 
cular food,  and  several  times  found  tubercular  lesions  of  the  mouth  and 
the  tonsils.  In  1884  Baumgarten,  who  made  similar  experiments,  produced 
tubercular  infection  of  the  tonsils,  and  subsequently  of  the  cervical  glands. 
Cadeac  induced  tuberculosis  in  the  tonsils,  and  subsequently  in  the  sub- 
maxillary glands  of  guinea-pigs,  by  food  rich  in  tubercular  products. 

During  the  experiments  in  question,  it  is  no  doubt  true  that  the  experi- 
menters made  use  of  food  which  was  largely  composed  of  tubercular 
matter.  These  conditions,  though  useful  in  experiments,  do  not  obtain 
in  the  ordinary  course  of  alimentation.  It  must,  nevertheless,  be  said  that 
certain  foods  and  drinks,  especially  milk,  whey,  some  kinds  of  cheese,  raw 
and  salt  meat,  may  all  carry  virulent  bacilli,  and  may  consequently  infect 
the  soil  with  which  they  happen  to  be  in  contact,  especially  if  it  is  pre- 
disposed. One  cow  with  tubercular  mastitis  can  infect  a  large  quantity  of 
milk,  when  all  the  milk  is  collected  in  the  same  vessel.  Galtier  of  Lyons 
has  produced  general  tuberculosis  in  guinea-pigs  with  salted  or  unsalted  cheese 
ten,  fourteen,  and  even  seventy  days  old.  The  whey,  separated  from  the 
cheese  a  fortnight  before  and  inoculated  into  guinea-pigs,  has  produced 
typical  tuberculosis.  Galtier  has  proved  that  salt  meat  is  virulent ;  the 
salting  may  not  destroy  the  virulence  of  the  bacillus,  especially  in  the 
centre  of  thick  pieces  of  meat. 

We  see,  therefore,  how  the  tubercle  bacillus  can,  by  respiration  or  by 
deglutition,  affect  the  lymphatic  tissue  of  the  three  tonsils. 

In  order  to  penetrate  this  tissue,  an  erosion  or  a  pre-existing  wound 
need  not  always  be  present.  We  know  that  the  tubercle  bacillus  can  traverse 
the  epithelium  without  previous  lesions,  and  that  the  tonsils,  larynx,  pharynx, 
bronchi,  trachea,  uterus,  or  intestine,  may  be  penetrated  by  the  bacillus, 
which  makes  its  way  through  the  epithelial  cells. 


DISEASES  OF  THE  THROAT  AND  PHARYNX  631 

The  bacillus,  once  installed  in  the  lymphoid  tissue  of  the  tonsils,  induces 
multiplication  of  phagocytes,  which  often  leads  to  considerable  hypertrophy 
of  the  tonsils.  Sometimes,  however,  the  reaction  is  almost  wanting,  and 
the  tonsils  remain  practically  normal  in  size. 

Tuberculosis  of  the  tonsils  is  often  painless,  but  it  does  not  by  any  means 
always  pass  unnoticed.  Many  children  or  adolescents  complain  of  "  sore 
throat  "  when  they  catch  cold  or  take  the  sUghtest  chill.  Acute  tonsillitis, 
with  or  without  enlarged  glands,  often  supervenes.  The  case  is  looked  on 
as  simple  acute  tonsilUtis,  and  there  is  an  apparent  return  to  the  normal 
condition.  The  tonsils  and  the  adenoids,  however,  remain  enlarged  and 
cause  discomfort. 

In  many  cases,  fortunately,  the  disease  does  not  proceed  beyond  the 
first  stage.  After  a  variable  length  of  time  the  phagocytosis  gains  the 
upper  hand.  The  tonsil  becomes  fibroid  (Grancher),  indurated,  and  atro- 
phied. Here,  as  in  all  cases  of  local  tuberculosis,  recovery  is  effected,  and 
the  infection  does  not  become  general. 

Second  or  Glandular  Stage. 

In  many  cases,  however,  the  first  stage  is,  unfortunately,  passed.  The 
bacillus  remains  for  a  variable  period  in  the  tissue  of  the  tonsils,  and  then, 
as  the  result  of  secondary  infection,  enters  the  lymphatic  network,  which 
drains  the  three  tonsils,  the  second  stage  betraying  itself  by  the  appearance 
of  glands  in  the  submaxillary  and  cervical  regions. 

Durochonsky  actually  observed  the  migration  of  the  tubercle  bacillus 
into  the  lymphatic  vessels  which  lead  from  the  tonsils  to  the  glands  of  the 
neck. 

One  fact  is  worthy  of  notice — namely,  that  larval  tuberculosis  of  the 
tonsils  reacts  more  surely  and  more  frequently  on  the  lymphatic  glands 
than  the  large  tubercular  ulcers  of  the  bucco-pharyngeal  cavity.  I  have 
often  noticed  this  fact,  which  other  authors  have  also  described  (Reclus, 
Pean).  Tubercular  ulcers  of  the  tongue  or  of  the  throat,  even  though 
large  and  deep,  may  not  lead  to  infection  of  the  glands,  while  a  tubercular 
lesion  of  the  tonsil,  though  apparently  trifling,  induces  considerable  enlarge- 
ment of  the  cervical  glands,  which  seems  at  first  to  have  no  connection  with 
the  masked  cause  that  has  given  rise  to  them. 

When  once  the  lymphatic  glands  of  the  neck  are  invaded,  the  lesion  may 
be  limited  to  a  small  number  of  glands,  or  else  the  whole  cliain  of  superficial 
and  deep  glands  may  be  affected.  The  trouble  is  always  descending.  It 
commences  in  the  upper  cervical  glands  with  which  the  lympluitics  of  the 
three  tonsils  communicate,  and  gradually  descends,  until  it  may  invade  the 
superficial  and  deep  glands  of  the  whole  cervical  and  clavicular  region. 

In  some  cases  the  glands  are  small,  hard,  painless,  and  separate,  but  in 


632  TEXT-BOOK  OF  MEDICINE 

others  they  are  enlarged,  painful,  and  matted  together.  The  disease  may 
sometimes  improve  or  disappear,  but  in  other  cases  the  glands  break 
down  and  suppurate.  This  condition  was  called  king's  evil.  We  may 
then  find  fistulse  and  chronic  suppuration  of  the  superficial  and  deep  glands, 
ending  in  scars,  which  occupy  the  submaxillary,  submental,  premastoid, 
retromastoid,  and  subclavicular  regions,  and  are  the  indehble  witnesses  of 
what  was  formerly  called  scrofula. 

Scarlatina,  whooping-cough,  influenza,  syphilis,  and  angina  of  every 
kind,  play  a  part  in  the  extension  of  the  process,  and  in  the  formation  of 
pus. 

Pizzini  has  shown  that  tubercular  adenitis  may  persist  indefinitely  in 
a  latent  state,  until  a  secondary  infection  brings  about  the  dissemination  of 
the  bacillus.  The  second  or  glandular  stage  does  not  always  run  a  progres- 
sive course.  Tuberculosis  of  the  cervical  glands  may  end  in  recovery.  An 
individual  who  in  childhood  or  youth  has  suffered  from  adenitis  of  the  glands 
in  the  neck,  caused  by  larval  tuberculosis  of  the  tonsils,  may  recover  from 
the  glandular  lesions,  and  escape  general  tuberculosis. 

We  are  not  yet  sufficiently  famihar  with  these  latent  forms  of  tubercu- 
losis, which  may  remain  in  the  glands  or  the  tonsils  for  an  indefinite  length 
of  time,  and  be  quite  harmless.  They  may,  however,  at  a  given  moment 
increase  in  virulence,  and  lead  to  general  infection. 

A  person  suffering  from  this  descending  adenitis,  then,  does  not  of  neces- 
sity become  phthisical,  but  it  can  never  be  stated  at  what  moment  the 
possibility  of  his  becoming  so  will  cease. 

Third  or  Pulmonary  Stage. 

When  the  bacillus  reaches  the  lung,  we  have  the  third  stage  of  tuber- 
culosis of  the  tonsil.  The  bacillus  may  finally  reach  the  great  lymphatic 
canal  or  thoracic  duct,  whence  it  is  launched  in  the  venous  circulation, 
passes  through  the  right  heart,  and  finally  reaches  the  lung,  causing  pul- 
monary tuberculosis. 

The  bacillus  may  enter  the  lung  in  such  small  numbers  that  the  disease 
can  be  arrested.  The  lung  defends  itself,  and  replies  to  the  attack  of 
the  bacillus  by  defensive  haemoptysis.  In  other  cases  the  disease  follows 
its  course,  and  ordinary  phthisis  results.  Finally,  the  bacillus  may  enter 
the  lung  in  such  large  numbers  as  to  cause  acute  tuberculosis. 

The  interval  between  the  pulmonary  and  glandular  stages  varies.  The 
disease  may  remain  latent  in  the  gland  for  many  years,  and  the  lung  is  only 
invaded  very  late.  The  cases  which  I  have  published  in  the  Bulletin  de 
r Academic  show  that  the  lung  infection  appeared  after  tliree  months 
(Case  1)  ;  five  months  (Case  2)  ;  four  years  (Case  3) ;  six  years  (Case  4)  ; 
ten  years  (Case  5)  ;  sixteen  years  (Case  6) ;  and  twenty-eight  years  (Case  7). 


DISEASES  OF  THE  THROAT  AND  PHARYNX  G33 

Case  1. — (Three  months'  interval  between  the  glandular  and  pulmonary  stages.) 

Ch ,  eighteen  years  of  age,  admitted  into  the  Necker  Hospital    under  my  care. 

Six  months  before  two  glands  at  the  angle  of  the  jaw  were  removed,  at  the  Beaujon 
Hospital.  Other  glands  have  since  appeared,  forming  a  descending  chain,  best  marked 
in  the  left  cervical  region.  The  glands  were  as  large  as  a  filbert  or  a  walnut ;  several 
of  them  were  adherent,  soft,  and  suppurating.     Bacilli  present  in  the  glandular  fluid. 

The  man,  who  had  never  been  ill,  commenced  to  cough  three  months  previously. 
At  the  same  time  he  had  attacks  of  haemoptysis,  which  were  the  first  symptoms  of  the 
pulmonary  stage,  and  appeared  three  months  after  the  glandular  stage.  Auscultation 
revealed  incipient  tuberculosis  at  the  apex  of  the  right  lung. 

Case  2. — (Five  months'  interval.)  In  consultation  with  Dr.  Gerard  Marchant,  I 
saw  a  young  girl,  thirteen  years  of  age,  suffering  from  plithisis,  with  numerous  bacilli 
in  the  sputum.  The  cough  and  other  symptoms  of  tuberculosis  had  set  in  about  two 
months  previously. 

Five  months  j^rior  to  these  pulmonary  symptoms  she  had  been  attended  by  Mar- 
chant  for  acute  inflammation  of  the  maxillary  and  cervical  glands  on  both  sides  (glan- 
dular stage).     The  inflammation  had  been  marked,  and  pus  had  formed  in  the  glands. 

It  is  very  interesting  to  note  that  the  glandular  trouble  had  been  preceded  two 
months  previously  by  hypertrophy  of  the  tonsil  (tonsillar  stage). 

Case  3. — (Four  years'  interval.)  A  young  man,  twenty-five  years  of  age,  was  ad- 
mitted to  the  Necker  Hospital  under  my  care  on  August  1,  1894.  Until  he  joined  his 
regiment  four  years  before,  he  had  never  shown  any  chest  symptoms.  In  1890  the 
submaxillary  glands  showed  such  marked  swelling  during  the  ■n-inter  that  Le  Fort 
removed  them.  Some  small  superficial  glands  were  not  removed.  He  was  able  to 
complete  his  military  service. 

Five  months  previously,  in  April,  1894,  cough,  expectoration,  and  two  attacks  of 
haemoptysis  appeared.  Loss  of  weight  and  night-sweats  followed,  and  we  found  advanced 
tuberculosis  at  the  apex  of  the  right  lurig  and  incipient  disease  at  tlie  apex  of  the  left. 

Case  4. — (Six  years'  interval.)  In  consultation  with  Dr.  Blocq,  I  saw  a  patient, 
aged  twenty-four,  suffering  from  advanced  tuberculosis  of  the  right  lung.  At  the  age 
of  seventeen  suppurative  adenitis  of  the  left  submaxillary  glands,  which  were  removed  ; 
no  chest  symptoms. 

Six  months  later  suppuration  in  the  left  cervical  glands,  which  were  removed. 

Some  months  later  suppuration  in  the  supraclavicular  glands  on  the  same  side  ; 
the  glands  were  removed. 

Some  months  later  suppuration  in  the  glands  on  the  right  side,  which  were  also 
removed. 

It  was  only  after  these  successive  attacks  of  descending  adenitis  that  pulmonary 
symptoms  appeared. 

Case  5. — (Ten  years'  interval.)  A  young  man,  twenty  years  of  age,  admitted  to 
the  Necker  Hospital.  Between  the  age  of  ten  and  twelve  years  he  was  subject  to  sore 
throat,  and  later,  when  about  seventeen,  suffered  from  double  tonsillitis. 

For  many  years  glands  had  appeared  in  the  cervical  region  ;  as  tliey  grew  larger  and 
suppurated,  operation  became  necessary. 

On  the  right  side  the  glands  were  soft  and  of  the  size  of  a  walnut,  while  those  on  the 
left  side  were  larger.     Fistula?  and  cicatrices  present  on  the  skin  of  the  cervical  region. 

The  pulmonary  stage  did  not  appear  till  ten  years  after  the  glandular  one.  Tuber- 
cular bronchitis  was  present,  though  the  patient  had  had  no  previous  cougli,  and  wo 
found  on  examination  phthisis  of  the  left  apex.  Marion  discovered  bacilli  in  the  pus 
from  the  glands  and  in  the  sputum. 

Case  G. — (Sixteen  years'  interval.)  In  1894  I  saw  a  patient,  aged  thirty-six,  suffer- 
ing from  early  plithisis  of  the  right  apex.  The  cougli  and  the  slightly  l)lo()(l-s(reaked 
sputum  appeared  to  be  recent,  but  the  glandular  stage  had  commenced  sixteen  years 


634  TEXT-BOOK  OF  MEDICINE 

before.  In  1877  he  had  an  attack  of  progressive  adenitis  in  the  glands  on  the  left  side 
of  the  neck.  The  adenitis  ended  in  suppuration,  which  lasted  for  several  months.  I 
found  two  large  cicatrices — one  below  the  jaw  and  the  other  on  the  posterior  edge  of 
the  sterno-mastoid  muscle. 

Case  7. — (Twenty-eight  years'  interval.)  A  patient,  forty-eight  years  of  age,  whom 
Potain,  in  consultation  with  me,  had  seen  several  times,  was  taken  ill  with  haemoptysis 
and  pulmonary  tuberculosis  in  May,  1893.  The  latter  ran  a  somewhat  rapid  course, 
and  the  patient  succumbed  a  year  later.  Though  he  had  never  had  any  symptoms  of 
phthisis,  he  had  in  his  youth  suffered  from  suppuration  of  the  cervical  glands.  He  had 
large  cicatrices.  After  a  latent  period  generalization  occurred,  and  the  glandular 
stage  ended  twenty-eight  years  after  in  the  pulmonary  stage. 

Case  8. — Quite  recently  I  had  at  the  Necker  Hospital  a  most  typical  case  of  this 
tubercular  infection  in  a  young  woman.  She  married  a  tubercular  husband,  who 
died  in  a  few  years  of  phthisis.  She  was  attacked  by  hypertrophy,  which,  though  simple 
in  appearance,  was  in  reality  larval  tuberculosis  of  her  three  tonsils.  In  spite  of  ener- 
getic treatment,  the  cervical  glands  had  been  invaded  about  a  year  previously,  and  a 
few  months  before  the  signs  and  symptoms  of  phthisis  had  supervened.  The  apex  of 
the  left  lung  was  tubercular. 

How  many  cases  of  this  kind  have  I  not  met  with  since  my  attention 
was  called  to  this  mode  of  propagation  in  tuberculosis !  It  is  surprising 
that  this  fact  has  not  been  demonstrated  earlier  by  experiment. 

The  invasion  of  the  lung  is  revealed  by  the  ordinary  signs  of  tuberculosis 
— namely,  haemoptysis,  suspicious  bronchitis  or  pleurisy,  wasting,  loss  of 
appetite  and  of  strength,  etc.  Percussion,  auscultation,  and  examination 
for  bacilli  readily  indicate  the  seat  of  the  disease. 

To  sum  up  :  It  is  truly  said  that  the  lymphoid  tissue  of  the  three  tonsils 
offers,  especially  in  young  and  predisposed  subjects,  an  entrance  and  a  sure 
asylum  to  the  tubercle  bacillus.  The  result  is  a  latent  form  of  tuberculosis, 
which  simulates  adenoids,  or  hypertrophy  of  the  tonsils.  Frequently  the 
tonsil  is  not  even  enlarged.  This  masked  tuberculosis  of  the  three  tonsils 
may  not  overstep  the  first  stage,  and  may  end  in  recovery. 

In  other  cases  the  infection,  at  first  limited  to  the  tonsils,  invades  the 
lymphatics  of  the  neck.  Numerous  varieties  of  tubercular  adenitis  are 
the  result.  This  glandular  stage  may  end  in  recovery  without  other  com- 
plications. 

Too  often,  however,  after  a  period  which  varies  from  some  months  to 
several  years,  the  second  stage  is  passed,  and  the  tuberculosis  affects  the 
lung,  or  becomes  general.  The  three  tonsils  must  therefore  be  reckoned  as 
one  of  the  most  formidable  portals  of  entry  in  human  tuberculosis. 

Treatment. — The  first  point  is  immediate  recourse  to  prophylactic 
measures.  In  practice  they  consist  in  preventing  the  entrance  of  the  bacillus 
during  respiration  and  aHmentation. 

Children  must  therefore  be  removed  from  all  sources  of  contamination, 
and  the  most  important  source  is  the  dust  of  the  dried  sputum.  It  is 
necessary,  as  far  as  possible,  to  change  the  infected  atmosphere,  in  which 


DISEASES  OF  THE  THROAT  AND  PHARYNX  635 

the  child  lives  for  an  inoffensive  medium.  I  know  well  that  the  matter  is 
easier  to  discuss  than  to  accomplish,  but  in  matters  prophylactic  we  must 
always  return  to  the  question  of  the  seed  and  the  soil.  Heredity  in  particular 
provides  the  soil,  and  it  is  our  duty  to  keep  the  seed  away  from  it.  Alimenta- 
tion may  be,  to  a  certain  extent,  a  source  of  infection.  From  the  experi- 
mental point  of  view  the  question  is  settled,  and  I  urged  this  when  considering 
the  modes  of  entrance  of  the  bacillus.  Hygiene,  in  the  case  of  a  predisposed 
child,  must  therefore  consist  of  many  precautionary  measures. 

And  even  though  the  seed  have  germinated,  and  the  bacillus  have  passed 
the  tonsillar  stage,  certain  prophylactic  measures  must  be  employed.  It  is 
often  only  through  secondary  infection  that  tuberculosis,  hitherto  latent, 
reveals  itself  in  a  subject  who  seemed  secure  from  harm.  Tuberculosis 
often  seems  to  break  out  after  measles,  whooping-cough,  scarlatina,  influenza, 
typhoid  fever,  or  syphihs,  when  these  infectious  diseases  are  only  the  occa- 
sional cause  of  a  hitherto  concealed  tuberculosis.  Children  and  young 
lymphatic  subjects  born  of  tubercular  stock,  whose  adenoid  tissue  is  already 
affected,  must  be  therefore  carefully  preserved  from  the  infectious  diseases 
which  I  have  just  enumerated. 

Let  us  now  consider  curative  measures.  What  treatment  are  we  to 
adopt  in  a  case  of  masked  tuberculosis  of  the  tonsils  ?  Before  approaching 
this  question,  which  is  both  medical  and  surgical,  I  must  confess  that  the 
means  at  our  disposal  are  not  always  efficient.  The  time  will  come,  no  doubt, 
when,  with  the  aid  of  serotherapy,  we  shall  be  able  to  fight  tubercular 
infection,  as  we  fight  diphtheritic  infection,  and  as  we  are  beginning  to  fight 
streptococcal  infection.  Until  then  let  us  employ  the  means  at  our  dis- 
posal, and  see  which  appear  to  be  the  best. 

Let  us  commence  with  the  general  treatment,  which  aims  at  placing  the 
system  in  a  state  of  defence.  Our  means  prepare  the  body  for  the  fight,  and 
sometimes  help  it  to  gain  the  victory.  Personally,  I  am  sure  that  the  best 
treatment  is  to  give  food  rich  in  fatty  substances,  such  as  cod-liver  oil,  caviare, 
sardines  in  oil,  tunny-fish,  pate  de  foie  gras,  slices  of  bread  and  butter,  etc. 

Hygienic  measures  occupy  an  important  place  in  cases  of  tonsillar  and 
glandular  tul^erculosis.  Sea  air  has  a  powerful  action.  Out  of  1,293  cases 
of  enlarged  cervical  glands  admitted  into  the  hospital  at  Berck,  the  glandular 
inflammation  disappeared  in  900  cases.  The  Arachon  cure  and  the  waters 
of  Salics-de-Bearn,  Safin,  or  Kreuznach,  are  all  means  to  the  same  end. 

Surgical  treatment  remains  to  be  discussed.  What  course  should  be 
adopted  in  a  case  of  enlarged  tonsils  or  of  adenoid  growths  ?  Ought  they  to 
be  removed,  or  destroyed  by  the  galvano-cautery  ?  Opinions  are  divided 
on  this  point.  Though  I  have  several  times  proved  the  necessity  for  surgical 
intervention,  great  judgment  is  required,  and  each  case  must  be  treated  on 
its  merits. 


CHAPTER  III 
DISEASES  OF  THE  OESOPHAGUS 

I.  (ESOPHAGITIS. 

Pathological  Anatomy— etiology. — CEsophagitis,  or  inflammation  of 
the  oesophageal  mucous  membrane,  may  be  primary  or  secondary.  The 
primary  form  is  always  caused  by  the  ingestion  of  hot  or  corrosive  hquids 
(sulphuric  acid,  solution  of  potash),  of  irritating  substances  (tartrate  of 
antimony),  or  by  the  presence  of  a  foreign  body  (fragment  of  a  bone,  fish- 
bone, pin).  Secondary  oesophagitis  develops  by  the  spreading  of  thrush 
or  of  diphtheritic  angina ;  it  supervenes  in  the  course  of  some  other  diseases 
(variola,  typhoid  fever). 

The  lesions  are  most  common  in  the  upper  third  of  the  oesophagus, 
and  differ  greatly  according  to  their  cause.  The  mucous  membrane  is  red, 
thick,  eroded,  or  ulcerated  ;  sometimes,  indeed,  the  walls  of  the  cesophagus 
are  perforated.  When  suppuration  occurs  (which  is  very  rare),  the  abscess 
may  be  either  submucous  or  peri- oesophageal.  In  the  latter  case  the  sup- 
puration may  invade  the  cellular  tissue  and  cause  a  cervical  abscess. 
Scarring  of  the  mucous  membrane  frequently  results  from  the  ingestion  of 
caustic  substances,  and  is  often  followed  by  stenosis  of  the  oesophagus.  In 
addition  to  the  causes  which  I  have  just  enumerated,  the  simple  ulcer  and 
syphilis  also  produce  cicatricial  stenosis. 

The  simple  ulcer  may  occur  in  the  oesophagus,  as  in  the  stomach  or 
duodenum,  and  cause  a  fibrous  stenosis  (Debove).  A  patient  who  had 
cicatricial  stenosis  of  the  oesophagus,  which  was  rightly  attributed  to  a  simple 
ulcer,  died  two  years  afterwards  from  perforation  of  a  gastric  ulcer.  Post 
mortem  the  gastric  ulcer,  which  was  the  cause  of  death,  was  found.  An 
ulcer  was  also  present  in  the  cicatrized  oesophagus  2  inches  above  the 
cardiac  orifice  ;  the  cicatrix  was  circular,  ^  inch  across,  and  of  the  same 
aspect  and  nature  as  the  simple  ulcer  of  the  stomach.  The  oesophagus, 
which  had  been  dilated  by  sounds  for  two  years,  was  somewhat  contracted 
at  the  cicatrix  and  slightly  dilated  above  it.  Syphilis  may  cause  cicatricial 
contractions  of  the  oesophagus,  which  result  from  ulcerated  gummata. 

Description. — The   initial  symptoms  are   only  marked  when  the  in- 

636 


DISEASES  OF  THE  (ESOPHAGUS  637 

flammation  is  very  acute.  Pain  may  be  felt  along  the  oesophagus,  in  the 
epigastric  region,  or  between  the  shoulders,  and  is  caused  by  the  passage 
of  food  and  of  hot  or  cold  hquids.  It  is  generally  accompanied  by  spasms 
of  the  oesophagus  and  regurgitation  of  ingested  substances. 

Foreign  bodies  in  the  oesophagus  may  produce,  not  only  inflammation 
and  ulceration,  but  also  perforation  of  the  oesophageal  vessels,  followed  by 
l^rofuse  haemorrhage.  Caustic  substances  cause  ulceration,  sloughing,  and 
perforation,  which -may  be  followed  by  death ;  and,  if  the  patient  recovers,  the 
cicatrices  usually  induce  stenosis  of  the  oesophagus.  The  formation  of  an 
abscess  is  announced  by  febrile  symptoms,  with  increase  of  pain  and  dys- 
phagia. If  the  abscess  is  submucous,  the  pus  may  be  rejected  by  the 
mouth,  or  may  pass  into  the  stomach.  If  it  is  peri- oesophageal,  the  pus 
burrows  into  the  neighbouring  tissues,  and  produces  very  grave  mischief. 

The  symptoms  of  cicatricial  contraction  of  the  oesophagus  at  first  closely 
resemble  those  due  to  mahgiiant  stricture.  I  shall  therefore  discuss  this 
question  under  Cancer  of  the  CEsophagus. 

Soothing  drinks,  apphcations  of  leeches  to  the  painful  region,  and 
injections  of  morphia,  are  employed  to  reheve  the  pain  and  the  inflammation 
in  acute  oesophagitis.  Catheterization  of  the  oesophagus  in  order  to  dilate 
the  stricture  is  the  usual  treatment  for  cicatricial  contractions.  (Esophago* 
tomy  should  be  reserved  for  special  cases.  In  the  case  of  syphihtic  stricture 
the  patient  must  be  put  on  a  course  of  iodide  of  potassium  and  mercury. 

II.  SPASM  OF  THE  (ESOPHAGUS. 

Description. — Spasms  of  the  oesophagus  are  often  described  under  the 
name  of  spasmodic  stenosis  of  the  oesophagus.  These  spasms  are  of  multiple 
origin,  being  idiopathic  in  hysteria,  in  hypochondriacs,  and  nervous  people  ; 
symptomatic  in  the  case  of  oesophageal  lesions  (foreign  bodies,  cancer) ;  and 
sympathetic  in  some  ill-determined  cases  (taenia,  uterine  affections).  It  is 
the  idiopathic  spasm  which  I  have  particularly  in  view  in  this  description. 

Spasm  of  tlio  (esophagus  comes  on  suddenly  at  the  sight  of  food,  with 
the  ftrst  mouthful,  or  during  the  course  of  a  meal.  Emotion,  annoyance, 
or  some  particular  kind  of  food  may  provoke  it.  If  the  dysphagia  is  com- 
plete the  food  does  not  pass  and  is  regurgitated,  or  if  it  should  pass,  it  is  only 
when  it  is  crumb-like,  well  moistened,  and  slowly  swallowed.  The  spasm  is 
generally  accompanied  by  choking  and  a  painful  feeling  of  constriction 
in  the  upper  third  of  the  a'sophagus.  By  the  use  of  tlie  catheter  tlie  pre- 
sence and  the  seat  of  the  spasmodic  contraction  are  proved  :  the  instrument 
is  sometimes  arrested  at  the  level  of  the  spasm ;  at  other  times  it  goes  through 
after  some  difliculty.  Transient  sj)asm  is  not  dangerous  ;  serious  anaemia 
and  weakness  may  follow  persistent  spasm. 


61)8  TEXT-BOOK  OF  MEDICINE 

The  diagnosis  of  spasmodic  contraction  from  cancer  of  the  oesophagus 
will  be  given  in  the  next  section.  The  treatment  consists  in  the  use  of  the 
catheter.  Bromide  of  potassium,  valerian,  and  belladonna,  are  also  adminis- 
tered.    Hydrotherapy  may  be  employed. 


III.  CANCER  AND  STRICTURES  OF  THE  (ESOPHAGUS. 

Pathological  Anatomy. — The  varieties  of  cancer  of  the  oesophagus 

are,  in  order  of  frequency  :  epithelioma,  encephaloid,  and  scLrrhus.  The 
middle  third  of  the  organ  is  the  most  common  seat  of  cancer,  and  next  the 
lower  third.  The  growth  occurs  in  the  form  of  a  patch  or  of  a  projecting 
tumour,  which  surrounds  the  oesophagus  like  a  ring  over  an  area  of 
half  an  inch  or  more,  and  gradually  narrows  the  lumen.  The  oesophagus  is 
almost  always  dilated  above  the  tumour  and  contracted  below  it.  The 
stricture  is  rarely  cyhndrical ;  it  is  usually  oblique  and  anfractuous.  The 
dilatation  above  the  tumour  may  form  a  pocket  or  a  lateral  diverticulum ; 
this  is  pecuhar  to  malignant  strictures,  and  is  hardly  ever  seen  in  those 
of  inflammatory  origin.  The  internal  surface  of  the  cancerous  oesophagus 
is  sometimes  normal,  and  the  mucous  membrane  preserves  its  integrity 
(scirrhus).  At  other  times  it  is  ulcerated  or  covered  with  f ungating  growths, 
the  mucous  and  submucous  coats  have  disappeared,  and  the  tunica  muscu- 
laris  is  thickened. 

The  trachea,  bronchi,  lungs,  pleura,  aorta,  glands,  and  vertebral  column 
may  be  invaded  by  the  growth,  and  we  find  adhesions,  ulcerations,  or  per- 
foration, with  or  without  fistulas,  which  establish  communication  between 
these  different  organs  and  the  oesophagus.  The  Dupuytren  Museum  has 
some  excellent  specimens,  showing  communications  between  the  oesophagus 
and  the  neighbouring  organs. 

Symptoms. — Pain  and  dysphagia  are  the  first  symptoms  of  cancer  of 
the  oesophagus.  The  pain,  however,  is  not  constant ;  it  consists  in  a  feehng 
of  constriction  behind  the  sternum  or  between  the  shoulders,  becomes  worse 
at  meal-times,  and  may  be  very  sharp,  but  the  radiation  is  not  always 
sufficient  to  localize  the  seat  of  the  disease.  Progressive  dysphagia  is  the 
chief  symptom  of  oesophageal  cancer.  The  troubles  in  deglutition  are  due 
to  the  thickening  and  induration  of  the  gullet,  and  often  to  the  gi'adual 
narrowing  of  its  cahbre.  The  patient  instinctively  takes  smaller  mouth- 
fuls  as  soon  as  he  feels  discomfort  in  swallowing,  and  takes  frequent  sips  to 
facihtate  the  passage  of  the  food  bolus.  For  some  time  the  food  passes 
fairly  well  if  it  is  well  masticated.  This  condition  lasts  weeks  and  months, 
with  alternate  improvement  and  aggravation,  but  later  the  dysphagia  becomes 
more  marked,  until  at  last  even  liquids  are  arrested  at  the  stricture.  Both 
solid  and  liquid  foods  are  frequently  regurgitated. 


DISEASES  OF  THE  (ESOPHAGUS  639 

The  foregoing  description  holds  good  in  most  cases.  In  many  instances 
the  dysphagia  associated  with  cancer  of  the  oesophagus  is  progressive  and 
continuous,  and,  while  sUght  at  first,  it  gradually  reaches  its  maximum 
as  the  lesion  progresses.  Events,  however,  do  not  always  take  this  course, 
and  several  cases  have  been  collected  in  which  the  dysphagia  was  sudden 
and  acute  from  the  outset,  just  as  in  simple  spasm.  In  some  patients  the 
dysphagia  comes  on  suddenly  during  the  swallowing  of  a  large  mouthful, 
or  in  consequence  of  vomiting  caused  by  a  hearty  repast.  The  dysphagia 
is  almost  absolute  for  two  or  three  days,  and  then  tlie  normal  condition 
returns,  deglutition  being  easy  for  several  weeks,  until  a  fresh  attack  comes 
on,  the  dysphagia  taking  on  this  intermittent  form  until  it  becomes  continu- 
ous. It  would  be  quite  wrong  to  rely  on  the  sudden  or  acute  onset  of  the 
dysphagia,  or  on  its  temporary  disappearance,  in  order  to  ehminate  the 
idea  of  cancer  and  show  that  a  case  of  stricture  is  simply  due  to  spasm. 
Spasm  of  the  oesophagus  plays  a  large  part  in  the  dysphagia,  even  when 
organic  lesions  are  present. 

Xo  matter  what  are  the  symptoms  at  the  commencement,  if  the  cancer 
terminates  in  stricture  of  the  oesophagus,  the  food  passes  with  difficulty 
and  is  regurgitated.  The  regurgitation  follows  immediately  on  the  inges- 
tion of  food  when  the  constriction  is  in  the  upper  part  of  the  oesophagus  ; 
it  occurs  later  when  the  growth  is  seated  in  the  lower  portion.  This  delay 
is  favoured  by  the  dilatation  of  the  tube,  which  forms  a  land  of  pouch,  where 
the  food  rests  for  a  time.  In  the  latter  case  food  is  rejected  some  time 
after  ingestion,  as  a  pulp-like  foul-smelling  mass.  It  has  undergone  but 
httle  modification  by  the  saliva.  The  accumulation  of  food  in  the  pouch 
causes  a  feehng  of  pain,  which  may  give  rise  to  choking,  and  only  ceases 
after  vomiting.  The  vomit  is  at  times  mixed  with  blood,  blackish  clots,  and 
detritus  from  the  fungating  growth. 

Some  patients  have  salivary  regurgitation,  or  "  fits  of  mucous  vomiting." 
Glue-like  masses  of  mucus,  which  the  patient  removes  from  his  mouth 
with  his  finger,  accumulate  at  the  level  of  the  stricture,  and  are  brought  up 
in  the  morning  on  awakening  or  prior  to  the  regurgitation  of  food.  Amongst 
the  symptoms  of  cancer  of  the  oesophagus  there  have  been  noted  hiccough 
(Mondiere)  and  the  "  gloo-gloo  "  sound  (Behier),  which  occurs  when  the  air 
swallowed  with  the  food  passes  the  stricture.  Alteration  in  the  voice  and 
paralysis  of  a  vocal  cord  from  destruction  of  one  recurrent  nerve  have  also 
been  noted.  Enlargement  of  the  glands  above  the  clavicle  is  a  valuable 
but  inconstant  sign. 

In  some  cases,  particularly  in  old  men,  cancer  of  the  oesophagus  is  latent, 
pain,  dysphagia,  and  regurgitation  being  absent;  so  that  we  should  think 
of  cancer  of  the  oesophagus  in  a  patient  suffering  from  mahgnant  cachexia, 
wiien  tho  site  of  the  growth  cannot  be  discovered. 


640  TEXT-BOOK  OF  MEDICINE 

Complications. — The  disease  lasts  from  one  to  two  years,  and  the 
prognosis  is  hopeless.  When  there  is  no  constriction,  and  the  patient  con- 
tinues to  take  food,  cachexia  may  appear  late  ;  but  when  the  cancer  ends  in 
stenosis,  the  loss  of  weight  progresses,  and  the  cachexia  is  earlier,  as  it 
depends  both  upon  the  presence  of  the  cancer  and  the  insufficiency  of  food. 
Death,  is,  however,  not  always  due  to  cachexia,  but  is  often  caused  or 
hastened  by  various  complications. 

In  purely  cicatricial  stenosis  the  danger  arises  only  from  the  inanition 
which  may  result,  but  in  stenosis  due  to  cancer  the  complications,  which 
depend  on  the  seat  of  the  cancer  and  its  propagation  to  neighbouring 
organs,  are  added  to  the  dangers  of  stenosis  and  inanition.  Amongst  the 
most  frequent  complications  I  shall  quote  compression  and  perforation  of 
the  trachea  and  the  bronchi.  The  perforation  is  sometimes  direct,  at  other 
times  fistulous,  involving  the  trachea  alone,  or  the  trachea  and  the  bronchi 
at  the  same  time.  This  compUcation  is  announced  by  fits  of  coughing  and 
suffocation,  which  come  on  as  soon  as  food  or  drink  enter  the  respiratory 
passages. 

Other  compHcations  comprise  :  communication  of  the  cancer  with  the 
pleura  and  lung,  especially  on  the  right  side  (Vigla) ;  pleuro-pulmonary 
inflammation  ;  perforation  of  the  pericardium  or  of  the  aorta  ;  and  the 
invasion  of  the  vertebrae.  According  to  some  authors,  constrictions  of  the 
oesophagus,  whether  they  are  cicatricial  or  cancerous,  are  apt  to  favour  tuber- 
culosis by  inanition. 

Diagnosis. — As  soon  as  a  patient  shows  symptoms  of  constriction  of 
the  oesophagus,  we  must  make  certain  that  it  is  a  case  of  constriction,  and 
not  of  compression  by  a  tumour  in  the  neighbourhood  (cancer  of  the  medi- 
astinum or  bronchial  glands,  aneurysm  of  the  aorta  or  of  the  subclavian 
artery).  The  signs  obtained  by  auscultation  and  percussion  and  the  various 
symptoms  inherent  in  each  of  these  diseases  generally  clear  up  the  point. 
When  we  have  proved  constriction  of  the  oesophagus,  the  next  question  is 
to  decide  whether  it  is  spasmodic,  cicatricial,  or  malignant. 

1.  Let  us  commence  with  the  diagnosis  from  spasmodic  constriction. 
I  have  described  in  the  second  section  the  characteristics  of  spasmodic 
constriction.  This  spasmodic  constriction,  which  is  usually  found  in 
hysterical,  nervous,  or  hypochondriacal  patients,  does  not  come  on  gradually ; 
it  appears  suddenly,  and  at  once  reaches  its  maximum.  In  spasmodic  con- 
striction the  symptoms  sometimes  disappear  suddenly,  and  return  some  days, 
weeks,  or  months  later.  They  often  recur  from  mental  causes,  or  from  the 
use  of  certain  foods  and  beverages.  In  cicatricial  or  cancerous  constriction 
these  symptoms  are  not  often  seen,  but  we  must  not  forget  that  organic 
lesions  of  the  oesophagus,  as  of  all  muscular  canals,  before  causing  persistent 
organic  constriction  may  give  rise  to  spasms  of   greater  or  less  duration, 


DISEASES  OF  THE  (ESOPHAGUS  641 

which  simulate  spasmodic  constriction.  Such  is  the  case  in  cancerous 
constriction.  On  the  other  hand,  spasmodic  constriction  may,  from  its 
duration  and  its  cachexia,  simulate  mahgnant  stricture,  and  Avriters  have 
recorded  cases  of  purely  spasmodic  constriction  which,  hke  the  permanent 
contractures  of  hysteria,  last  for  weeks  at  a  time,  and  bring  about  a  state 
of  inanition  and  emaciation  which  might  give  rise  to  the  idea  of  cancer. 
It  will  therefore  be  seen  that  dysphagia  alone  is  often  insufficient  to  prove 
that  a  stricture  is  maUgnant,  and  that  hysterical  oesophagismus,  in  order 
to  have  an  absolute  diagnostic  value,  must  be  associated  with  other  symp- 
toms common  to  hysteria. 

In  certain  rare  cases  the  spasm  comes  on  in  fits,  which  are  due  to  stimula- 
tion of  the  recurrent  nerve  by  a  neighbouring  tumour.  This  symptom 
belongs  to  the  category  of  spasmodic  constrictions  described  under 
Aneurysms  of  the  Aorta  of  the  Recurrent  Type. 

1.  Let  us  now  consider  the  diagnosis  of  cancerous  and  cicatricial  con- 
strictions. Certain  symptoms  aid  us  in  distinguishing  between  these  two 
forms.  I  shall  divide  cicatricial  constrictions  into  three  varieties.  In  the 
first  variety  the  constriction  is  due  to  the  ingestion  of  corrosive  substances. 
Behier  has  collected  a  large  number  of  cases  in  which  the  patients  had 
swallowed  liquor  potassae,  nitric  acid,  or  sulphuric  acid,  and  had,  in  conse- 
quence, suffered  from  cicatricial  constrictions,  which  were  sometimes 
multiple,  and  more  or  less  extensive.  In  these  cases,  however,  the  symp- 
toms of  constriction  are  preceded  by  acute  (Bsophagitis.  This  acute  stage, 
with  the  information  given  by  the  patient,  proves  the  case.  Several  con- 
strictions may  be  present  in  such  cases  at  various  points  of  the  oeso- 
phagus, and  as  they  may  be  some  inches  in  extent,  catheterization  is  very 
difficult. 

2.  In  the  second  variety  the  constriction  is  due  to  a  simple  ulcer  of  the 
oesophagus,  which  is  identical  with  the  simple  ulcer  of  the  stomach  and 
duodenum.  Its  cicatrization  may  lead  to  constriction  of  the  oesophagus, 
as  was  evident  in  Debove's  case,  where  the  ulcer  and  the  consequent 
constriction  were  situated  2  inches  above  the  cardia.  In  such  cases,  how- 
ever, the  dysphagia  and  the  symptoms  of  constriction  are  preceded  by 
symptoms  resembling  those  of  ulcer  of  the  stomach.  Sharp  pains  are 
present  at  the  pit  of  the  stomach,  and  in  the  vertebral  region,  they  radiate 
to  the  shoulders,  around  the  thorax,  or  in  other  directions.  Vomiting  of 
blood,  accompanied  by  pain,  is  the  second  prominent  symptom  of  ulcer 
of  the  oesophagus.  The  haemorrhage  consists  of  red  rather  than  of  black 
blood;  It  may  be  profuse  and  recurrent.  This  first  phase,  which  may 
last  months  and  years,  is  succeeded  by  dysphagia  and  symptoms  of  stricture. 
These  symptoms  appear  slowly,  and  the  difficulty  in  deglutition  increases 
gradually,  until  the  catheter  is  passed,  and  the  seat  of  the  constriction  is 

41 


642  TEXT-BOOK  OF  MEDICINE 

established.     The  succession  and  the  course  of  these  symptoms  allow  us 
to  ehminate  the  idea  of  cancer. 

3.  The  third  variety  of  cicatricial  constriction  is  due  to  syphilis.  We 
find  neither  the  acute  stage  seen  in  corrosive  strictures,  nor  the  pain  and 
haemorrhage  which  precede  constriction  due  to  a  simple  ulcer.  Cases  of 
syphilitic  stricture  are  rare,  and  Potain  has  been  able  to  collect  only 
seven  cases.  Virchow  found  breaking-down  gummata  in  the  scar  of  a 
stricture.  Lubinski  cites  two  cases  of  syphihtic  constriction.  In  the  first 
case  a  young  man,  twenty-nine  years  of  age,  had  been  syphihtic  for 
some  y^ars,  and  the  stenosis,  which  was  almost  complete,  was  probably  due 
to  an  ulcerated  gumma,  and  developed  in  about  three  weeks.  Specific 
treatment  brought  about  rapid  improvement.  Palmar  psoriasis  confirmed 
the  diagnosis.  The  second  case  is  that  of  a  man  who  had  had  syphilis  of 
the  tongue.  In  syphihtic  constriction  the  diagnosis  will  be  made  by  the 
process  of  eUmination.  The  constriction  takes  place  either  quickly  or 
slowly,  and  is  not  preceded  by  the  preliminary  stage  noticed  in  the  other 
varieties  of  cicatricial  constriction,  and  the  patient  has  already  had  syphihtic 
troubles. 

As  we  have  just  seen  by  this  lengthy  discussion  of  the  symptoms,  it  is 
by  ehmination  that  the  cancerous  nature  of  the  lesion  will  be  recognized  in 
difficult  cases.  It  is  at  first  difficult  to  diagnose,  but  the  age  of  the  patient, 
conditions  of  heredity,  and  careful  study  of  the  preliminary  stage,  will 
most  frequently  allow  us  to  say  whether  it  is  a  case  of  cancer  or  not. 

In  making  a  diagnosis,  cachexia  must  never  be  rehed  on,  for  it  may 
appear  late,  if  nourishment  can  be  taken.  Vomiting  of  blood-stained  matter 
mixed  with  particles  of  food  is  in  favour  of  cancer. 

The  use  of  the  catheter,  which  must  be  carried  out  with  the  greatest 
care,  in  order  to  avoid  false  passages  and  perforations  of  the  canal,  may 
furnish  valuable  information.  In  the  case  of  spasmodic  constriction  serious 
resistance  is  sometimes  met  with.  We  can,  however,  pass  a  large  ohvary 
catheter  more  easily  than  a  small  one,  and  when  the  instrument  has  been 
passed  the  patient  can  usually  swallow  without  difficulty — at  any  rate,  for 
the  first  few  moments.  In  cicatricial  stricture,  especially  when  annular, 
the  catheter  passes  with  a  jerk,  as  through  an  obstacle  which  does  not  give 
way.  On  the  contrary,  the  catheter  when  passing  a  cancerous  constriction 
seems  to  go  through  a  less  rigid  obstacle, 'which  is  more  yielding,  and  it  is  often 
streaked  with  blood  on  withdrawal,  even  though  the  manipulation  has  been 
carried  out  with  dexterity.  In  some  cases  the  presence  of  supraclavicular 
glands  or  the  appearance  of  phlegmasia  alba  dolens  will  help  to  prove  the 
existence  of  cancer. 

Treatment. — In  the  cicatricial  strictures  the  use  of  the  catheter  has  a 
twofold  object :  on  the  one  hand,  it  is  possible  to  feed  the  patient,  and,  on 


DISEASES  OF  THE  (ESOPHAGUS  643 

the  other,  it  leads  to  the  gradual  dilatation  of  the  constriction.  It  is  often 
preferable  to  perform  gastrostomy,  in  order  to  feed  the  patient  and  allow 
time  for  systematic  catheterization.  I  did  this  for  a  patient  of  mine  and  the 
result  was  excellent. 

When  there  is  a  maUgnant  stricture,  a  gastric  fistula  must  at  once  be 
made  ;  the  patient  is  fed  through  it  (gastrostomy),  and  in  a  few  weeks  gains 
several  pounds  in  weight,  while  hfe  may  be  prolonged  considerably. 

I  have  seen  several  cases  of  this  kind  in  patients  of  mine  operated  on  by 
Routier  and  Marion. 


41—2 


CHAPTER  IV 
DISEASES  OF  THE  STOMACH 

I.  GASTRIC  DISTRESS— ACUTE  CATARRHAL  GASTRITIS. 

The  terms  "  gastric  distress  "  and  "  gastric  fever  "  have  been  variously 
interpreted  by  different  writers,  because  each  has  the  drawback  of  referring 
to  an  ill-defined  morbid  condition.  Some  authors  consider  catarrhal 
gastritis  as  a  local  infection,  whilst  others  class  it  amongst  the  group  of 
fevers.     It  seems  easy  to  me  to  reconcile  these  contrary  opinions. 

Gastric  Distress — Catarrh  of  the  Stomach.— The  conditions  united 
under  the  name  of  gastric  distress  or  acute  gastric  catarrh  may  be  the  result 
of  a  local  trouble ;  or  the  expression  of  a  general  condition,  which  is  quite 
different.  If  an  individual  takes  a  heavy  meal,  drinks  too  much  wine,  eats 
rich  food,  alters  his  course  of  living  completely  for  a  few  days,  smokes  too 
much,  or  keeps  late  hours,  he  will  suffer  from  headache,  loss  of  appetite, 
distaste  for  food,  nausea,  and  vomiting.  His  tongue  will  be  thick  and 
coated,  and  he  may  have  sUght  fever.  This  condition  is  due  to  local  gastric 
trouble,  and  this  acute  catarrh  of  the  stomach  cannot  be  mistaken  for  the 
manifestation  of  a  general  condition.  In  other  cases,  in  consequence  of 
the  ingestion  of  tainted  meat,  of  "  high  "  game,  or  indigestible  food,  the 
gastric  disorder  is  the  result  of  auto-intOxication.  The  digestion  is  impaired 
by  the  defective  production  of  hydrochloric  acid,  fermentation  occurs,  and 
the  absorption  of  toxic  substances  causes  gastritis,  with  its  train  of  symptoms 
(Bouchard).  The  ingestion  of  bad  food  may  cause  fatal  ptomaine- poisoning 
(Brouardel  and  Boutmy). 

The  distress  sometimes  appears  under  quite  different  conditions.  A 
person,  without  any  appreciable  cause,  is  taken  ill  with  rigors,  malaise, 
headache,  and  perhaps  epistaxis.  In  the  meanwhile  the  digestive  troubles 
which  I  have  just  described  supervene — complete  anorexia,  pain  in  the 
pit  of  the  stomach,  nausea  or  vomiting,  constipation,  ballooning  of  the 
abdomen,  etc.  The  patient  has  acute  catarrh  of  the  stomach  with  fever, 
but  in  this  case  the  trouble  has  been  preceded  by  a  period  of  invasion,  and 
is  accompanied  by  unmistakable  symptoms.  The  remittent  nature  of  the 
fever,  the  rapid  loss  of  strength,  the  possible  appearance  of  an  exanthem, 

644 


DISEASES  OF  THE  STOMACH  645 

and  the  slowness  of  convalescence,  are  evidence  of  a  morbid  condition  in 
which  the  digestive  troubles  form  only  a  part. 

Gastric  Fever.— Febrile  gastritis  owes  to  the  seasons,  to  localities,  or 
to  the  medical  constitution  of  the  moment,  certain  characteristics  which 
permit  the  description  of  certain  varieties.  It  is  chiefly  in  spring  and 
autumn,  under  the  influence  of  sudden  changes  of  temperature  and  atmo- 
sphere (changes  which  our  predecessors  called  circumfusa),  that  we  meet 
with  epidemic  gastritis.  I  shall  sketch  the  principal  types,  some  of  which 
at  least  belong  to  the  class  of  infectious  diseases. 

Acute  catarrh  of  the  stomach  may  last  a  few  days,  and,  as  it  often  appears 
in  the  remittent  form,  the  disease  has  been  called  remittent  gastric  fever 
by  some  authors.  In  some  cases  it  is  accompanied  by  excessive  secretion 
of  bile  (polychoUa),  and  is  then  called  bilious  gastric  fever.  The  skin  and 
the  conjunctivaB  are  yellowish,  the  hepatic  region  is  tender,  the  liver  is 
sometimes  enlarged,  the  vomit  contains  bile,  and  the  stools  are  hquid,  foetid, 
and  often  bihous.  The  pulse  is  soft,  the  headache  is  intense,  and  the  fever 
is  clearly  remittent.  This  type  of  fever,  which  may  be  observed  in  the 
Mediterranean  region,  and  more  often  in  tropical  countries,  is  generally  the 
result  of  malarial  poisoning. 

In  other  cases  gastric  fever,  especially  in  our  cHmate,  occurs  in  epidemic 
form,  and  is  accompanied  by  headache,  epistaxis,  insomnia,  intestinal 
troubles,  and  diarrhoea,  so  that  the  diagnosis  is  very  difficult  at  first  between 
these  cases  and  typhoid  fever.  Certain  writers  have  expressed  the  opinion, 
which  I  share,  that  this  gastric  fever  is  a  mild  form  of  typhoid  fever.  A 
fact  in  favour  of  this  view  is  that  such  cases  generally  appear  at  the  com- 
mencement of  epidemics  of  typhoid  fever.  After  all,  the  diagnosis,  formerly 
so  diSicult,  is  now  siraphfied  by  Widal's  reaction. 

Prognosis — Treatment. — The  prognosis  is  not  grave.  The  symptoms, 
however,  may  be  comphcated  by  palpitations,  dyspnoea,  or  fits  of  choking, 
which  are  due  to  dilatation  of  the  right  heart.  This  dilatation  is  passive, 
due  to  the  influence  of  gastric  troubles,  and  disappears  with  them  (Potain). 

The  treatment  consists  chiefly  in  the  use  of  purgatives.  In  simple 
catarrh  of  the  stomach  sahne  purgatives  are  sufficient.  Sulphate  of  soda  is 
given  for  two  or  three  days  in  half-ounce  doses  in  vegetable  broth  ;  Birmen- 
storft'  water,  PuUna  water,  etc.,  may  be  given.  If  the  condition  is  more 
severe,  we  must  employ  emetics,  such  as  ipecacuanha  or  ipecacuanha  and 
tartar  emetic,  and  the  next  day  a  saline  purgative.  The  patient  is  dieted, 
and  according  to  circumstances,  is  allowed  acid  drinks,  cold  broth,  and  cold 
milk,  with  Vichy  or  other  alkaline  water  (Vals  or  Saint-Galmier). 


646  TEXT-BOOK  OF  MEDICINE 

II.  ACUTE  GASTRITIS. 

Acute,  phlegmonous,  and  toxic  gastritis  demand  notice  here.  Appen- 
dicular ulcerative  gastritis  will  be  dealt  with  in  a  separate  section. 

Acute  gastritis  is  acute  inflammation  of  the  mucous  membrane  of  the 
stomach.  The  mucosa  is  inflamed,  and  is  sometimes  the  seat  of  erosions 
and  superficial  ulcerations.  The  vessels  are  dilated  and  form  a  fine  net- 
work, while  the  glands  are  enlarged  and  the  stomach  is  covered  with  mucus. 
The  causes  given  under  Gastric  Catarrh  apply  to  this  form.  The  onset  is 
sudden,  and  fever  may  be  present ;  the  patient  complains  of  pain  in  the 
epigastric  region,  vomiting  of  mucus  and  bile  comes  on,  and  is  accom- 
panied by  pain.  The  anorexia  is  complete,  the  thirst  is  great,  the  mouth  is 
dry,  the  tongue  is  red  or  coated  at  times,  and  the  urine  is  scanty  and  high- 
coloured.  Cough  is  fairly  common  ;  it  is  frequent  and  dry  or  succeeded  by 
the  rejection  of  mucus  from  the  stomach. 

Acute  simple  gastritis  is  not  dangerous,  as  comphcations  do  not  occur,  and 
the  patient  recovers  after  a  convalescence  which  requires  care. 

Phlegmonous  Gastritis. — This  form  of  gastritis,  which  is  also  called 
submucous  gastritis,  is  characterized  by  the  formation  of  pus  in  the  sub- 
mucous tissue  of  the  stomach.  The  pus  may  be  spread  out  in  more  or  less 
extensive  sheets,  or  form  abscesses  varying  in  size  from  a  lentil  to  a  walnut. 
The  abscesses  are  most  common  at  the  pylorus,  and  may  be  submucous  or 
subperitoneal.  The  former  may  open  into  the  stomach  by  one  large  opening 
or  by  several  apertures,  which  are  the  orifices  of  the  gUnds  ;  and  the  latter 
may  cause  acute  peritonitis,  unless  adhesions  have  previously  formed  between 
the  stomach  and  the  peritoneum. 

The  symptoms  are  those  of  acute  gastritis,  but  the  pain  is  severe,  the 
vomiting  is  acute,  and  the  fever  is  high  ;  while  dyspnoea,  prostration,  and 
icterus  are  also  seen.  Death  may  supervene  before  the  opening  of  the 
abscess.  If  it  opens  into  the  stomach,  the  contents  are  vomited  ;  if  it  opens 
into  the  peritoneum,  it  causes  acute  fatal  peritonitis.  The  disease  may  end 
in  recovery,  but  the  scar-tissue  sometimes  causes  stricture  of  the  stomach 
or  of  the  pylorus. 

Phlegmonous  gastritis  may  be  primary  or  secondary,  the  latter  form 
being  observed  in  the  infectious  diseases  (smallpox,  pysemia,  or  typhus). 

Toxic  Gastritis. — The  mineral  acids  and  caustic  alkahs  destroy  the 
tissues  of  the  stomach,  but  do  not  cause  inflammation  in  the  true  sense  of 
the  word.  Arsenic,  phosphorus,  the  silver  salts,  and  vegetable  poisons  cause 
necrosis  of  the  coats  of  the  stomach,  but  only  after  an  acute  inflammatory 
stage.  We  find  haemorrhage,  ulceration,  perforations,  and  eschars  which 
may  affect  the  mucous  membrane  or  all  the  coats  of  the  organ.  The  mouth, 
pharynx,  oesophagus,  and  intestine  show  traces  of  the  passage  of  the  poison. 


DISEASES  OF  THE  STOMACH  647 

The  symptoms  are  sudden,  and  their  severity  depends  on  the  nature  of 
the  poison.  Acids  and  caustic  alkaUs  caitse  agonizing  pain  and  absolute 
intolerance  of  the  stomach,  while  the  vomit  often  contains  blood.  The 
pulse  is  small,  the  skin  is  cold  and  covered  with  sweat,  and  the  patient  dies 
of  collapse  or  of  superacute  peritonitis.  When  recovery  does  occur,  it  is 
only  after  a  tedious  convalescence,  followed  in  some  cases  by  stenosis  of 
the  oesophagus,  stomach,  or  pylorus.  When  the  patient  has  swallowed 
toxic  substances  which  act  on  the  whole  organism  (arsenic,  phosphorus, 
vegetable  poisons),  the  gastritis  and  the  poisoning  demand  relief. 

Treatment. — In  simple  acute  gastritis  leeches  may  be  appUed  to  the 
pit  of  the  stomach,  and  the  diet  carefully  regulated.  The  patient  may 
suck  ice  ;  he  may  take  cold  drinks  or  small  quantities  of  cold  milk  to  which 
lime-water  and  cocaine  are  added.  An  ice-bag  or  cold  compresses  are 
apphed  to  the  epigastrium.  The  pain  is  relieved  by  injections  of  morphia. 
Similar  measures  may  be  employed  in  phlegmonous  gastritis.  The  first 
indication  in  the  case  of  toxic  gastritis  is  to  get  rid  of  the  poison  by  vomiting 
at  the  earliest  possible  moment,  and  then  to  administer  an  antidote.  Treat- 
ment is  only  effective  when  it  is  applied  soon  after  the  intoxication. 

III.  CHRONIC  GASTRITIS. 

^Etiology. — Chronic  gastritis  often  follows  acute  or  subacute  gastritis, 
and  even  when  it  seems  to  be  chronic  from  the  first,  it  is  preceded  by  dyspeptic 
symptoms,  which  indicate  its  gradual  onset.  Of  all  the  causes  which  I  have 
enumerated  under  Acute  Gastritis,  and  which  I  might  again  mention  in  con- 
nection with  chronic  gastritis,  alcohoHsm  is  the  most  important  and  the 
most  frequent.  The  abuse  of  alcoholic  drinks,  especially  of  those  of  inferior 
quahty,  is  the  usual  cause  of  chronic  gastritis.  By  alcoholism  I  do  not 
refer  only  to  the  excessive  use  of  alcoholic  diinks,  but  I  also  allude  to  the 
excess  of  alcohol  taken  by  people  who  never  get  drunk,  but  who  in  the 
course  of  years  poison  themselves  slowly,  and  so  contract  gastritis  and 
cirrhosis.  Amongst  other  contributory  causes  I  may  mention  gout,  tuber- 
culosis, and  most  of  the  infectious  diseases. 

Pathological  Anatomy. — The  mucosa  is  red,  pigmented,  studded  with 
lia-morrhagic  erosions,  thick  and  smooth,  or  mammillated.  It  sometimes 
has  a  polypoid  appearance,  especially  at  the  pylorus.  The  submucous  and 
muscular  coats  are  thickened,  giving  a  special  firmness  and  resistance  to 
the  walls  of  the  stomach.  This  hypertrophic  sclerosis  of  the  sul)mucous 
layer  is  the  chief  lesion  in  some  cases.  Under  the  microscope  these  lesions 
are  seen  to  be  glandular  and  interstitial.  As  far  as  the  glands  are  con- 
cerned, the  epithcliuiu  is  granular  ;  the  cul-de-sac  is  granulo-fatty,  and 
some  glands  have  undergone  cystic  dilatation. 


648  TEXT-BOOK  OF  MEDICINE 

The  cells  of  the  glands  undergo  a  retrogressive  change,  become  flattened, 
and  have  the  appearance  of  cubical  epithehal  cells.  These  atypical  cells 
block  some  of  the  ducts,  and  when  we  notice  how  closely  the  condition 
resembles  epithelioma  we  are  tempted  to  admit  that  there  is  no  sharp  line 
of  demarcation  between  chronic  gastritis,  adenoma,  and  cancer.  The 
adenomatous  changes  in  the  glands  assume  various  forms.  We  find  flat 
(Andral),  pedunculated  (Cruveilhier),  or  nodular  adenoma,  which  some- 
what resembles  the  convolutions  of  the  brain.  The  interstitial  and  inter- 
muscular tissue  is  hyperplastic.  When  the  fibrosis  chiefly  affects  the 
pylorus,  it  produces  stenosis,  and  later  dilatation  of  the  stomach. 

As  the  interstitial  tissue  increases  the  glands  disappear,  which  explains 
the  almost  entire  absence  of  free  hydrochloric  acid  and  pepsin.  In  other 
cases,  however,  the  adenomatous  degeneration  is  more  marked  than  the 
formation  of  fibrous  tissue,  and  as  a  result  the  chronic  gastritis  assumes 
the  adenomatous  type.  Superficial  ulcerations  are  sometimes  found  which 
do  not  extend  beyond  the  mucosa.  Small  abscesses  may  also  be  present  in 
the  walls  of  the  stomach. 

Symptoms. — In  very  many  cases  the  symptoms  at  first  resemble  those 
of  simple  dyspepsia  so  closely  that  a  separate  description  is  not  possible. 
As  the  disease  progresses  the  patient  complains  of  epigastric  pain,  which  is 
more  acute  after  a  meal.  Loss  of  appetite,  eructations,  and  ballooning  of 
the  abdomen  are  constant.  Vomiting  is  frequent,  and  besides  the  food 
which  has  remained  a  longer  or  shorter  period  in  the  stomach,  the  patient 
brings  up  mucus,  especially  in  the  morning.  This  mucus  is  composed  of 
the  gastric  secretions  and  the  saHva  swallowed  during  the  night.  Chronic 
gastritis  is  often  accompanied  by  buccal  catarrh,  obstinate  constipation, 
and  congestion  of  the  Hver.  Duodenitis,  with  or  without  ulceration  of  the 
mucous  membrane,  has  also  been  noticed. 

Examination  of  the  epigastric  region  sometimes  reveals  induration  of 
the  stomach.  While  it  simulates  cancer,  it  is  really  due  to  the  fibrosis  of 
the  submucous  tissue.  Heematemesis  may  also  occur,  as  in  a  case  quoted 
by  Trousseau.  When  the  stomach  is  dilated,  the  enlargement  is  revealed 
on  percussion  by  a  tympanitic  note.  If  the  stomach  contains  fluid,  we  can 
obtain  a  succussion  splash  by  gently  shaking  the  patient. 

Wasting  and  loss  of  strength  result  from  chronic  gastritis.  Under  the 
influence  of  treatment  improvement  is  often  noticed,  with  long  remissions 
and  even  cure  may  occur ;  in  severe  cases,  especially  when  cirrhosis  of  the 
liver  or  Bright's  disease  is  present,  the  disease  runs  a  progressive  course, 
and  is  generally  incurable. 

Diagnosis — Treatment. — The  diagnosis  of  chronic  gastritis  from  ulcer 
and  from  cancer  of  the  stomach  will  be  given  later.  The  treatment  will 
be  discussed  under  Dyspepsia. 


DISEASES  OF  THE  STOMACH  649 

I  must  specially  mention  the  diagnosis  of  chronic  gastritis  from  the  gastric 
manifestations  of  uraemia.  Ursemic  vomiting  and  gastritis  are  easily  recog- 
nizable when  they  supervene  in  a  patient  with  confirmed  Bright' s  disease.  In 
some  cases,  however,  vomiting  is  the  first  apparent  manifestation  of  Bright's 
disease,  and  if  this  cause  is  not  thought  of,  an  error  in  diagnosis  will  result. 

Milk  diet  often  gives  excellent  results  in  chronic  gastritis.  Gastrorrhoea 
and  flatulence  which  resist  medical  measures  are  sometimes  improved  by 
lavage. 

IV.  DYSPEPSIA. 

Dyspepsia,  or  difficulty  in  digestion,  is  a  symptom  common  to  many 
acute  or  chronic  diseases.  Even  when  this  symptom  becomes  so  prominent 
as  to  constitute  a  pathological  species,  it  remains  subordinate  to  morbid 
conditions  which  differ  widely  from  each  other  (Trousseau).  Dyspepsia, 
therefore,  is  only  a  symptom  ;  it  is  not  a  morbid  entity. 

Several  classifications  have  been  proposed.  Dyspepsia  has  been  looked 
upon  as  a  kind  of  neurosis  or  as  a  chronic  affection  of  the  glands  of  the 
stomach.  Glandular,  mucous,  or  neuro- vascular  dyspepsia,  and  dyspepsia 
ah  ingestis,  have  all  been  described.  Giibler  has  divided  dyspepsia  into 
painful,  atonic,  catarrhal,  and  inflammatory. 

As  I  cannot  enter  here  into  full  details,  I  must  be  content  to  mention  its 
principal  characteristics  and  its  most  important  varieties,  and  I  refer  the 
reader  to  special  monographs  for  fuller  details. 

Pathogenesis. — It  is  unnecessary  to  give  details  of  the  chemistry  of  the 
stomach,  because  authors  are  not  unanimous  in  opinion.  The  question  is 
at  present  somewhat  obscure.  I  have  had  a  recent  proof  of  this  in  a  patient 
whom  I  had  sent  to  Vichy.  Fremont  wrote  to  me  :  "  Striking  dispro- 
portion between  the  chemical  reactions,  which  are  almost  normal,  and  the 
dyspepsia,  which  is  extreme." 

In  reducing  gastric  digestion  to  its  simplest  physiological  expression  we 
find  two  factors  :  (1)  movements,  (2)  secretions.  If  the  movements  of  the 
stomach  become  irregular  or  lose  their  force,  if  they  become  too  slow  or 
too  quick,  or  if  there  is  no  harmony  between  the  mechanical  (movement) 
and  the  chemical  acts  (secretion),  dyspepsia  is  the  result.  If  the  secretions 
of  the  stomach  are  changed  in  quantity  or  quality,  if  the  acid  and  the 
pepsin  of  the  gastric  juice  are  no  longer  in  the  proper  proportions,  then 
the  chemical  act  of  digestion  is  imperfect,  and  we  have  dyspepsia.  I  hasten 
to  state  that  the  chemical  trouble  is  the  essential  factor  in  dyspepsia. 

The  gastric  juice  owes  its  antiseptic  action  to  the  hydrochloric  acid, 
which  prevents  abnormal  fermentation  in  the  stomach.  Oxygen,  nitrogen, 
carbonic  acid  gas,  hydrogen,  and  sulphuretted  hydrogen,  may  be  set  free 


650  TEXT-BOOK  OF  MEDICINE 

by  abnormal  fermentation,  which  is  one  of  the  most  common  causes  of 
tympanites  and  of  eructation  of  gas. 

The  bacilU  of  lactic  and  butyric  acid  fermentation,  the  spores  of  the 
Mycodenna  aceti,  and  many  other  micro-organisms,  have  a  useful  or  harmful 
action.  They  may  irritate  the  mucosa,  thus  favouring  distension  of  the 
stomach.  They  may  also  produce  toxic  matter,  and  neutralize  the  hydro- 
chloric acid.  When  we  remember  that  the  various  factors  of  digestion 
must  act  in  perfect  harmony  in  order  that  the  function  may  be  normal, 
and  that,  on  the  other  hand,  if  one  of  these  factors  is  altered,  the  digestive 
process  as  a  whole  is  deranged,  it  is  easy  to  see  that  many  causes  may  bring 
on  dyspepsia.  According  to  Ewald's  happy  expression,  there  is  "  gastric 
insufficiency." 

"In  the  stomach,"  says  Guyon,  "the  fermentations  are  of  two 
types  :  in  the  one  they  result  from  organic  stenosis,  and  are  only  an  epipheno- 
menon  which  occasions  no  trouble ;  in  the  other,  they  exist  apart  from  any 
organic  lesion  and  distension.  We  then  speak  of  fermentative  dyspepsia, 
described  formerly  under  the  name  of  flatulent  or  acid  dyspepsia."  Naunym 
was  the  first  to  draw  attention  to  these  gastric  fermentations.  As  A.  Kobin 
has  proved,  this  form  of  dyspepsia  may  be  primary,  and  lead  to  functional 
troubles,  or  secondary  to  hyperchlorhydria  or  hypochlorhydria.  As  a 
matter  of  fact,  we  do  not  know  whether  there  are  special  types  of  fermenta- 
tion, accompanied  by  special  symptoms  and  characterized  by  special  micro- 
organisms. 

The  causes  of  dyspepsia  are  at  times  easily  grasped  ;  in  other  cases 
they  are  but  hypotheses.  In  the  enumeration  of  the  causes  I  do  not  include, 
of  course,  acute  and  chronic  gastritis,  dilatation  of  the  stomach,  or  ulcer 
and  cancer,  where  dyspepsia  is  merely  symptonaatic  of  the  different  morbid 
entities,  and  is  only  of  importance  as  regards  the  diagnosis. 

Amongst  the  most  frequent  causes  of  dyspepsia,  some  are  local  and  the 
direct  result  of  the  inefficient  action  of  the  stomach,  while  others  depend 
upon  some  general  disease  or  remote  lesion.  Amongst  the  former  we  must 
place  the  question  of  foods.  A  person  who  has  been  in  the  habit  of  stimu- 
lating the  stomach  by  means  of  highly-spiced  foods  or  alcohol  will  suffer 
from  dyspepsia  if  he  suddenly  stops  the  stimulant.  So,  too,  indefinite 
stimulation  will  end  in  catarrh  and  gastritis.  In  large  eaters  and  heavy 
drinkers  the  stomach  becomes  dilated  and  the  muscular  irritability  is 
reduced.  This  muscular  asthenia  is  a  cause  of  dyspepsia.  The  opposite 
excess — viz.,  deprivation  of  food — also  favours  dyspepsia.  Excessive  work, 
sedentary  habits,  night  work,  and  worry  produce  a  Hke  result,  and  produce 
a  form  of  dyspepsia  which  we  shall  study  later  under  the  name  of  Gastroxia. 

In  the  second  category  we  must  place  dyspepsia  due  to  disease  of  a  more 
or  less  remote  organ.     Dyspepsia  is  often  associated  with  diseases  of  the 


DISEASES  OF  THE  STOMACH  651 

liver  or  of  the  uterus,  with  pregnancy,  and  with  diseases  of  the  heart,  the 
kidneys  (Bright's  disease),  or  the  bladder  and  the  urethra  (Guyon). 

To  a  third  category  belong  the  dyspeptic  troubles,  resulting  from 
ansemia,  chlorosis,  tuberculosis,  syphihs,  gout,  and  neuroses,  of  which 
neurasthenia  deserves  special  mention. 

Each  of  these  causes  should  be  studied  in  detail.  Thus,  the  dyspepsia 
which  is  associated  with  genito-urinary  diseases  may  result  from  fever  or 
from  some  infection  (catarrh  of  the  bladder,  pyehtis).  It  may  also  be  the 
consequence  of  Bright's  disease  and  uraemia. 

Dyspepsia  in  tubercular  patients,  which  is  often  associated  with  lesions 
of  the  stomach,  and  is  often  so  marked  at  an  advanced  period  of  the  disease, 
may  be  present  from  the  first,  and  exactly  simulate  dyspepsia  of  anaemic 
origin,  although  it  is  really  a  question  of  tuberculosis. 

Gouty  dyspepsia,  so  characteristic  and  so  frequent  that  it  may  be  said 
that  the  stomach  is  to  gout  what  the  heart  is  to  rheumatism,  shows  various 
forms.  It  may  precede  the  attack  of  gout  or  may  exist  apart  from  any 
joint  trouble  in  gouty  people. 

Dyspepsia  in  neurasthenic  patients  seems  to  be  rather  the  cause  than 
the  effect  of  the  neurasthenia. 

Symptoms. — The  functional  troubles  may  be  divided  into  several 
varieties.  These  divisions,  however,  are  artificial,  and  the  different  varieties 
are  sometimes  associated  in  the  same  patient. 

As  a  rule,  dyspepsia  is  accompanied  by  loss  of  appetite.  The  patient 
does  not  feel  hungry,  and  even  when  fasting  experiences  a  feeUng  of  fulness 
in  the  stomach.  He  sometimes  complains  of  cramp  in  the  stomach,  due  in 
part  to  spasms  of  the  pylorus.  When  he  has  begun  his  meal,  he  eats 
sufficient,  but  is  careful  to  avoid  certain  foods,  such  as  meat,  fish,  fats,  and 
vegetables  which  do  not  agree.  Digestion  is  retarded.  It  is  sometimes 
accompanied  by  pains  in  the  stomach,  ballooning  of  the  epigastric  region, 
congestion  of  the  face,  drowsiness,  pain,  eructations,  and  in  some  cases  by 
retching  and  vomiting.  The  pain  and  tympanites  may  not  appear  till  two 
or  three  hours  after  a  meal.  In  the  morning  the  patient  suffers  from  dry- 
ness of  the  mouth,  bitter  taste,  and  coated  tongue.  The  epigastric  region 
is  sensitive  ;  constipation  is  the  rule.  This  condition  of  the  digestive  tract 
(gastro-intestinal  dyspepsia)  often  affects  the  entire  economy.  The  affec- 
tion may  be  the  result  of  reflex  action,  such  as  arrhythmia  or  dilatation  of  the 
riglit  side  of  the  heart  (Potain),  or  of  auto-intoxication  (Bouchard).  The 
dyspeptic  complains  of  headaclie,  vertigo,  and  inaptitude  for  work  ;  anaomia, 
loss  of  flesh,  hypochondria,  and  neurasthenia  supervene.  If  the  reader  will 
refer  to  Neurasthenia,  he  will  find  the  relation  between  neurasthenia  and 
dyspepsia. 

The  general  symptoms  may  in  time  become  very  severe.     The  patient 


652  TEXT-BOOK  OF  MEDICINE 

complains  of  palpitation  and  shortness  of  breath.  The  skin  becomes  pale 
and  earthy,  and  the  emaciation  is  so  great  that  we  are  apt  to  suspect  cancer 
of  the  stomach. 

Flatulent  dyspepsia  is  characterized  by  abundant  formation  of  gas, 
which  is  associated  with  the  other  dyspeptic  troubles.  After  a  meal,  gas 
forms  in  the  stomach  and  the  intestine,  the  swelhng  being  so  marked  that 
the  patient  is  compelled  to  loosen  his  clothes.  Eructations  are  at  times 
abundant,  and  afford  rehef.  The  gastro-intestinal  pneumatosis  is  not 
exclusively  due  to  abnormal  fermentation,  but  results  sometimes  from  a 
secretion  of  gas  analogous  to  that  seen  in  hysterical  patients.  It  has  also 
been  stated  that  the  gas  forms  in  the  intestine,  and  is  driven  back  into  the 
stomach  by  antiperistalsis  (Leven). 

In  acid  dyspepsia  the  vomit  is  acid,  and  causes  a  burning  sensation  in 
the  throat  (pyrosis).     Acid  vomiting  is  most  pronounced  in  gastroxia. 

In  one  form  of  dyspepsia,  boulimia  replaces  loss  of  appetite.  It  is 
generally  met  with  in  women  suffering  from  hysteria  or  gastralgia.  The 
patient  experiences  a  continual  sensation  of  emptiness  in  the  stomach,  and 
is  always  hungry.  Even  when  the  hunger  is  satisfied,  it  is  accompanied 
with  a  feeling  of  faintness.  This  form  is  not,  as  a  rule,  accompanied  by 
eructations,  flatulence,  or  constipation.     Diarrhoea  is  more  often  present. 

In  gouty  persons  dyspeptic  troubles  are  often  associated  with  congestion 
of  the  liver  and  hypersecretion  of  bile  (polycholia).  These  hepato-gastric 
troubles  often  alternate  or  coincide  with  eczematous  eruptions. 

Writers  have  described  under  the  name  of  gastroxi^  nervosa  a  dyspeptic 
condition  that  comes  on  in  fits,  and  is  perhaps  a  variety  of  migraine.  The 
attacks  are  most  common  during  mental  strain.  They  come  on  every  month 
or  two,  and  disappear  under  the  influence  of  rest  or  of  change  of  air.  The 
health  is  excellent  between  the  attacks.  The  attack  is  characterized  by 
violent  headache,  burning  pain  in  the  stomach,  and  vomiting  of  acid  fluid, 
which  leaves  an  acrid  feeling  in  the  pharynx  for  several  hours.  Analyses 
have  shown  the  presence  of  an  excess  of  hydrochloric  and  lactic  acids. 
The  attacks  may  be  checked  by  very  hot  water.  Unless  treatment  is 
given,  they  last  for  a  longer  or  shorter  period. 

Course — Diagnosis — Treatment. — Dyspepsia  is  essentially  chronic,  and 
subject  to  recurrence,  especially  in  the  gouty  form.  Though  we  have 
separated  it  from  chronic  catarrh  of  the  stomach,  it  must  be  remarked  that 
the  symptoms  of  dyspepsia  and  of  gastritis  are  so  closely  allied  that  we  are 
frequently  compelled  to  include  both  in  the  same  description.  The  difiiculty 
in  diagnosis  is  not  the  recognition  of  dyspepsia  ;  it  consists  in  discovering 
whether  the  trouble  is  purely  functional  or  whether  it  is  the  result  or  the 
cause  of  some  nervous  condition  (neurasthenia),  and  also  whether  it  is  a 
manifestation  of  some  remote  lesion  (tuberculosis,  pyelitis,  nephritis),  or  the 


DISEASES  OF  THE  STOMACH  653 

forerunner  of  disease  of  the  stomach,  such  as  ulcer  or  cancer.  The  problem 
is  sometimes  difficult  to  solve,  because  the  symptoms  of  cancer  are  at  times 
preceded  by  a  long  period  of  dyspepsia,  wliich  may  be  associated  or  not  with 
chronic  gastritis  and  adenomatous  changes  in  the  stomach. 

The  treatment  varies  with  the  nature  and  the  cause.  Analysis  of  the 
chyle  may  help  to  show  whether  the  acid  is  in  excess  or  not.  Proper  foods 
(milk,  strong  meats,  white  meats)  and  beverages  (alkaUne,  bitter  or  fer- 
mented drinks),  regular  meals,  and  suitable  exercise— or,  in  a  word,  a  correct 
regime — play  a  great  part  in  the  treatment  of  dyspepsia.  In  many  cases 
(simple  or  gouty  dyspepsia)  alkaUs,  lime  -  water,  Vichy  water,  Pouges, 
Carlsbad,  or  Homburg  waters  are  indicated.  In  gastro-intestinal  catarrh 
mild  purgation  is  needed  (BirmenstorfE  or  Pullna  water).  Belloc's  charcoal 
is  indicated  in  flatulent  dyspepsia,  wliich  is  often  accompanied  by  acid 
eructations.  Alkaline  preparations  are  also  of  use  if  replaced  in  a  few  days 
by  quassia,  calumba,  or  other  bitter  tinctures.  If  anaemia  is  present, 
chalybeate  waters  (Spa  and  Forges)  should  be  selected. 

In  my  opinion.  Trousseau's  plan  is  the  best.  Flatulent  dyspepsia  is  the 
most  frequent  form,  and  its  usual  symptoms  are  loss  of  appetite,  constipa- 
tion, foul  tongue,  ballooning  of  the  abdomen,  eructations  after  a  meal, 
headache,  congestion  of  the  face,  and  vertigo.  In  these  cases  I  advise  the 
following  measures  : 

1.  Take  every  morning  when  fasting  half  a  glass  of  Vichy  water 
(Celestins). 

2.  Before  the  two  principal  meals  take  3  drops  of  Baume's  bitter  tincture 
in  a  spoonful  of  water. 

3.  During  the  meal  take  a  cachet  composed  of — 

Prepared  chalk  ^ 

Bicarbonate  of  soda  [^  . .  . .  . .     aa  2  grains. 

Magnesia  J 

•1.  If  constipation  is  severe,  the  cachets  are  replaced  by  the  following  : 

Bicarbonate  of  soda  . .  . .  . .     4  grains. 

Rhubarb  . .  . .  . .     3  grains. 

5.  Take  after  the  meal  1  or  2  tablespoonfuls  of  lime-water. 

6.  If  pain  is  present,  xV  grain  cocaine  is  added  to  the  hme-water. 

7.  In  the  case  of  constipation,  take  a  mild  purgative  on  going  to  bed  — 
either  a  teaspoonful  of  Vichy  laxative  powder  in  half  a  glass  of  ]^ivian  water, 
or  a  cascara  pill. 

8.  Eat  foods  that  agree  well.  Drink  at  meals  Evian,  Alet,  or  Vittel 
water,  with  or  without  red  or  white  wine. 

9.  Avoid  alcoholic  beverages  and  pure  wine.  Hot  infusions  after  meals, 
such  as  tea,  coffee,  or  camomile,  are  permitted. 

10.  Take  a  cure  at  Vichy  or  Pouges. 


654  TEXT-BOOK  OF  MEDICINE 

Some  kinds  of  dyspepsia  are  not  relieved  by  alkalis,  and  must  therefore 
be  treated  with  acids.  The  patient  is  given  hydrochloric  acid,  diluted  with 
water,  after  each  meal. 

Dyspepsia,  accompanied  by  bouhmia,  sensation  of  emptiness  in  the 
stomach,  and  diarrhoea,  which  comes  on  directly  after  taking  food,  is  reheved 
by  small  doses  of  opium.  One  or  two  drops  of  Sydenham's  laudanum 
before  each  meal  will  suffice. 

Lavage  of  the  stomach  is  sometimes  very  useful,  especially  if  the 
dyspepsia  results  from  catarrh,  with  or  without  dilatation  of  the  organ. 

Fremont  has  suggested  the  employment  of  gasterine  (animal  gastric 
juice).  I  have  found  it  useful,  especially  in  obstinate  dyspepsia.  "  Gas- 
terine is  an  acid,  watery  fluid,  with  great  digestive  power.  It  is  the  type 
of  stomachic  opotherapy,  and  is  apphcable  in  all  cases  of  insufficient  secretion 
by  the  stomach,  except  cancer."  Gasterine  is  administered  in  doses  of 
3  to  10  ounces  daily,  mixed  with  milk,  beer,  broth,  water,  or  wine,  either 
during,  before,  or  after  a  meal. 

V.  GASTRALGIA. 

etiology. — Gastralgia  (cramp  in  the  stomach)  is  neuralgia  of  the 
nerves  of  the  stomach.  It  is  sometimes  essential  and  compiises  the  whole 
disease,  but  at  other  times  it  is  secondary  and  appears  as  a  symptom  of 
various  morbid  conditions. 

It  may  be  brought  on  by  cold,  fatigue,  worry,  or  the  use  of  stimulants. 
It  is  a  frequent  symptom  in  dyspepsia,  hysteria,  neurasthenia,  anaemia,  and 
uterine  diseases.  It  is  caused  by  phthisis,  gout,  malaria,  and  certain 
affections  of  the  spinal  cord,  notably  locomotor  ataxy.  In  one  case  it  was 
undoubtedly  connected  with  the  reduction  of  a  varicocele. 

Description. — Pain  is  the  essential  and  at  times  the  only  symptom. 
It  occurs  in  paroxysms,  which  are  generally  spontaneous  and  independent 
of  the  ingestion  of  food.  The  pain  is  sometimes  preceded  by  eructations, 
nausea,  or  pyrosis.  The  attack  of  pain  may  be  slight  and  Hmited  to  the 
epigastric  region,  with  or  without  spasms  of  the  pylorus.  At  other  times 
it  is  acute,  and  accompanied  by  vomiting  and  syncope.  The  pain  is  of  the 
most  varied  character ;  it  may  be  stabbing  or  agonizing,  and  radiates  to 
the  back,  the  thorax,  and  the  base  of  the  chest.  It  may  invade  the  abdomen 
and  reach  the  hypochondria,  the  kidneys,  or  even  the  spermatic  cord.  In 
severe  attacks  the  face  is  white  and  pinched,  and  the  patient  is  obliged  to 
press  upon  the  painful  region,  seeking  to  diminish  his  suffering  by  assuming 
every  possible  position.  The  attack  may  last  for  some  minutes,  but  in 
other  cases  the  duration  may  vary  from  a  quarter  of  an  hour  to  an  hour. 
It  may  return  several  times  in  the  twenty-four  hours,  and  on  several  con- 
secutive days. 


DISEASES  OF  THE  STOMACH  655 

If  gastralgia  is  associated  with  dyspepsia  or  gastric  catarrh,  digestive 
troubles  are  also  present.  In  other  cases  digestion  is  normal,  and  the 
appetite  is  good,  or  at  times  increased.  In  hysterical  and  chlorotic  women 
the  taste  is  perverted  (pica).  In  locomotor  ataxy  the  attacks  (gastric 
crises)  have  the  characteristics  which  are  described  in  the  chapter  on  Tabes, 
and  may  be  the  first  symptom.  The  duration  of  gastralgia  is  subordinate 
to  its  cause.     It  may  be  transient  or  persistent  and  subject  to  repetitions. 

Diagnosis. — Simple  ulcer  of  the  stomach  provokes  pains  hke  those  of 
gastralgia,  but  the  ulcer  is  recognized  by  other  symptoms,  such  as  intoler- 
ance of  certain  foods,  the  appearance  or  the  aggravation  of  the  pain  after 
meals,  the  xiphoidal  or  spinal  seat  of  the  pain,  and  the  presence  of  blood  in 
the  vomit  (hsematemesis).  Cancer  of  the  stomach  causes  less  pain,  but  this 
lesion  is  sometimes  ushered  in  by  persistent  epigastric  pain,  and  the  diagnosis 
must  be  made  from  gastralgia.  The  age  of  the  patient,  the  gradual  wasting, 
liaBmatemesis,  melsena,  phlegmasia  alba  dolens,  presence  of  gastric  tumour, 
and  hypochlorhydria,  are  important  points  in  cancer.  Gastralgia  must  not 
be  confounded  with  superficial  neuralgia  of  the  skin  or  of  the  muscular 
layers  of  the  epigastric  region.  Epigastralgia  and  neuralgia  of  tlie 
intercostal  nerves  are  accompanied  by  hypersesthesia,  which  is  easily 
provoked  by  pressure  at  the  exit  of  the  nerve  branches.  Slight  attacks  of 
hepatic  colic,  particularly  if  jaundice  is  absent,  are  frequently  mistaken 
by  patients  for  gastralgia.  In  order  to  avoid  this  mistake  we  must  localize 
the  seat  of  the  pain,  which  in  hepatic  colic  is  in  the  right  hypochondrium, 
and  frequently  radiates  to  the  right  shoulder.  The  Uver,  which  is  often 
painful  and  enlarged,  must  be  percussed,  and  the  urine  tested,  as  it  often 
contains  bile  pigment.  Hepatic  colic,  even  if  slight,  is  at  times  accom- 
panied by  vomiting,  and  followed,  if  not  by  icterus,  at  least  by  a  subicteric 
tinge  of  the  conjunctivae. 

It  is  not  sufficient  to  diagnose  gastralgia  ;  the  cause  must  also  be  ascer- 
tained, for  the  prognosis  largely  depends  on  it.  We  must  find  whether  the 
gastralgia  is  purely  nervous,  symptomatic  (ulcer,  cancer,  tabes),  or  an  early 
symptom  of  pulmonary  tuberculosis. 

Treatment. — In  the  attack  the  first  point  is  to  relieve  the  pain.  Ice- 
bags  are  applied  over  the  stomach,  aspirin  or  antipyrin  is  prescribed,  and  an 
injection  of  morpliia  in  the  epigastric  region  is  administered,  according  to 
the  duration  and  intensity  of  the  attack. 

In  the  intervals  the  cause  must  be  treated  :  antispasmodics  (valerian, 
bromide  of  potassium)  in  cases  where  the  nervous  element  predominates, 
alkalis  and  bitters  if  the  gastralgia  is  associated  with  one  of  tlie  forms  of 
dyspepsia  previously  described.  Laudanum  sliould  be  given  before  meals 
if  the  attacks  of  pain  are  provoked  by  the  ingestion  of  food.  Milk  diet  is 
also  indicated.     In  many  cases  hydrotherapy  renders  valuable  services. 


656  TEXT-BOOK  OF  MEDICINE 

VI.  ULCERATION  OF  THE  STOMACH— GENERAL 
CONSIDERATIONS. 

Erosions  and  Ulcerations.— Ulceration  of  the  stomach,  from  a  simple 
erosion  to  the  complete  destruction  of  the  wall,  occurs  in  widely  different 
conditions.  Hsemorrhagic  erosions  are  found  in  alcoholic  or  uraemic 
gastritis  (Treitz),  and  in  gastritis  of  the  new-born,  which  is  called  "  ulcerous 
gastropathy  "  (Parrot). 

1.  If  in  an  infant  the  skin  dries  quickly  and  becomes  bluish,  the  eyes  are 
sunken,  and  the  face  is  pinched,  and  the  vomit  contains  brownish  flakes, 
ulceration  of  the  stomach  should  be  suspected.  Post  mortem,  the  stomach 
is  found  covered  with  a  thick  layer  of  mucus,  and  studded  with  blackish 
clots  of  blood,  modified  by  the  gastric  juice.  Beneath  the  mucus  the 
erosions  form  circular  ulcers,  some  being  hardly  visible  to  the  naked  eye, 
while  others  are  more  than  a  milhmetre  in  diameter.  They  are  chiefly 
found  on  tlie  greater  curvature  and  in  the  pyloric  region.  Histological 
examination  shows  that  the  ulceration  affects  the  entire  mucous  membrane 
(Parrot).  Sometimes  it  destroys  the  superficial  part  of  the  glands,  and  at 
other  times  the  glandular  layer:     The  venous  congestion  is  marked, 

2.  Haemorrhagic  erosions  of  the  stomach  are  also  seen  in  venous  stasis 
(obstruction  in  the  portal  circulation,  diseases  of  the  Uver  and  heart).  The 
erosions  are  generally  small  and  rounded,  with  flat  edges,  but  they  some- 
times follow,  in  a  more  or  less  capricious  manner,  Hnes  or  circles  in  relation 
to  the  submucous  veins.  Half  a  dozen  are  found,  on  an  average,  to  a  square 
centimetre,  and  the  largest  never  exceed  2  milhmetres  in  diameter.  The 
lesion  seems  to  be  both  inflammatory  and  necrobiotic.  The  blood-stasis 
and  the  inflammation  succeed  one  another,  or  combine  to  bring  about  the 
death  of  the  tissue. 

3.  Tuberculosis,  which  is  essentially  a  destructive  affection,  does  not 
always  spare  the  stomach.  Functional  troubles  are  frequent,  but  tubercu- 
lar ulcerations  of  the  stomach  are  so  rare  that  Marfan  quotes  but  fourteen 
cases,  and  Letorey  has  collected  only  twenty-one  authentic  cases.  The 
ulcers  vary  much  in  character.  Sometimes  they  are  as  small  as  a  pin's 
head  ;  at  other  times  they  are  4  to  5  centimetres  in  diameter.  The  edges 
are  ragged  and  irregular.  Tubercles  are  often  seen  on  the  floor  and  the 
circumference  of  the  ulcer.  Bacteriological  examination  has  several  times 
revealed  bacilh.  Tubercular  ulcers  of  the  stomach  are  nearly  always 
secondary,  and  develop  in  patients  already  suffering  from  tuberculosis. 
They  are  usually  latent,  and  are  found  by  chance  at  the  post-mortem 
examination.  The  tubercular  ulcer,  unhke  the  simple  ulcer  of  Cruveilhier, 
has  little  tendency  to  perforation.  Hsematemesis,  though  rare,  is  a  possible 
comphcation.     It  may  be  fatal,  as  in  two  cases  quoted  by  Letorey. 


DISEASES  OF  THE  STOMACH  657 

On  microscopic  examination  the  subglandular  zone  of  the  mucous 
membrane  and  the  tunica  submucosa  are  found  to  be  infiltrated  with 
tubercles ;  the  tubercular  infiltration  also  follows  the  vessels  of  these 
regions.  The  ulceration  attacks  the  mucous  membrane,  as  a  rule,  and 
rarely  extends  beyond  the  submucous  layer.  The  peritoneum  over  the 
ulcer  is  thickened,  but  tubercles  are  rare.  In  exceptional  cases  the  ulcera- 
tion may  involve  the  gastro-epiploic  vessels,  and  produce  fatal  haemorrhage, 
or  cause  perforation  of  the  stomach,  with  acute  peritonitis.  Perforation 
of  the  stomach  in  the  six  known  cases  has  always  been  produced  from 
without  inwards,  by  peritonitis,  colitis,  or  tubercular  adenitis. 

F.  Arloing,  who  has  written  an  important  monograph  on  tubercular 
ulceration  of  the  stomach,  comes  to  the  following  general  conclusions  : 

"  Tubercular  ulceration  of  the  stomach  is  not  common  in  man  and  in 
animals.  It  is  always  accompanied  by  other  tubercular  lesions  in  the 
viscera.  The  different  forms  of  tubercular  ulcerations  seen  in  man  may 
be  reproduced  experimentally. 

"  Direct  penetration  of  Koch's  bacillus  through  the  healthy  or  diseased 
mucous  membrane,  either  naturally  or  experimentally,  seems  doubtful. 
Clinically,  it  is  probable  that  the  infectious  agent  (bacillus  or  toxine)  selects 
the  blood-passages  in  order  to  reach  the  mucous  membrane.  The  ulcera- 
tion may  be  either  histologically  tubercular  or  toxi-infectious  without 
histological  manifestations." 

4.  Typhoid  fever  may  cause  ulceraition  of  the  stomach  (Chauffard)  in 
very  exceptional  cases.  Millard's  case  is  usually  quoted,  but  in  the  section 
on  Appendicular  Ulcerative  Gastritis  we  shall  find  that  this  case  must  be 
revised,  because  it  has  perhaps  not  been  interpreted  correctly.  Ulceration 
of  the  stomach,  though  appearing  in  the  course  of  enteric  fever,  may  still 
persist  as  a  sequela  after  recovery  from  the  fever,  as  Cazeneuve's  observa- 
tions prove. 

5.  Large  burns  on  the  surface  of  the  body  and  contusions  of  the  epi- 
gastric region  may  also  be  followed  by  ulcer  of  the  stomach.  Cases  in  which 
epigastric  traumatism  has  induced  ulcus  simplex  have  been  quoted. 

G.  Syphilitic  ulceration  of  the  stomach  will  be  described  separately. 
Gummatous  ulcers  are  common,  and  often  coincide  with  tertiary  lesions 
in  other  regions. 

7.  The  next  three  sections  are  devoted  to  the  study  of  erosions  and 
of  acute  ulceratioji  of  the  stomach  due  to  toxic  poisoning.  Haemorrhage 
is  frequent,  and  it  may,  indeed,  be  said  that  haematemesis  is  the  chief 
symptom. 


42 


658  TEXT-BOOK  OF  MEDICINE 

VII.  PNEUMOCOCCAL  GASTRITIS  WITH  ULCERATION. 

In  the  next  three  sections  I  shall  discuss  the  following  subjects  ; 

1.  Pneumococcal  gastritis. 

2.  Appendicular  vomito  negro. 

3.  Exulceratio  simplex. 

Let  us  commence  with  the  study  of  pneumococcal  gastritis. 

Description. — In  the  past  "  pneumonia  "  summed  up  the  infection 
which  we  now  call  "  pneumococcal  infection."  Bacteriology,  however, 
has  revealed  this  infection  in  numerous  organs  where  it  had  not  been 
suspected.  Pleurisy,  pericarditis,  peritonitis,  both  cerebral  and  cerebro- 
spinal meningitis,  endocarditis,  otitis,  tonsilUtis,  and  arthritis  have  been 
placed  amongst  the  pneumococcal  infections.  These  lesions  are  found 
not  only  as  secondary  complications  of  pneumonia,  but  also  as  primary 
affections,  due  to  the  pneumococcus  (peritonitis,  otitis,  meningitis,  etc)., 
and  quite  independent  of  pneumonia. 

One  form  of  pneumococcal  infection  has,  however,  passed  almost  unnoticed 
— viz.,  pneumococcia  of  the  stomach.  I  give  here  two  cases  which  I  have 
already  described  in  my  lectures  at  the  Hotel-Dieu  :* 

A  patient  was  admitted  to  the  hospital  with  dyspnoea,  cyanosis,  temperature  of 
105°  F.,  respirations  42,  and  acute  pain  under  the  right  breast.  We  found  pneumonia 
at  the  right  base  ;  friction  sounds  showed  that  the  pleura  was  also  involved.  The 
dyspnoea  was  so  severe  that  it  was  impossible  to  auscultate  the  heart.  The  abdomen 
was  painful  and  distended.  He  brought  up  rusty  sputum-,  was  restless  at  night, 
vomited,  and  had  diarrhoea.  The  urine  contained  albumin,  and  urobiUn.  The  abdo- 
minal symptoms  of  pain,  tympanites,  vomiting,  and  diarrhoea,  which  are  rare  in  pneu- 
monia, attracted  attention.  Next  day  the  dyspnoea  was  worse  ;  the  abdomen  was 
more  painful  and  distended  ;  the  nausea  and  diarrhoea  continued.  What  was  the 
meaning  of  these  abdominal  symptoms  ?  Was  peritonitis  the  cause  ?  Twelve  ounces 
of  blood  were  taken.  He  had  a  bad  day,  though  the  dyspnoea  was  improved  by  the 
bleeding.  Next  day  great  restlessness  and  complete  insomnia.  He  complained  of  pains 
in  the  stomach  and  of  a  desire  to  vomit ;  at  5  a.m.  he  vomited  about  IJ  pints  of 
blackish  fluid,  like  coffee-grounds.  In  view  of  the  severe  hsematemesis,  I  was  at  a  loss 
for  a  diagnosis.  There  was  no  doubt  that  the  patient  was  suffering  from  pneumonia, 
but  why  this  severe  haematemesis  ?  As  far  as  I  know,  haematemesis  does  not  appear 
in  pnuemonia.  Many  theories  were  possible.  Could  he,  prior  to  the  pneumonia,  have 
had  an  ulcus  simplex,  which  had  previously  been  latent  ?  Or  else,  was  not  this 
a  case  of  exulceratio  simplex  ?  He  grew  worse  from  hour  to  hour.  The  tympanites, 
pain,  and  diarrhoea  became  more  marked  ;  the  diarrhoea,  so  common  in  primary 
pneumococcal  peritonitis,  made  us  think  of  peritonitis.  Melsena  was  present — a  point 
which  agreed  well  with  the  hsematemesis,  but  did  not  clear  up  the  diagnosis.  At  noon 
slight  haematemesis,  and  at  three  o'clock,  after  a  severe  attack,  the  patient  succumbed, 
the  temperature  being  104°  F.  The  chief  feature  was  :  severe  attacks  of  haematemesis 
and  gastro-peritoneal  complications  in  a  patient  with  pneumonia. 

*  "  Gasterite  Ulcereuse  Pneumococcique :  Grandes  Hematemeses "  (Clinique 
Medicale  deV Hotel-Dieu,  1899,  ll°"le9on,  p.  219). 


Plate  V. 


Fig.  35. 


'  t'i ' 

■  '$  ■■■     -   •-  . 

.:i:fi-.m-'-- 

'•    t  4  <      •.■^  • 
.■■'  ■':    ':  :.■    '  ■  ',  .fr^ 


*'5:t?t]!«r"»rtl' 


111%  -^mm 


Fig.  36.  ' 


■vi 


Fio.  37. 


Fig.  35.  —  a,  Erosion  which  affects  the  whole  thickness  of  the  glandular 
la^'er,  and  which  stops  on  the  confines  of  the  muscularis  mi]Cos;t.  The  base 
of  the  erosion  in  the  necrosed  glandular  tissue  is  in  process  of  elinnnation.  In 
the  vicinity  of  the  erosion  the  mlerglandular  connecti\e  tissue  has  undergone 
slight  embryonic  infiltration,  c,  Intact  muscularis  mucosas.  rf,Tunica  muscularis. 

Fio.  36.  —  A  tanj^cntial  section  of  the  mucosa  on  a  level  with  the  bottom  of 
the  erosion,  a,  the  healthy  glandular  tissue,  with  a  section  of  its  tubes;  b,  the 
small  glandular  region,  where  the  necrosis  is  taking  place  which  will  form 
the  erosion.  This  is  the  earliest  phase  of  the  lesion. 

Fk;.  37.  —  A  section  of  the  mucosa,  perpendicular  to  its  surface,  passing 
through  an  erosion.  The  preparation  has  been  stained  by  thionine  and  Gram's 
method,  a.  The  edge  of  the  erosion;  b.  The  glandular  tubes;  c,  Pneumococci. 
The  microbes  infiltrate,  not  only  the  edge  of  the  erosion,  but  are  found  in 
numbers  in  the  interglandular  connective  tissue  at  some  distance  from  it.  It 
mi^ht  be  called  pnetimocorrhagia  —  a  name  which  appears  to  me  the  more 
acceptable  as  the  capillaries  of  the  mucous  membrane  are  also  infiltrated 
with  pneumococci. 

To  f.ice  p.  658 


DISEASES  OF  THE  STOMACH  659 

Post-mortem  examination  :  On  opening  the  thorax,  the  pericardium  was  found  to 
contain  13  ounces  of  reddish  fluid,  rich  in  red  corpuscles.  The  pericardium  was  covered 
with  fibrinous  exudate,  villous  and  studded  with  bright  spots  ;  the  pneumococcus  was 
the  cause  of  the  pericarditis.  The  heart  was  of  normal  size  ;  in  the  right  cavities,  post- 
mortem, clots.  The  orifices  of  the  heart  and  the  large  vessels  showed  nothing  pecuUar. 
The  right  pleural  cavity  contained  10  ounces  of  reddish  fluid,  similar  to  that  in  the 
pericardium,  but  not  so  clear.  At  certain  points  the  two  layers  of  the  pleura  were 
adherent.  The  parietal  pleura  was  slightly  thickened,  and  covered  with  shreds  of 
fibrin.  The  visceral  pleura  over  the  lung  formed  a  kind  of  connective  shell  of  a 
lardaceous  aspect.  Pneumonia  of  the  right  lung  ;  congestion  of  the  left.  The  left 
pleura  was  healthy.     The  tracheo-bronchial  glands  were  enlarged. 

The  abdominal  cavity  showed  peritonitis.  Turbid  reddish  fluid  in  the  pelvis.  The 
intestines  were  matted  together,  and  covered  with  a  viscid,  non-purulent  exudate, 
studded  with  granules,  several  of  which  did  not  exceed  a  pin's  head  in  size.  The 
pneumococcus  was  the  cause  of  the  peritonitis,  and  the  abdominal  symptoms  present 
during  life  were  explained  :  he  had  had  secondary  pneumococcal  peritonitis.  The 
spleen  was  enlarged  ;  the  liver  and  pancreas  were  normal.  The  lesions  of  the  stomach 
were  noteworthy.  When  it  was  opened  and  cleaned,  several  brown  points  of  the  size 
of  a  pin's  head  were  seen  ;  one  of  these  points  was  as  large  as  a  small  lentil.  These 
brownish  points  were  erosions,  and  showed  clearly  under  the  lens.  The  edges  were 
clean-cut  and  adherent,  and  the  floor  was  filled  up  with  a  small  hsemorrhagic  eschar. 
The  diameter  of  the' erosions  was  from  2  to  3  milUmetres.  They  were  scattered  over 
the  whole  mucous  membrane,  but  especially  in  the  pyloric  region,  at  the  bottom  of  the 
folds  and  on  the  surface.  Bacteriological  examination  showed  that  the  man  had 
succumbed  to  general  pneumococcal  poisoning.  The  pneumococcus  was  found  in  the 
fluid  from  the  jileura,  pericardium,  and  peritoneum. 

The  nature  of  the  hsemorrhagic  erosions  that  had  caused  the  hsematemesia  had 
still  to  be  cleared  up.  The  histological  and  bacteriological  preparations,  reproduced 
in  Plate  V.,  were  made  by  Jolly.  I  think  this  is  the  first  case  in  which  pneumococcal 
infection  of  the  stomach  has  been  seen  in  a  complete  form  with  pneumococci,  hsemor- 
rhagic erosions,  and  huematemesis. 

The  erosions  were  formed  by  the  elimination  of  an  eschar,  and  the  process  is  clearly 
shown  in  Plate  V. 

The  erosions  were  due  to  rapid  and  Umited  necrosis  of  a  small  portion  of  the  mucous 
membrane,  with  an  inflammatory  reaction  that  was  nil  or  trifling.  They  were  caused 
by  the  pneumococcus,  and  were  therefore  part  of  the  general  pneumococcia.  These 
erosions  explained  the  severe  haematemeses  which  had  been  so  obscure  during  life. 
I  have  proposed  for  this  condition  the  name  of  pneumococcal  haemorrhagic  ulcerative 
gastritis. 

By  a  strange  coincidence,  I  had  in  my  wards  at  the  same  time  a  similar  case.  A 
man  was  admitted  to  the  Hotel-Dieu  on  the  sixth  day  of  pneumonia.  Abdominal 
symptoms  appeared  on  the  same  day — diarrhica,  jiain,  and  tympanites — pointing  to 
pneumococcal  peritonitis.  He  also  complained  of  pain  in  his  left  wrist  (pneumococcal 
arthritis).  On  the  eighth  day  the  abdoinen  was  tympanitic  and  painful,  especially  at 
(he  j)it  of  the  stomach  and  in  the  right  flank.  During  the  nigiit  lie  vomited,  and  passed 
two  loose  stools.  The  diagnosis  of  pneumococcal  peritonitis  was  dear.  The  abdominal 
condition  Ijecame  worse,  and  the  arthritis  of  the  left  wTist  more  marked.  A  surprise 
occurred.  The  patient,  like  his  neighbour  opposite,  was  seized  with  pains  in  thestomach, 
nausea,  and  hujmatcmesis,  and  vomited  a  quart  of  blackish  fluid  like  coffee-grounds. 

For  two  days  peritonism  was  marked,  with  vomiting,  hiccough,  ballooning  of  the 
abdomen,  and  diarrhoea,  which  is  the  usual  symptom  in  pneumococcal  peritonitis. 
As  the  threatening  peritonitis  began  to  resolve,  the  vomiting  ceased,  the  abdominal 
pain  grow  less,  the  ballooning  disai^peared,  and  the  prognosis  was  more  hopeful. 

42—2 


660  TEXT-BOOK  OF  MEDICINE 

One  morning  he  felt  weak,  and  complained  of  violent  headache,  with  buzzing  in  the 
ears.  He  refused  nourishment,  and  lay  on  his  right  side  in  a  state  of  coma.  This 
symptom-complex  pointed  to  meningitis.  Death  occurred  on  the  nineteenth  day  of 
the  disease. 

The  post-mortem  examination  revealed  the  following  lesions  :  The  lower  lobe  of  the 
left  lung  was  splenized  and  infected  by  the  pneumococcus  ;  the  right  lung  was  con- 
gested. The  left  pleura  was  adherent,  and  a  similar  condition  was  found  in  the  inter- 
lobar fissure,  in  which  three  small  abscesses  were  found.  Adhesions  and  abscesses 
also  existed  in  the  diaphragmatic  pleura.  The  abscesses,  both  interlobular  and 
diaphragmatic,  contained  creamy  pus,  rich  in  pneumococci. 

False  membranes  and  a  small  quantity  of  liquid  were  found  in  the  pelvis,  in  front 
of  the  rectum.  Bacteriological  examination  revealed  the  pneumococcus,  so  that  these 
lesions  were  the  result  of  pneumococcal  peritonitis,  and  showed  the  spontaneous  cura- 
bility of  this  secondary  variety.  On  examining  the  heart,  a  small,  prominent,  friable 
vegetation,  from  4  to  5  millimetres  in  diameter,  was  found  at  the  insertion  of  the  right 
sigmoid  valve.  The  pneumococcus  was  found  in  smears  taken  from  the  vegetation. 
The  symptoms  of  meningitis  observed  during  life  were  also  explained.  On  opening 
the  skull,  we  found  purulent  pneumococcal  meningitis  and  thick  yellowish  pus  spread 
along  the  Sylvian  arteries,  and  over  the  peduncles  and  upper  surface  of  the  cerebellum. 
There  was  nothing  noticeable  in  the  cavity  of  the  tympanum. 

The  radio-carpal  articulation  and  the  sheaths  of  the  extensor  tendons  contained 
about  I  ounce  of  creamy  greenish  pus.  The  articular  surfaces  of  the  ulna  and  radius, 
and  the  radial  surface  of  the  carpal  articulation  presented  a  velvet-like  change,  re- 
sulting in  complete  disappearance  of  the  cartilage  at  certain  points.  Bacteriological 
examination  proved  the  presence  of  the  pneumococcus. 

On  opening  the  stomach,  we  found  congestion  of  the  mucous  membrane,  but  no  active 
erosions,  as  in  the  preceding  case.  The  histological  examination  of  the  mucosa  showed 
small  haemorrhagic  foci,  some  in  the  submucous  tissue,  and  others,  more  numerous, 
in  the  interglandular  tissue.  These  foci  (the  origin  of  the  hsematemesis)  pushed  the 
glands  aside,  and  formed  distinct  masses,  that  were  separated  from  the  exterior  by  a 
thin  layer  of  mucous  membrane.  Around  the  foci  no  trace  of  inflammatory  reaction 
was  to  be  seen.     The  search  for  microbes  was  negative. 

In  these  two  cases,  by  a  singular  coincidence,  we  have  two  men,  both 
suffering  from  pneumococcia,  who  are  seized  within  a  few  days  with  peritoneal 
symptoms  and  severe  hsematemesis.  The  first  patient  had  several  attacks, 
and  finally  succumbed  to  hsomatemesis.  The  bleeding,  as  we  have  seen, 
was  due  to  pneumococcal  infection,  with  liaemorrhagic  erosions. 

In  the  first  patient,  who  died  while  the  gastric  stage  was  active,  we  were 
able  to  surprise  the  infection  in  actual  progress.  In  the  second  patient,  who 
Uved  some  time  after  the  hsematemesis,  we  found  only  the  remains  of 
hsemorrhagic  foci  in  the  gastric  mucous  membrane. 

In  an  old  woman  who  had  suffered  from  pneumonia  at  the  right  apex,  but  had 
during  her  life  shown  neitlier  gastric  nor  intestinal  symptoms.  Griffon  found  pneumonia 
with  abscesses,  the  pus  of  which  contained  only  pneumococci.  In  the  first  portion  of 
the  duodenum  were  two  symmetrical  ulcers.  In  the  pyloric  region  there  were  two  ulcers 
and  several  punctate  haemorrhages.  Although  the  bacteriological  examination  did 
not  show  the  pneumococcus  in  the  ulcers,  it  is  probable  that  they  were  due  to  a  toxi- 
infection,  caused  either  by  the  microbes  or  their  toxines. 

Gastric  ulcers  occurring  in  the  course  of  pneumococcia  have  been  studied 
experimentally  in  the  guinea-pig.     According  to  Bezan9on  and  Griffon,  the 


DISEASES  OF  THE  STOMACH  661 

pneumococcus  is  apt  to  cause  hsemorrhagic  lesions  when  its  virulence  has 
been  increased  by  successive  passages,  whilst  the  fibrino-purulent  changes 
are  due  to  the  pneumococcus  of  less  exalted  virulence.  The  peritoneum  of  a 
healthy  guinea-pig  was  inoculated  with  a  few  drops  of  peritoneal  exudation 
from  a  guinea-pig  infected  with  virulent  pneumococci.  The  inoculated 
guinea-pig  succumbed  in  twenty-one  hours,  and  the  post-mortem  examina- 
tion showed  petechiae  in  the  mesentery  and  the  large  intestine,  and  haemor- 
rhagic  nodules  in  the  spleen.  The  mucosa  of  the  stomach  was  studded  with 
about  fifteen  haemorrhagic  erosions.  The  histological  examination  of  these 
erosions  showed  that  the  process  affected  only  the  mucous  and  submucous 
layers.  Pneumococci  were  present  in  the  ulcer,  as  in  all  the  organs.  These 
experiments  are  of  value,  in  that  they  allow  us  to  place  clinical  and  experi- 
mental cases  side  by  side. 

Summary. — The  stomach,  like  other  organs,  may  be  infected  by  the 
pneumococcus.  This  organism  may  perhaps  locaUze  itself  from  the  first  in 
the  stomach,  causing  a  primary  gastritis.  Why  should  we  not  find  primary 
and  secondary  forms  of  pneumococcal  gastritis,  just  as  we  do  in  meningitis  ? 
Pneumococcal  infection  of  the  stomach  may  be  revealed  by  gastric  symp- 
toms. Still,  nausea  and  vomiting  of  food  or  bile  are  of  no  great  significance, 
because  they  may  occur  in  simple  pneumonia.  On  the  other  hand,  attacks 
of  hsematemesis  in  the  course  of  pneumonia  point  to  pneumococcal  gastritis 
with  ulceration.  Meleena  has  the  same  signification,  whether  it  is  due  to 
ulcerative  gastritis  or  enteritis. 

Although  the  erosions  are  very  small,  there  is  nothing  to  show  that  they 
may  not  be  more  extensive.  They  may  get  well  quickly  (as  in  my  second 
case),  but  it  is  equally  probable  that  they  may  survive  the  gastritis.  An 
individual,  though  cured  of  pneumonia  and  apparently  of  pneumococcal 
gastritis,  may  yet  have  an  invading  gastric  ulcer,  which  will  perhaps  in  time 
assume  the  form  of  Cruveilhier's  ulcus  simplex.  In  other  words,  it  is  not 
impossible  that  the  ulcus  simplex  may  in  some  cases  arise  from  a  pneumo- 
coccal erosion.  This  view  of  the  transformation  of  infective  gastric  ulcera- 
tions into  ulcus  has  gained  ground  during  the  past  few  years.  Gandy  has 
written  a  remarkable  monograph  on  this  subject,  to  which  I  shall  refer 
under  Exulceratio  Simplex. 


VIII.  APPENDICULAR  VOMITO  NEGRO. 

Amongst  the  innumerable  misdeeds  of  the  appendix  there  is  one  which 
I  shall  now  discuss — namely,,  vomiting  of  blood.  A  few  years  ago  no  one 
thought  of  ha^matemesis  in  connection  with  appendicitis,  and  until  recent 
years  text- books  of  medicine  and  surgery  were  silent  on  this  point ;  and  yet 
haematemesis  resulting  from  appendicitis  is  far  from  being  rare. 


662  TEXT-BOOK  OF  MEDICINE 

I  do  not  refer  to  slight  haematemesis,  which  is  only  an  epiphenomenon, 
and  may  be  lightly  passed  over.  On  the  contrary,  we  usually  find  severe 
attacks  of  haematemesis.  The  black  vomit  may  amount  to  |  pint  of  blood, 
the  attacks  may  be  repeated,  and  the  patient  may  die  from  haemorrhage. 

I  have  given  the  name  of  appendicular  vomito  negro  to  this  tragic 
event,  and  in  addition  to  a  communication  to  the  Academie  de  Medecine  I 
have  dehvered  a  chnical  lecture  on  it.*  The  following  cases  will  give  us 
full  details  : 

On  June  6,  1900,  in  consultation  with  Gros  and  Cazin,  I  saw  a  young  American  lady 
who  was  suffering  from  appendicitis  of  four  days'  duration,  complicated  by  peritonitis. 
She  was  operated  upon  by  Cazin  on  the  same  day.  In  spite  of  the  operation,  her  con- 
dition remained  gi-ave,  aad  the  fever  persisted.  Two  days  later  jaundice  was  just 
beginning.  Urine  scanty  and  high-coloured.  In  -spite  of  treatment,  complete  suppres- 
sion (toxic  anuria).  The  first  severe  attack  of  haematemesis  now  appeared.  During  the 
night,  delirium,  alternating  with  restlessness  and  coma  ;  the  anuria  persisted.  Next 
day  the  jaundice  had  become  general.  Blood  was  repeatedly  vomited.  The  delirium 
continued,  and  the  patient  died  a  few  hours  later,  after  an  attack  of  copious  haemate- 
mesis. 

On  October  8,  1900, 1  saw,  with  Sevestre  and  Quenu,  a  young  girl  of  ten  years  of  age, 
who  had  appendicitis.  The  attack  had  commenced  forty  hours  previously,  with  vomit- 
ing and  pain.  When  we  arrived,  at  half -past  seven,  she  was  very  restless.  Her  features 
were  drawn  ;  her  pulse  was  140,  and  her  temperature  nearly  104°  F.  Suppression  of 
urine  since  the  morning.  The  abdomen  was  distended,  and  the  region  of  the  appendix 
painful.     The  prognosis  was  alarming,  and  \^e  decided  on  immediate  operation. 

On  opening  the  abdomen,  diffuse  peritonitis ;  serous  and  foetid  pus  in  the  pelvis. 
The  appendix  lay  behind  the  caecum,  and  its  tip  was  gangrenous.  The  restlessness  per- 
sisted all  night. 

Next  morning  the  general  condition  was  bad  ;  temperature  103°  F. ;  pulse  122.  In- 
^'octions  of  serum  given.  Restless  night.  Next  morning  temperature  rose  to  104°  F., 
and  pulse  to  130.  Everything  went  well  as  far  as  the  abdomen  was  concerned,  but  the 
child  was  poisoned,  and  complications  soon  appeared.  At  ten  o'clock  temperature  was 
104-3°  F.,  pulse  140,  and  respirations  45.  We  saw  her  at  noon,  when  she  had  an 
earthy  complexion  and  small,  irregular  pulse.  The  urine  was  scanty  and  albuminous. 
From  the  vomit,  in  which  I  saw  some  shreds  of  black  blood,  I  foretold  an  attack  of 
haematemesis,  which  came  on  two  hours  later  ;  it  was  profuse.  Ice  was  given,  and  the 
injections  of  serum  continued,  but  her  condition  became  worse  every  hour.  Other 
attacks  of  haematemesis  occurred  at  6  p.m.  and  at  8  p.m.  The  breathing  was  quick  ; 
the  extremities  were  cold  ;  she  passed  several  large  foetid  stools,  and  died  at  9.15  p.m. 

On  January  13,  1900,  with  Bergeron  and  Widal,  I  saw  a  patient  who  had  been 
operated  upon  by  Delbet  on  the  fourth  day  of  an  attack  of  appendicitis.  Next  day 
the  patient  was  seized  with  haematemesis  and  died. 

On  October  30,  1900,  I  saw,  with  Charrier,  a  young  man  who  for  three  days  had 
been  suffering  from  appendicitis.  The  yellowish  tinge  of  the  conjunctivae  and  the  con- 
dition of  the  urine  showed  general  infection.  The  situation  appeared  to  be  most  grave, 
and  an  operation  was  performed  that  evening  by  Segond.  On  opening  the  abdomen 
a  foetid  abscess  and  diffuse  peritonitis  were  found ;  the  intestine  was  of  a  purple  colour. 
The  abscess  passed  up  behind  the  caecum,  the  limiting  membranes  being  very  friable. 
The  appendix  was  perforated  and  gangrenous.     Next  morning  he  seemed  a  little  better, 

*  "  Vomito  Negro  Appendiculaire "  {Cliniqtie  Medicale  de  VHotel-Dieu,  1903, 
10""=  leQon). 


DISEASES  OF  THE  STOMACH  663 

but  in  the  evening  tie  had  an  attack  of  haematemesis,  and  vomited  about  3  ounces  of 
dark  blood,  like  coffee-grounds.  The  pulse  rose  to  140,  and  nervous  symptoms  of  a 
toxic  nature  appeared — viz..  stupor,  loss  of  consciousness,  and  oscillations  of  the  head, 
which  lasted  till  death. 

On  January  27,  1900,  I  saw,  with  Segond  and  Ramond,  a  young  girl  who  had 
been  operated  upon  by  Segond  on  the  fourth  day  of  an  attack  of  appendicitis.  During 
the  next  few  days  she  had  several  attacks  of  baematemesis,  which,  fortunately,  did 
not  prevent  recovery. 

A  youth  was  operated  upon  by  Piechaud  on  the  sixth  day  of  an  attack  of  appendi- 
citis ;  a  few  hours  later  he  felt  much  better.  At  five  o'clock  in  the  afternoon  he  was 
in  extremis.  An  injection  of  serum  was  administered,  but  the  patient  was  seized  with 
fulminant  haBmatemesis,  and  died  at  one  o'clock  in  the  morning.  At  the  post- 
mortem we  found  the  appendix  perforated  at  its  tip.  The  stomach  was  distended  with 
black  blood,  as  the  result  of  the  haemorrhage ;  the  mucous  membrane  showed  ecchymotic 
patches. 

Pathogenesis. — Post-mortem,  ecchymotic  patches  are  found  on  the 
mucosa  of  the  stomach,  and  erosions  which  are  of  heemorrhagic  origin  and  the 
result  of  the  appendicular  toxines.  I  have  shown  {vide  Appendicitis)  that 
the  appendicular  focus  developed  in  a  closed  cavity  causes  not  only  infection, 
but  also  intoxication.  It  is  the  appendicular  toxines  that  provoke  the 
jaundice,  albuminuria,  anuria,  and  nervous  troubles  which  I  shall  discuss 
under  Appendicitis.  It  is  this  same  toxi-infection  which  causes  the  gastric 
erosions  and  the  consequent  haematemesis.  When  the  toxic  syndrome  is 
complete,  as  in  the  first  case  quoted,  the  jaundice  and  black  vomit  confirm 
the  name  of  appendicular  vomito  negro. 

Since  attention  has  been  called  to  this  compUcation  of  appendicitis  1 
have  asked  myself  what  gastric  lesion  was  capable  of  producing  such  attacks 
of  haematemesis.  My  researches  on  pneumococcal  erosions  and  exulceratio 
simplex  had  taught  me  that  the  attacks  of  haematemesis  consequent  on 
these  toxi-infections  are  due  to  ulceration  of  the  arterioles  ramifying 
under  the  muscularis  mucosae.  I  have  found  that  the  process  is  identical 
in  the  gastric  erosions  which  follow  strangulation  of  the  gut,  as  in  the 
following  case  : 

On  Saturday,  Juno  16,  a  man  was  admitted  for  strangulated  hernia,  and  was 
immediately  operated  upon.  Next  morning  tlio  conjunctivro  and  the  face  were  yel- 
lowish ;  during  the  night  two  severe  attacks  of  hSBmatemesis  took  place.  On  Monday 
the  jaundice  was  more  marked.  Kahn,  who  examined  the  urine,  found  albumin, 
urobilin,  and  brown  pigment.  My  prognosis  was  grave.  During  the  day  fresh  htcma- 
temesis  occurred.  On  Tuesday  the  urine  was  scanty  and  albuminous  ;  he  had  a  large 
hajmatemesis.  On  Wednesday  he  passed  only  5  ounces  of  urine,  containing  brown 
pigment,  urobilin,  and  albumin.  Ho  was  delirious,  and  was  seized  during  tlie  night  with 
several  epileptiform  fits.  On  Thursday  fresh  fits,  complete  anuria,  and  another  attack 
of  ha-niatcmosis.  On  Friday  death.  The  results  of  the  post-mortem  examination 
were  as  follows:  Cure  of  the  strangulated  hernia  ;  nothing  in  tlic  intestine  or  peritoneura. 
The  liver  (50  ounces)  and  the  kidney  (7  ounces)  showed  acute  degeneration  of  the 
epithelium.  The  stomach  contained  blood  in  abundance,  but  the  mucous  surfivce 
was  intact,  except  in  the  pyloric  region,  where  there  was  a  hsemorrhagic  eschar  as 


664  TEXT-BOOK  OF  MEDICINE 

big  as  a  small  lentil.  This  eschar  was  prominent,  adherent,  and  surrounded  bv  a 
furrow. 

The  histological  examination  made  by  Gandy  is  shown  in  Figs.  38-40. 

Summary — Necrosis  of  an  extensive  portion  of  the  mucosa  in  the  form  of  an  eschar, 
cutting  the  glandular  layer  cleanly,  injuring  the  muscularis  mucosa,  the  superficial  part 
of  the  submucosa  ;  after  aflfecting  other  anatomical  parts  in  the  course  of  its  progress, 
it  finally  reached  the  superior  wall  of  an  arteriole  situated  below  the  muscularis  mucosae, 
which  gave  way.  In  the  neighbourhood  of,  and  at  a  distance  from,  this  focus  of  necrosis 
there  were  some  submucous  haemorrhages  and  secondary  inflammatory  reaction,  shown 
chiefly  by  embryonic  infiltration  in  the  form  of  large  subglandular  masses. 


*'  •  "'*  -ni  m. 

^5  m. 

o     -t.m. 

-J-S.S 


Fig.  38. — One  of  the  Sections  (Low  Power). 

P,  Gastric  side  of  the  pyloric  valve  ;  T>,  mucosa  of  the  dupdenum  ;  B,  Briinner's 
glands  ;  I,  inflammatory  subglandular  islets  ;  E,  eschar  breaking  up  the  glandular 
layer  ;  G,  glandular  layer  of  the  stomach  ;  m.m.,  muscularis  mucosae  ;  s.m.,  submucous 
layer  ;  /.to.,  tunica  muscularis  ;  s.s.,  subserous  layer. 


>^l^-^=5i 


niiri; 


\ 

\ 

\ 


i;i- 


Fig.  39. — One  of  the  Sections  (High  Power). 
G,  Glandular  layer  of  the  pyloric  region  ;  m.m.,  muscularis  mucosae  ;  s.m.,  submucous 
layer  infiltrated  with  fibrinous  exudation  ;  t.m.,  tunica  muscularis  ;  E,  eschar ;  n,  in- 
vading zone  of  the  necrosis  ;  A,  arteriole  of  the  submucosa,  injured  by  the  necrosis  at 
the  base  of  the  eschar. 

The  experiments  made  by  Talma  (Utrecht,  1890)  on  the  pathogenesis  of 
simple  ulcer  of  the  stomach  show  the  part  played  by  intestinal  strangula- 
tion in  the  production  of  erosions  and  ulceration.  Talma  repeated  his 
experiments  several  times.  He  ligatured  a  coil  in  an  animal,  or,  in  other 
words,  estabhshed  a  closed  cavity,  and  amongst  other  lesions  he  found 
erosions  and  ukeration  of  the  stomach.     The  cUnical  and  experimental 


DISEASES  OF  THE  STOMACH  C65 

facts,  therefore,  agree.  Similar  gastric  erosions  existed  in  three  cases 
reported  by  Chariot. 

We  have  now  gained  some  idea  of  the  lesions  which  provoke  hsema- 
temesis  consequent  on  appendicitis  and  strangulated  hernia.  The  toxic 
process  is  identical  in  both  cases.  The  infection  causes  acute  hsemorrhagic 
erosions  and  ulcerations  of  the  stomach  comparable  to  the  ulcerations  found 
in  pneumococcal  infection  and  to  exulceratio  simplex. 

Description. — ^Vomito  negro  is  part  of  the  appendicular  toxi-infection. 
I  have  often  endeavoured  to  prove  that  appendicitis  is  not  only  a  focus  of 
infection,  but  also  of  intoxication.*  The  toxines  are  responsible  for  changes 
in  the  liver,  with  jaundice,  urobiUnuria,  and  sometimes  symptoms  of  icterds 
gravis.  They  are  also  responsible  for  changes  in  the  kidneys,  with  albu- 
minuria, oHguria,  anuria,  and  sometimes  symptoms  of  uraemia.     The  lesions 


Fig.  40. — Section  through  Stjbmtjcosa. 

A,  Arteriole  with  the  superior  wall  openeil,  communicating  with  a  large  lacuna,  I, 
made  by  the  eschar. 

of  the  stomach,  with  the  attacks  of  hsematemesis,  therefore  appear  to  me 
to  form  part  of  the  toxic  syndrome  of  appendicitis.  Hsematemesis  is 
sometimes  independent  of  other  toxi-iufectious  manifestations,  but  at  other 
times  it  is  associated  with  them. 

Jaundice  of  the  conjunctivae  and  skin,  urobilinuria,  and  albuminuria 
often  precede  the  appearance  of  haematemesis.  In  the  first  case  quoted,  the 
jaundice  was  general  when  the  black  vomit  appeared. 

Appendicular  haematemesis  may  assume  different  forms.  The  atta  'ks 
are  sometimes  preceded  by  naiLsea  and  vomiting.  On  examining  the  vomit, 
blackish  streaks  and  clots  like  coffee-grounds,  which  are  the  forerunners  of 
an  attack  of  haematemesis,  may  be  seen.  Sometimes  the  attack  comes  on 
suddenly  without  prodromata,  even  when  an  operation  for  appendicitis  had 

*  Diculafoy,  "  Toxicite  do  1' AiJpcndititc  "  (communication  a  rAcademie do  MWecino, 
1899,  ot  ('lini<iHc  Mcdualc  deVHoUi-Dku,  1899,  17""=  k'von). 


666  TEXT-BOOK  OF  MEDICINE 

apparently  averted  complications.  A  single  attack  of  haematemesis  is  rare ; 
six  or  more  may  occur  in  a  few  hours.  Sometimes  the  attacks  are,  so  to  say, 
fulminant,  and  carry  off  the  patient  in  a  few  moments. 

I  have  so  far  considered  only  heematemesis  due  to  ordinary  appendicitis. 
The  paratyphoid  form  of  appendicitis,  which  appears  during  the  dechne  of 
typhoid  fever,  may  also  give  rise  to  gastric  ulceration  and  fatal  hsematemesis, 
as  in  the  following  case  : 

In  1876  Millard  communicated  to  the  Societe  Medicale  des  Hopitaux  the  case  of  a 
patient  who,  during  convalescence  from  typhoid  fever,  was  attacked  by  acute  peri- 
tonitis, and  died  a  few  days  later,  after  attacks  of  very  profuse  htematemesis.  At  the 
port-mortem  examination  diffuse  purulent  peritonitis  was  found  ;  it  was  not  due  to  the 
intestinal  lesions,  for  they  had  quite  healed.  It  was  necessary  to  seek  elsewhere,  says 
Mallard  ;  and,  indeed,  he  discovered  "  in  the  vermiform  appendix  the  evident  cause 
of  the  peritonitis.  The  appendix,  which  had  perforated  in  its  middle  third,  no 
longer  communicated  with  the  caecum  ;  the  opening  into  the  caecum  was  completely 
obliterated." 

The  attacks  of  haematemesis  from  which  he  suffered  during  the  course  of  the  peri- 
tonitis were  due  to  ulceration  of  the  stomach  near  the  pyloric  region.  One  of  the  ulcers 
was  oval,  2  inches  in  its  larger  diameter,  and  very  deep,  with  irregular,  clean-cut  edges. 
Millard  discusses  the  cause  and  origin  of  these  ulcers,  and  recalls  the  excessive  rarity 
of  gastric  ulcer  in  typhoid  fever.  With  wise  prudence,  he  refrains  from  coming  to  a 
conclusion,  and,  with  great  intuition,  he  asks  himself  if  there  is  not  some  connection 
between  the  purulent  peritonitis  and  the  ulcerative  process  in  the  stomach.  We 
know  the  connection,  and  we  can  explain  the  pathogenesis  of  the  complications  in  this 
case  :  paratyphoid  appendicitis,  with  its  toxi-infection,  had,  as  in  common  appendicitis, 
caused  peritonitis  on  the  one  hand,  and  gastric  ulceration,  with  haematemesis,  on  the 
other.  This  explanation  at  once  clears  up  this  case,  which  has  been  regarded  as  a  typhoid 
ulcer  of  the  stomach  ;  for  even  supposing  that  the  typhoid  infection  had  played  some 
part,  it  is  the  appendicular  toxi-infection  which  claimed  the  larger  share. 

In  appendicular  vomito  negro  the  prognosis  is  most  grave.  Some 
cases  of  cure,  however,  have  been  reported. 

Absolute  rest  for  the  stomach,  no  hquid  by  the  mouth,  and  large  injec- 
tions of  serum,  appear  to  me  to  be  the  rational  treatment  of  this  comphca- 
tion.     Lucas-Champonniere,  however,  advises  lavage. 

The  terrible  compUcation  just  described  darkens  the  prognosis  of  appen- 
dicitis, and  is  a  further  plea  in  favour  of  early  operation.  The  more  time 
the  appendicular  focus  has  to  elaborate  its  poisons,  the  more  threatening 
the  situation ;  the  less  time  the  focus  has  to  poison  the  victim,  the  less  are 
the  complications  to  be  feared.  We  must,  then,  remove  the  focus.  This 
statement  is  self-evident. 


IX.  EXULCERATIO  SIMPLEX  OF  THE  STOMACH. 

The  two  preceding  sections  have  been  devoted  to  haemorrhagic  erosions 
in  which  the  course  was  rapid.  There  are,  however,  cases  in  which  acute 
ulceration,  with  severe  haematemesis,  occurs,  although  we  cannot  find  the 


DISEASES  OF  THE  STOMACH  667 

infectious  origin  of  the  gastric  lesion,  just  as  it  often  happens  that  the 
simple  ulcer  of  Gruveilhier  develops  in  the  stomach  without  the  original 
cause  being  found.  I  have  reserved  for  these  acute  ulcers  which  supervene 
without  apparent  cause  the  name  of  exulceratio  simplex.  In  future  it 
will  be  necessary  to  describe  exulceratio  simplex,  which  is  an  acute  lesion, 
and  ulcus  simplex,  which  runs  a  chronic  course. 

I  have  made  a  communication  to  the  Academic  de  Medecine  on  exul- 
ceratio simplex,  and  I  shall  here  quote  two  cases  from  my  cUnical  lectures* 
on  this  subject : 

A  man,  twenty-seven  years  of  age,  was  admitted  under  my  care.  His  pallor  at  once 
pointed  to  severe  haemorrhage.  He  had  had  several  attacks  of  hcsmatemesis,  and 
passed  much  blood  per  anum.  He  put  the  quantity  of  blood  vomited  at  3  pints.  The 
pallor  of  the  skin,  the  feebleness  of  the  pulse,  and  the  coldness  of  the  extremities,  all 
indicated  that  the  bleeding  must  have  been  profuse.  Although  the  classical  signs  of 
gastric  ulcer  were  absent,  I  thought  of  a  latent  ulcer  which  had  perhaps  opened  a  large 
vessel.  In  spite  of  treatment,  the  bleeding  recurred  during  the  night ;  next  morning 
two  basins  were  nearly  filled  with  blackish  blood  and  clots.  The  haematemesis  had  been 
foUoAved  by  melsena,  as  on  the  previous  day.  Three  pints  of  artificial  serum  were 
injected  into  the  veins,  and  produced  slight  improvement.  At  one  o'clock  in  the  after- 
noon fresh  haematemesis  and  death.  He  had  lost  about  7  pints  of  blood  in  less  than 
thirty  hours. 

Here  are  the  results  of  the  autopsy  :  The  exterior  aspect  of  the  stomach  was  normal. 
A  ligature  was  placed  around  the  cardia  and  the  pylorus  ;  an  incision  was  made  in  the 
stomach,  which  contained  a  point  of  blood,  but,  to  our  great  surprise,  we  did  not  find 
the  simple  ulcer. 

The  mucous  membrane  was  carefully  washed,  and  we  then  discovered,  half  an  inch 
from  the  cardia,  a  superficial  circular  exulceration. 

The  specimens  made  by  Caussade  showed  the  characters  of  the  ulceration.  It  was 
so  superficial  as  to  affect  only  the  tunica  mucosa,  with  its  muscularis  mucosae  ;  it  had 
only  broken  down  in  places.  At  the  bottom  of  the  ulcer  we  saw  the  gaping  arteriole 
which  caused  the  fatal  haemorrhages.     These  details  are  shown  in  Fig.  41. 

Fig.  42  shows  miliary  abscesses  in  the  mucous  membrane  ;  they  open  on  the 
surface  of  the  mucosa,  and  have  made  breaches  of  surface,  which  have  left  the 
muscularis  mucosa;  uncovered.  This  may  have  allowed  the  gastric  juice  to  help 
in  the  work  of  destruction.  The  origin  of  the  exulceration  and  of  the  fulminant  haema- 
temesis is  thus  clear. 

It  seems  strange  tliat  this  superficial  ulcer  and  this  small  arteriole  should  have  caiised 
such  profuse  haematemesis.  The  calibre  of  an  empty  arteriole  cannot,  however,  be 
correctly  estimated  in  anatomical  specimens,  and  the  arterioles  of  the  stomach,  even 
those  which  are  separated  from  the  mucosa  only  by  the  muscularis  mucosae,  are  rela- 
tively of  large  calibre  ;  they  equal  in  size  the  collateral  arteries  of  the  little  finger.  The 
ulceration  had  been  latent  and  rapid  in  its  progress,  for  our  specimens  showed  recent 
lesions  only.  I  was  sorry  on  seeing  this  limited  lesion  in  the  stomach.  I  said  to  myself 
that  surgical  intervention  might  have  saved  the  life  of  this  man,  and  determined  to  seize 
the  opportunity  as  soon  as  it  presented  itself. 

The  opportunity  did  present  itself.  On  October  7,  1897,  at  11  p.m.,  a  young  man, 
twenty-two  years  of  age,  brought  up  much  blood.  "  I  must  have  vomited,"  said  he, 
"  2  or  .3  pints,  for  there  was  a  regular  pool  on  the  pavement."     The  next  day,  "  to  pick 

*  "  E.xulceratio  Simplex  "  (Clinique  Medicale  de  I'Hotel-Dieu,  1898,  l",  2""  et  3""' 
lemons). 


668 


TEXT-BOOK  OF  MEDICINE 


up  strength,"  he  ate  well.  About  two  o'clock  next  morning  he  again  brought  up 
blood.  The  vomited  blood  was  brownish,  part  liquid  and  part  clotted.  On  October  9 
and  during  the  following  days  he  had  neither  pain  nor  vomiting,  though  he  was  very 
weak.     He  came  to  the  Hotel-Dieu  on  October  13.     Next  morning  I  was  struck  with 


Fig  41. — Section  through  the  Wall  of  the  Stomach. 

U,  Ulceration  formed  at  the  expense  of  the  tunica  mucosa  M  and  of  the  muscularis 
mucosae  mm  ;  a,  small  submucous  artery  destroyed  at  the  point  h,  where  a  quantity  of 
red  blood-corpuscles  are  found  en  masse  (it  was  from  this  spot  that  the  fatal  haemor- 
rhages proceeded)  ;  v,  th,  thrombosed  vein  ;  sm,  tunica  submucosa ;  mtr  and  ml,  tunica 
muscularis  ;  s,  tunica  serosa  ;  1,  2,  3,  miliary  abscesses,  situated  in  the  depth  of  the 
mucosa. 


Fig.  42. — Ttjnica  Mucosa,  with  its  Muscularis  Mucosa. 

1,  Miliary  abscess  in  formation  in  the  depths  of  the  mucosa  above  the  muscularis 
mucosae  ;  2,  miliary  abscess,  opening  through  the  tunica  mucosa,  and  communicating 
with  the  cavity  of  the  stomach  at  the  point  3. 

the  pallor  of  the  skin  and  mucous  membranes.  The  pulse  was  small,  the  temperature 
100°  F.,  and  the  patient  complained  of  great  weakness.  I  am  sure  that  he  spoke  the 
truth  when  he  claimed  to  have  lost  5  pints  of  blood,  for  the  blood-count  gave  only 


DISEASES  OF  THE  STOMACH  669 

1,600,000  red  corpuscles.  Though  we  had  not  verified  the  haemorrhage,  it  was  neces- 
sary to  make  a  diagnosis,  and  to  find  out  the  origin  of  the  bleeding.  The  case  was 
evidently  one  of  hsematemesis,  and  not  of  haemoptysis,  because  the  blood  had  been 
vomited  in  streams,  with  enormous  clots,  and  without  the  least  cough  ;  moreover,  the 
lungs  were  absolutely  healthy.  On  the  other  hand,  it  was  evident  that  the  attacks 
were  not  due  to  the  rupture  of  oesophageal  varices,  for  he  had  no  sign  of  cirrhosis. 
Some  lesion  of  the  stomach  was  therefore  the  cause.  It  was  certainly  not  cancer,  which 
is  never  ushered  by  violent  attacks  of  gastrorrhagia.  A  simple  ulcer,  whicli  so  often 
causes  hsematemesis,  remained  ;  he  had  never  showed  any  symptoms  of  ulcer  or  other 
gastric  trouble. 

I  felt  sure  that  he  had  an  exulceration  like  my  other  patient.  The  idea  of  surgical 
intervention  at  once  entered  my  mind.  We  had  not  saved  the  first  patient,  in  spite 
of  intravenous  injections,  and  therefore  we  must  not  let  the  second  one  die  through 
indecision. 

I  commenced  medical  treatment,  giving  milk,  which  the  patient  vomited  repeat- 
edly.    The  analysis  of  the  vomit  showed  that  the  hydrochloric  acid  was  diminished. 

Next  day  and  the  day  following,  the  patient,  who  wished  to  get  up,  had  a  fainting 
fit ;  fresh  comphcations  were  arising. 

When  I  arrived  at  the  Hotel-Dieu  next  day  I  was  shown  a  basin  containing 
56  ounces  of  liquid  blood  with  clots.  During  the  night  he  had  had  a  sudden  attack  of 
hsematemesis.  He  was  pale,  drowsy,  and  prostrate.  The  pulse  was  almost  absent. 
Further  delay  was  impossible  ;  fresh  haemorrhage  might  come  on,  and  the  patient 
would  assuredly  die,  as  my  other  patient  did. 

After  a  preUminary  injection  of  artificial  serum  Cazin  operated.  An  incision 
5  inches  long,  parallel  to  the  edge  of  the  false  ribs  on  the  left  side,  opened  the  peritoneal 
cavity.  The  stomach,  partly  hidden  by  the  false  ribs,  was  brought  out  of  the  wound 
and  examined  ;  it  appeared  quite  normal.  Neither  by  sight  nor  by  touch  could  we  find 
any  lesion  ;  ecchymosis,  adhesions,  and  induration  were  absent.  For  a  moment  it 
appeared  unnecessary  to  open  the  stomachy  which,  from  the  external  examination, 
appeared  healthy.  Nevertheless,  as  the  diagnosis  of  exulceration  had  been  made,  the 
operation  was  continued,  and  we  showed  the  value  of  exact  diagnosis  and  timely  inter- 
vention. The  contents  of  the  stomach  were  squeezed  into  the  intestine,  and  the  viscus 
was  clamped  near  the  pylorus,  to  prevent  regurgitation  from  the  intestine.  An  incision 
4  inches  long  was  made  in  the  anterior  surface  of  the  stomach,  which  was  turned  inside 
out  to  make  the  exploration  easier.     The  stomach  was  empty. 

Cursory  examination  seemed  to  show  that  the  operation  was  ill-advised.  The 
previous  example,  however,  was  not  to  be  lost.  When  Cazin  wiped  tlie  mucous 
membrane  with  sterile  gauze,  a  bleeding  spot  appeared  ;  it  was  as  big  as  a  sixpence,  and 
was  situated  in  the  mucous  membrane. 

When  the  ulcerated  surface  was  gently  rubbed  with  a  tampon,  the  hremorrhage 
reappeared  over  an  area  as  large  as  a  crown-piece.  The  case  was  one  of  exulceratio 
simplex  in  the  mucous  membrane,  discernible  only  by  careful  search,  and  comparable 
to  the  exulceration  which  liad  killed  my  first  patient. 

I  omit  the  details  of  the  operation  and  subsequent  treatment.  Food  was  gradually 
given.  Three  weeks  after  the  operation  the  patient's  appetite  was  good  ;  lie  grew 
fat,  and  was  discharged  from  the  hospital  five  weeks  after  the  operation,  completely 
cured.  The  red  corpuscles  amounted  to  nearly  4,000,000.  I  saw  him  a  year  later, 
when  he  was  in  perfect  health. 

The  third  case  I  owe  to  the  kindness  of  Michaux  ;  it  is  identical  with  the  preceding 
ones.  A  healtliy  young  woman  suddenly  vomited  2  or  3  pints  of  blood.  During  the 
night  of  October  22  and  also  next  day  she  had  fresh  hasmatcmesis  and  mchcna.  She 
was  admitted  into  liospital  on  the  2oth,and  had  lost  so  much  blood  tliat  her  skin  and 
mucous  membranes  were  colourless.     As  the  hicmatemesis  recurred,  in  spite  of  medical 


670 


TEXT-BOOK  OF  MEDICINE 


treatment,  and  as  danger  was  imminent,  Michaux  decided  on  operation.  The  stomach 
was  opened  and  explored  with  care,  but  the  operator  did  not  find  the  simple  ulcer  which 
he  expected.  No  adhesions ;  no  induration  ;  walls  of  the  stomach  supple.  The  patient 
was  so  weak  that  further  manipulation  was  abandoned.  During  the  next  few  days  the 
situation  became  worse  ;  the  meltena  persisted,  and  death  supervened  on  October  31. 


Fig.  43. — Showing  the  Ulceration, 

The  ulceration  hars  taken  place  at  the  expense  of  the  tunica  mucosa  M  with  the 
muscularis  mucosae  mm  ;  the  other  tunicse  of  the  stomach,  the  tunica  sub-mucosa  sm, 
the  tunica  mHSCulari?  m,  thetunica  serosa  s,  are  quite  healthy.  The  superficial  slanting 
arteriole  a  is  destroyed  at  h. 


Fig.  44. 


-Section  of  the  Artery  (no  Arteritis)  at  the  Point  where  it  reaches 

THE    UlCERATEB   SURFACE. 


Fig.  45. — Section  of  the  Artery  at  the  Point  where  its  Walls,  eroded  by  the 
Ulcerative  Process,  open  into  the  Cavity  of  the  Stomach. 

Michaux  has  been  kind  enough  to  give  me  his  specimens.  The  mucosa  of  the 
stomach  shows  a  superficial  circular  ulceration,  which  has  attacked  the  mucous  mem- 
brane only,  and  is  as  large  as  a  florin.  In  the  centre  there  is  a  small  cup-Uke  erosion, 
traversed  by  an  open  arteriole. 

Sections  made  by  Du  Pasquier  show  all  the  details.  Fig.  43  represents  the 
ulceration. 

The  arterial  lesion  which  caused  tlie  ha?morrhage  is  seen  in  Figs.  44  and  45.  The 
artery  is  healthy,  and  there  is  not  a  trace  of  arteritis  ;  the  vessel  is  seen  running  up  to  the 
aunica  mucosa,  until  its  walls  are  involved  in  the  ulceration.  It  opens  by  a  gaping  aper- 
ture into  the  cavity  of  the  stomach. 


DISEASES  OF  THE  STOMACH  671 

In  this  case,  as  in  my  first  one,  we  find  acute  exulceration  without  previous  vascular 
lesions.  The  ulcer  has  destroyed  the  mucosa  and  the  muscularis  mucosfe,  and  pro- 
duced the  fulminating  hsematemesis  by  erosion  of  one  of  the  arterioles  which  ramify 
under  the  muscularis  mucosae. 

In  my  clinical  lectures  on  exulceratio  simplex  several  cases  are  men 
tioned.     They  are  absolutely  identical  with  the  preceding  ones,  and  show 
that  this  lesion  is  far  from  being  rare.     Since  my  paper  on  this  subject, 
several  new  cases  have  been  pubhshed  in  France  (Chauffard,  Bichelonne 
and  Petges)  and  abroad  (John  Lindsay  Steven,  Quintard,  and  Restis). 

Pathological  Anatomy. — The  exulceration  is  generally  circular  ;  it  may 
be  elliptical  or  stellate.  It  often  affects  a  large  area,  since  it  may  be  as 
large  as  a  sixpence  (my  second  case),  a  florin  (Michaux's  case),  or  more 
(my  first  case).  We  have  not  to  deal  here — at  least,  as  far  as  appearance 
is  concerned — with  the  small,  punctiform,  hsemorrhagic  erosions  described 
by  Balzer  and  Fillet,  and  found  in  alcohohc,  cardiac,  or  cirrhotic  patients. 
In  our  cases,  cirrhosis,  heart  disease,  and  alcohohsm  were  not  in  evidence. 

The  exulceration  may  occur  in  any  region  of  the  gastric  mucosa.  It  is 
supple  ;  its  edges  are  neither  adherent  nor  thickened.  They  are  fairly 
distinct  from  the  surrounding  healthy  parts.  The  ulceration  is  in  the 
mucosa,  which  must  be  smoothed  out  in  order  to  show  the  lesion.  Its 
depth  is  so  Uttle  that  in  the  living  patient  at  the  time  of  operation,  and  in 
the  cadaver  at  the  post-mortem  examination,  it  may  easily  pass  unnoticed 
without  careful  examination  and  a  preconceived  idea  of  its  presence.  In 
the  neighbourhood  of  the  ulceration  reddish  spots  of  an  ecchymotic  appear- 
ance are  sometimes  seen.  In  some  cases  it  is  possible  to  distinguish  with 
the  naked  eye — or,  better,  with  a  lens — on  the  ulcerated  part  the  open 
arteriole  which  has  caused  the  bleeding. 

I  shall  not  dwell  on  the  histological  points  of  this  lesion.  Microscopic 
examination  has  always  proved  that  the  ulceration  is  due  to  the  disappear- 
ance of  the  mucous  coat,  with  its  muscularis  mucosae.  The  rest  of  the  , 
mucosa  of  the  stomach  is  generally  healthy  throughout  its  whole  extent, 
and  the  arterioles  of  the  ulcerated  portion  hardly  ever  show  arteritis.  In 
my  two  cases  and  in  those  reported  by  Brault  and  Giraudeau  there  was  not 
a  trace  of  it.  The  arterioles  attacked  by  the  ulcerative  process  were  healthy, 
a  proof  that  pre-existing  arterial  lesions  are  not  needed  to  explain  the  ulcera- 
tion and  the  resulting  ha3matemesis. 

Some  authors  consider  that  alcoholism  is  of  importance  as  leading  to 
simple  ulcer,  but  "  everyone  is  aware,"  says  Letulle,  "  that  the  simple 
ulcer  is  common  in  sober  persons  whose  arteries  are  healthy."  Tliis  rcniarlc 
applies  to  most  cases  of  exulceration,  and  amongst  the  cases  which  I  have 
collected,  I  can  only  find  alcoholic  gastritis  in  two  of  them. 

Summary. — Exulceratio  simplex  is  not  due  to  tuberculosis,  syphilis, 


672  TEXT-BOOK  OF  MEDICINE 

alcohol,  or  uraemia.  What  is  it,  then  ?  Everything  considered,  we  must 
admit  that  it  is  the  result  of  an  acute  toxi-infectious  process,  and  I  may- 
add  that  in  two  of  my  cases  the  deep  parts  of  the  ulcerated  mucous  coat 
were  the  seat  of  small  collections,  probably  httle  mihary  abscesses,  resulting 
from  toxi-infection.  These  abscesses,  as  may  be  seen  in  Fig.  42,  had 
destroyed  the  mucosa  in  places,  and  emptied  themselves  into  the  cavity 
of  the  stomach,  leaving  the  underlying  layers  without  any  defence.  Similar 
abscesses  were  found  in  the  cases  of  Lepine  and  Bret.  In  one  of  Giraudeau's 
cases  the  exulceration  did  not  extend  beyond  the  muscularis  mucosae,  and 
attacked  an  arterial  branch.  The  vessel  was  not  quite  divided,  and  no 
trace  of  arteritis  was  present  in  the  walls,  which  had  resisted  the  ulcerative 
process.  Furthermore,  and  an  important  point,  in  the  neighbourhood  of 
this  vessel  masses  of  leucocytes  were  seen  representing  true  mihary  abscesses, 
with  numerous  micro-organisms  in  Httle  chains. 

The  process  which  ends  in  exulceration  is  rapid  in  its  progress.  The 
exulceration  in  my  patient  was  of  recent  date,  and  the  histological  examina- 
tion did  not  reveal  any  chronic  lesion.  It  was  the  same  in  Michaux's 
patient,  and  the  exulceration  in  Giraudeau's  patient  was  hkewise  the  result 
of  a  recent  process.  In  the  case  reported  by  Luys  everything  leads  to  the 
supposition  "  that  the  lesion  was  of  recent  date,"  and  Brault  also  insists  that 
the  exulceration  which  caused  the  death  of  his  patient  was  "  of  recent  date." 

The  toxi-infectious  origin  of  exulceratio  simplex  and  the  rapidity  of  its 
course  agree  with  what  we  know  of  the  pathogenesis  of  acute  ulcerations  of 
the  stomach.  This  fact  was  explained  in  Sections  VII.  and  VIII.  Letulle 
has  expressed  the  opinion  that  "  the  ulcus  is  often  the  hidden  rehc  of  an 
infectious  disease."  In  a  woman  who  had  died  from  puerperal  fever  Letulle 
found  in  the  stomach  two  small  clean-cut  ulcerations.  The  underlying  veins 
were  thrombosed,  and  contained  many  streptococci.  Following  the  same 
idea,  Widal  and  Meslay  have  reported  the  case  of  a  youth  who  had  a  corn 
on  his  right  foot.  After  incision  cutaneous  abscesses  and  symptoms  of 
toxi-infection  soon  appeared,  and  caused  death.  Post  mortem,  signs  of 
general  infection  were  found,  abscesses  or  suppurative  infarcts  in  the  myo- 
cardium, kidneys,  lung,  and  epididymis,  due  to  Streptococcus  aureus.  In 
the  stomach  there  was  an  acute  ulcer  of  large  size. 

The  experibiental  investigation  of  acute  ulceration  of  the  stomach  is 
also  in  favour  of  a  toxic  origin.  Letulle  produced  ulceration  of  the  stomach 
in  a  guinea-pig  by  injecting  staphylococci  into  the  peritoneum,  after  having 
first  filled  the  stomach  with  solution  of  bicarbonate  of  soda.  Enriquez  and 
Halhon  have  produced  gastric  ulcerations  in  the  guinea-pig  by  injecting 
diphtheritic  toxine  under  the  skin  of  the  abdomen,  and  Bezan9on  and 
Griffon  have  induced  acute  gastric  erosions  by  the  introduction  of  the 
pneumococcus  into  the  peritoneum  of  a  guinea-pig. 


DISEASES  OF  THE  STOMACH  673 

It  was  still  essential  to  determine  the  origin  of  the  toxi-infection.  Was 
it  preceded  by  infectious  lesions,  such  as  angina,  furuncles,  otitis,  etc.  ? 
It  was  not  possible  to  prove  this  fact  in  my  patients.  In  them  the  exul- 
ceration  superv^ened  whilst  they  were  in  perfect  health. 

Description. — Events  usually  run  the  following  course  :  A  young  person 
who  has  previously  had  neither  gastric  pain  nor  dyspeptic  troubles,  and  is 
apparently  free  from  any  gastric  lesion,  is  suddenly  seized  with  malaise, 
vertigo,  nausea,  and  weight  in  the  stomach,  and  vomits  1  or  2  pints  of  blood, 
which  may  be  Uquid  or  partly  clotted.  The  bleeding  is  followed  by  weakness, 
and  if  the  first  stools  are  examined,  melsena  will  be  found.  The  first  attack 
is  rarely  fatal,  but,  on  the  other  hand,  it  very  rarely  happens  that  the 
attack  does  not  recur,  and  a  few  hours  later  or  on  the  following  day  or  the 
day  after,  a  second,  third,  or  fourth  severe  attack  of  haematemesis  takes 
place,  and  is  accompanied  by  vertigo  and  syncope,  so  that  in  twenty-four 
to  forty-eight  hours  the  patient  vomits  several  pints  of  blood.  You  find 
him  breathless  and  Uvid,  with  colourless  mucosas  and  inaudible  voice.  The 
pulse  is  small  and  quick,  and  the  temperature  is  often  raised ;  but  the 
patient  feels  no  pain,  and  the  stomach  is  not  tender  on  palpation. 

The  exulceration  is  almost  always  rapid  and  latent ;  it  may,  indeed,  be 
said  that  its  clinical  history  commences  with  the  haemorrhage.  Let  us 
review  our  cases,  and  it  will  be  seen  that,  with  the  exception  of  two  or  tlu'ee 
amongst  them,  who  complained  of  some  gastric  symptoms,  the  others  had 
experienced  nothing  that  might  draw  attention  to  the  condition  of  the 
stomach.  They  were  not  dyspeptic,  and  had  had  neither  pains  in  the 
stomach,  nor  fits  of  vomiting,  nor  gastric  intolerance.  They  were  taken 
suddenly  ill  whilst  in  perfect  health  with  these  severe  attacks  of  haemorrhage. 
In  my  first  patient  who  died,  the  attacks  of  haematemesis  came  on  suddenly 
without  previous  warning  ;  my  second  patient,  who  was  cured  by  the  opera- 
tion, was  walking  home  when  he  commenced  to  vomit  blood,  without  any 
previous  gastric  symptoms.  A  young  woman  whom  we  had  in  the  St. 
Jeanne  Ward  was  seized  with  severe  and  unexpected  haematemesis.  A 
young  girl  whom  I  saw  in  consultation  with  Griinberg  had  never  had  any 
gastric  symptoms,  when  she  was  attacked,  while  walking,  with  fulminant 
haematemesis.  The  patient  operated  upon  by  Michaux  had  never  had  any 
fits  of  vomiting  or  gastric  pains.  The  first  symptom  of  the  exulceration 
was  haematemesis.  The  young  girl  who  died  whilst  under  the  care  of  Brault 
had  never  had  any  stomach  troubles  when  the  severe  attacks  of  luema- 
temesis  which  ended  fatally,  suddenly  appeared.  A  patient  whom  I  had 
in  the  Hotel-Dieu,  and  who  had  not  the  slightest  gastric  trouble  previously, 
was  seized  with  such  severe  attacks  of  haematemesis  that  the  blood-count 
showed  only  630,000  red  blood-corpuscles. 

Another  fact  has  attracted  my  attention — namely,  that  haemorrhages 

43 


674  TEXT-BOOK  OF  MEDICINE 

in  exulceratio  simplex  are  severe  from  the  first,  and  are  not  preceded  by 
slight  premonitory  bleeding ;  they  are  not  preceded  by  vomiting  of  blood 
like  coffee-grounds,  which  is  so  frequent  in  ulcus  simplex.  From  the  very 
first  they  amount  to  a  pint  or  more,  and  this  severe  haemorrhage  takes  place 
in  a  few  moments,  and  is  at  times  followed  by  melaena.  Whilst  fatal 
gastrorrhagia  is  relatively  rare  in  ulcus  simplex,  lightning-like  haematemesis 
is  much  more  frequent  in  exulceratio  simplex,  in  which  it  constitutes  the 
most  important  sign  and  the  sole  danger.  Pathological  anatomy  will 
perhaps  be  able  to  enlighten  us  on  these  differences  between  gastrorrhagia 
in  ulcer  and  in  exulceration. 

The  chronic  course  of  the  ulcer  lends  itself  better  to  vascular  obhtera- 
tion,  whilst  the  acute  process  in  the  exulceration  rapidly  affects  the  muscu- 
laris  mucosae  and  the  arterioles.  It  attacks  the  vessel  and  destroys  its  wall 
laterally.  The  haemorrhage  is  much  worse  when  an  artery  is  opened 
laterally  than  when  it  is  completely  cut  across.  In  the  former  case  the 
retraction  of  the  walls  and  the  formation  of  the  clot  are  not  enough  to 
arrest  the  haemorrhage.  Accordingly,  in  exulceratio  simplex  the  haemor- 
rhage is  terrible  and  in  some  cases  fulminant.  My  first  patient  lost  7  pints 
in  less  than  thirty  hours  ;  my  second  patient  had  lost  7  pints  of  blood  when 
I  advised  operation.  Michaux's  patient  lost  several  pints  of  blood,  and 
the  same  may  be  said  of  Brault's  case ;  Gilbert's  patient  died  of  fulminant 
haematemesis.  Two  young  women,  of  whom  I  shall  speak  later,  lost  several 
pints  of  blood  in  forty-eight  hours.  The  greatest  peril  of  exulceratio  simplex 
Ues,  then,  in  the  quasi-fulminant  attacks  of  gastrorrhagia,  which  show 
themselves  by  haematemesis  and  melsena. 

We  are  ill  acquainted  with  the  chemical  composition  of  the  gastric 
juice  during  exulceratio  simplex.  It  might,  a  priori,  be  supposed  that 
here,  as  in  ulcus  simplex,  excess  of  acid  would  be  found,  and  yet  in  Lepine 
and  Bret's  case  no  free  hydrochloric  acid  was  discovered.  In  my  second 
patient  I  found  a  condition  of  hypochlorhydria.  I  bring  forward  this  fact, 
which  does  not  agree  with  the  theories,  and  which  proves  in  any  case  that 
exulceration,  like  ulcer,  may  occur  although  the  amount  of  hydrochloric  acid 
is  diminished.  Another  point  to  be  noticed  is  the  febrile  condition  of 
patients  suffering  from  exulceration,  and  we  find  in  almost  every  case  a  rise 
of  temperature.  W^hy  this  rise  of  temperature  ?  The  youth  in  St.  Chris- 
topher Ward  had  a  temperature  of  100°  F.,  and  in  Michaux's  patient  the 
reading  was  102°  F.  In  the  case  of  the  young  woman  in  St.  Jeanne  Ward 
the  temperature  remained  high  for  three  days,  and  the  young  girl  whom  I 
saw  with  Grlinberg  had  a  temperature  of  102°  F.  for  several  days.  Another 
point  to  be  noted  is  the  predilection  of  exulceration  for  young  people. 

Diagnosis. — We  have  said  that  the  evolution  of  exulceratio  simplex  is 
rapid  and  latent,  revealing  its  presence  suddenly  by  terrible  attacks  of 


DISEASES  OF  THE  STOMACH  675 

hgematemesis,  and  but  imperfectly  heralded  by  weight  in  the  stomach, 
with  or  without  nausea,  vertigo,  and  tendency  to  syncope.  These  attacks 
of  hsematemesis  may  be  fatal,  unless  recourse  be  had  to  operation,  so  that 
the  question  resolves  itself  into  making  a  correct  diagnosis. 

If  the  patient  is  seized  with  sudden  and  severe  haematemesis,  a  double 
diagnosis  must  be  made — firstly,  to  prove  that  it  is  a  case  of  hsematemesis  ; 
and,  secondly,  to  ascertain  the  lesion  that  has  provoked  it.  A  patient 
tells  you  that  he  has  been  vomiting  blood.  Has  he  had  an  attack  of 
haematemesis  or  of  haemoptysis  ?  Haemoptysis  is  sometimes  so  copious 
and  the  blood  is  brought  up  with  such  violence  that  the  patient  speaks  of 
vomiting,  though  the  blood  really  comes  from  the  lung,  and  not  from  the 
stomach.  The  blood  in  haemoptysis  is  brought  up  during  fits  of  coughing  ; 
it  is  frothy  and  bright  red,  which  is  not  the  case  in  haematemesis.  Further- 
more, the  pulmonary  lesion  which  causes  haemoptysis  indicates  the  cause 
and  seat  of  the  haemorrhage.  The  opening  of  an  aortic  aneurysm  into  the 
trachea  or  bronchi  must  also  be  considered.  In  this  case  the  patient  vomits 
an  enormous  quantity  of  blood,  which  must  be  differentiated  from  haema- 
temesis.    It  is  true  that  death  is  the  immediate  consequence. 

When  haematemesis  is  proved,  it  is  necessary  to  locahze  its  origin.  Blood 
may  pass  from  the  nose  into  the  stomach  and  be  vomited.  I  have  seen 
two  cases  of  this  kind. 

A  bloodless  patient  came  under  my  care  for  haematemesis,  attributed  to  a  lesion 
of  the  stomach.  Examination  showed,  not  a  gastric  lesion,  but  an  angioma  of  the  nasal 
fossee.  The  blood  ran  down  the  cesophagus  and  accumulated  in  the  stomach,  whence 
it  was  rejected  by  haematemesis.  The  angioma  was  cauterized  by  Luc,  and  the  bleeding 
at  once  ceased. 

(Esophageal  and  gastric  varices  (Letulle)  in  cirrhosis  of  the  liver  may 
rupture  and  cause  haematemesis. 

A  patient  came  under  my  care  for  cirrhosis  of  the  liver.  Whilst  we  were  examining 
him,  he  was  seized  with  nausea,  and  twice,  at  a  quarter  of  an  hour's  interval,  he  brought 
up  2  pints  of  blood.  In  spite  of  treatment,  he  died  the  next  day.  At  the  post-mortem 
examination  cirrhosis  of  the  liver  was  found  ;  at  the  lower  end  of  the  oesophagus  there 
was  a  varicose  plexus  ;  one  of  the  veins  was  ulcerated,  and  the  blood  had  filtered  into  the 
stomach  and  had  been  subsequently  vomited. 

In  such  a  case  we  have  as  a  guide  the  symptoms  of  hepatic  cirrhosis. 
If  the  cirrhosis  is  early,  it  is  possible,  thanks  to  "  the  minor  signs  of  cirrhosis  " 
(Hanot) — urobilinuria,  subicteric  tint,  haemorrhoids,  epistaxis,  alimentary 
glycosuria,  and  abdominal  tympanites — to  recognize  the  disease  and  the 
origin  of  the  haemorrhage. 

Severe  haematemesis  with  melacna  has  also  been  found  as  a  coniplicatioji 
of  gall-stones.  In  this  case  the  bleeding  is  due  to  an  aneurysm  of  the  hepatic 
artery,  which  opens  into  the  large  bile-ducts.  I  have  seen  a  case  of  this 
kind. 

43—2 


676  TEXT-BOOK  OF  MEDICINE 

It  has  been  thought  that  hsematemesis  might  be  due  to  infective  angio- 
choHtis.  Rondot  has  pubhshed  the  history  of  two  patients  who  had  symp- 
toms of  ulcer  of  the  stomach  and  severe  hsematemesis.  At  the  post-mortem 
examination  an  abscess  of  the  hver  was  found  in  one  patient  and  suppurative 
cholecystitis  in  the  other.  The  report  mentions  that  the  stomach  also 
presented  traces  of  ulceration,  which  were  examined  microscopically.  I 
therefore  put  the  question  whether  the  trouble  must  not  be  laid  rather  to 
the  charge  of  the  ulceration  than  to  the  angiocholitis  ? 

Cancer  of  the  stomach  causes  attacks  of  hsematemesis,  but  they  are 
preceded  by  many  other  signs,  and,  moreover,  the  bleeding  is  not  copious. 
Severe  hsematemesis  is  seen  in  ulcer.  If  cancer  of  the  stomach  is  accom- 
panied by  severe  hsematemesis,  it  is  because  the  cancer  is  grafted  on  an 
ulcer. 

From  this  discussion  it  is  evident  that,  with  a  few  exceptions  recog- 
nizable by  clinical  examination  (varices  of  the  oesophagus  and  stomach, 
hepatic  cirrhosis),  profuse  hsematemesis  is  due  to  simple  ulcer  and  exulceratio 
simplex.     Let  us  attempt  a  differentiation. 

In  exulceration,  hsematemesis  is  generally  the  first  symptom ;  previous 
gastric  troubles  are  absent  or  slight.  In  ulcer,  hsematemesis  is  preceded  or 
accompanied  by  the  classical  symptoms.  The  ulcer  may,  it  is  true,  have 
been  latent,  but  scrutiny  shows  that  this  so-called  latent  state  is  often  only 
relative.  Hsematemesis  in  exulceration  presents  some  interesting  features. 
When  I  refer  to  my  case-book,  I  find  that  the  hsematemesis  is  severe  from 
the  first,  and  is  not  preceded  by  the  slight  attacks  of  vomiting  of  blood 
like  coffee-grounds  which  are  so  frequent  in  ulcus  simplex.  The  latter,  it 
is  true,  also  causes  hsemorrhage,  which  may  become  fatal  on  account  of  its 
abundance  or  its  repetition.  I  consider,  however,  the  hsematemesis  of 
exulceration  as  more  to  be  feared  than  that  of  ulcer.  I  have  had  many 
patients  suffering  from  ulcer,  but,  though  several  died  from  perforation, 
cachexia,  or  malignant  changes,  and  others  had  severe  attacks  of  hsema- 
temesis, fulminant  hsemorrhage  was  exceedingly  rare. 

Let  us  see  what  happened  in  the  ten  cases  of  exulceratio  simplex  discussed 
in  my  clinical  lectures.  Seven  died  more  or  less  quickly,  after  losing  several 
pints  of  blood,  from  ulceration  of  an  arteriole.  Post  mortem  the  same 
lesion  was  found  in  every  case,  the  exulceration  having  attacked  or  destroyed 
the  arteriole.  As  for  the  patients  who  recovered,  they  also  looked  as  if 
the  hand  of  death  had  been  placed  upon  them  in  the  midst  of  perfect  health. 
The  gastrorrhagia  was  so  copious  that  the  blood-count  showed  only 
1,200,000  red  corpuscles,  and  in  a  recent  case  at  the  Hotel-Dieu  the  corpuscles 
were  only  630,000.  I  am  therefore  correct  in  stating  that  hsematemesis 
in  exulceration  is  more  acute  and  more  sudden,  as  a  rule,  than  in  ulcer.  In 
a  word,  sudden  hsematemesis,  which  is  threatening  from  the  very  outset. 


DISEASES  OF  THE  STOMACH  677 

and  often  fatal,  is  the  dominant  symptom  in  the  chnical  picture  of  exulceratio 
simplex. 

Prognosis. — I  have  just  explained  how  death  from  exulceratiou  comes 
about,  and  I  should  hke  to  mention  those  cases  that  recover.  What  is 
their  future  ?  Are  they  freed,  once  and  for  all,  from  this  terrible  eventu- 
ahty  ?  Does  exulceration  predispose  to  a  second  attack,  like  ulcer,  or  is  it 
not  the  initial  stage  of  Cruveilhier's  ulcus  simplex,  arrested  in  its  course  by 
fulminant  haematemesis  or  by  appropriate  treatment  ?  To  prove  this 
hypothesis,  it  would  be  necessary  to  find  a  typical  ulcer  and  an  exulceration 
in  the  same  stomach.  It  would,  then,  be  rational  to  suppose  that  we  had 
before  our  eyes  the  simple  ulcer  in  the  various  stages  of  its  development. 
With  this  idea  in  view,  I  have  succeeded  in  finding  a  case  which  seems  clear. 
The  case  is  as  follows  : 

A  man  who  had  had  no  previous  gastric  symptoms  was  admitted  into  hospital  with 
signs  of  internal  haemorrhage — viz.,  pallor,  cold  sweat,  and  tendency  to  syncope.  After 
dinner  he  suffered  from  severe  malaise,  was  seized  with  fulminant  htematemesis,  and 
died.  At  the  jjost-mortem  examination  three  ulcers  were  found,  placed  one  behind  the 
other,  on  the  lesser  curve  of  the  stomach.  The  middle  ulcer  was  a  typical  ulcus  simplex  ; 
it  was  the  size  of  a  shilling,  round,  and  had  prominent,  clean-cirt  edges.  The  floor  was 
reddish,  mammillated,  and  a  divided  artery,  obliterated  by  a  clot  of  fibrin,  was  found 
on  section.  To  the  right  and  left  of  this  ulcer  there  were  two  slight  ulcerations,  one  of 
which  was  of  the  size  of  a  lentil,  while  the  other  ulceration  was  superficial,  eUiptical  in 
shape,  and  about  as  large  as  a  halfpenny.  Although  no  histological  examination  was 
made,  it  had  all  the  characteristics  of  ah  exulceratio.  The  floor  was  traversed  by  a 
vessel,  with  a  lateral  opening  visible  under  water  and  under  the  lens.  On  reading  of 
this  ease,  I  thought  I  had  found  a  case  in  which  the  lesion  existed  both  in  the  stage  of 
confirmed  ulcer  and  of  limited  exulceration. 

We  may,  then,  admit  that,  until  the  contrary  has  been  proved,  exulceratio 
simplex  may  be  an  initial  stage  of  Cruveilhier's  ulcus  simplex.  Moreover, 
Cruveilhier,  in  his  excellent  description  of  simple  ulcer,  has  rightly  said 
that  "  In  the  first  degree  the  ulceration  is  hmited  to  the  mucous  membrane, 
and  is  generally  a  follicular  erosion." 

I  believe  that  exulceratio  simplex  is  not  subject  to  recurrences.  A 
patient  who  is  cured  of  exulceration  need  not  fear  a  return  thereof,  because 
the  toxi-infectious  process  which  produced  the  ulceration  is  extinct. 

Treatment. — Let  us  take  the  situation  in  a  case  analogous  to  one  of 
those  wliich  we  have  just  described.  You  are  called  to  a  patient  who  has 
been  seized  with  severe  haematemesis  while  in  good  health.  The  blood  is 
there,  liquid  or  in  clots,  and  the  quantity  is  alarming,  for  2  or  3  pints  have 
been  brought  up  at  one  time.  The  patient  is  anxious,  ready  to  faint,  and 
extremely  pale.  The  pulse  is  quick,  and  the  temperature  slightly  raised. 
You  make  inquiries,  and  formulate  the  following  diagnosis  :  The  patient  has 
just  had  a  terrible  attack  of  haematemesis,  in  consequence  of  ulceration  of 
the  stomach,  and  everything  points  to  exulceratio  simplex. 


678  TEXT-BOOK  OF  MEDICINE 

What  are  you  going  to  do  ?  Are  you  to  advise  immediate  operation  ? 
As  you  know  that  death  has  followed  the  first  or  second  attack  of  haema- 
temesis,  be  ready  in  case  surgical  intervention  should  become  urgent,  but 
first  try  medical  treatment.  The  immediate  indication  is  to  keep  your 
patient  absolutely  at  rest,  with  an  ice-bag  on  the  abdomen.  In  my  opinion, 
the  patient  should  take  absolutely  nothing — not  even  a  spoonful  of  water 
nor  a  morsel  of  ice.  I  consider  that  anything  which  may  induce  movement 
of  the  stomach  or  secretion  of  the  gastric  juice  is  harmful.  An  arteriole  has 
been  opened,  and  the  haemorrhage  has  been  stopped  for  the  moment  by  a 
clot  which  will  later  obliterate  the  vessel.  Do  not  give  an5^hing  which 
may  hamper  the  process  of  repair.  Fluid  by  the  mouth  provokes  contrac- 
tion of  the  stomach  and  secretion  of  the  gastric  juice,  conditions  which  are 
unfavourable  to  the  sohdification  of  the  occluding  clot.  I  reject,  therefore, 
in  the  most  absolute  manner,  preparations  of  gelatine  and  haemostatic 
draughts.  All  medication  must  be  carried  out  hypodermically  or  per 
rectum.  The  patient  must  be  fed  by  means  of  nutritive  enemata  of  peptones, 
eggs  and  milk,  while  ergotin  or  ergotinin  is  given  hypodermically ;  and 
even  then  these  remedies,  though  most  efficacious  in  uterine  haemorrhage, 
are  here  of  less  utility.  Artificial  serum  should  be  given  by  subcutaneous 
injection.  It  may  be  asked  theoretically  if  these  injections  do  not  afiect  the 
process  of  coagulation  in  the  vessel,  by  raising  the  arterial  tension,  or  if  too 
large  a  quantity  of  serum,  rapidly  introduced,  has  not  a  bad  effect  on  the 
small  quantity  of  blood  still  remaining  in  the  body  ?  Experience  proves 
that  careful  injections  of  serum  are  of  service.  It  is  not  necessary  that  they 
be  intravenous.  The  injections  may  be  repeated  several  times  a  day,  and 
10  to  15  ounces  of  serum  may  be  given  at  a  time. 

The  young  woman  whom  I  saw  with  Griinberg  took  some  26  pints  in 
twenty-nine  days.  You  may  employ  a  serum  containing  0"7  per  cent,  of 
chloride  of  sodium  (Malassez's  formula),  or  a  serum  containing  75  grains 
of  chloride  of  sodium  and  150  grains  of  sulphate  of  soda  (Hayem's  formula), 
to  35  ounces  of  water.  The  serum  which  I  employ  contains  105  grains  of 
chloride  of  sodium  and  2  grains  of  benzoate  of  caffein  to  35  ounces  of  water. 
I  have  held  to  this  formula,  because  it  seems  to  me  to  answer  all  purposes. 
(For  further  details,  see  Appendix  on  Therapeutics.) 

Inhalations  of  oxygen  and  injections  of  ether  are  of  benefit  in  case  of 
syncope.  The  above  treatment  is  carefully  watched.  The  patient  must 
take  no  food  for  three  or  four  days  ;  after  that  time  a  few  spoonfuls  of 
water,  and  then  a  few  spoonfuls  of  milk  diluted  with  water,  are  given,  the 
amounts  being  gradually  increased.  You  rarely  succeed  in  stopping  the 
haemorrhage  at  first,  and  fresh  attacks  of  haematemesis  may  occur.  In 
certain  cases  the  situation  becomes  dangerous :  the  restlessness  increases, 
the  pulse  becomes  quicker,  the  pallor  more  pronounced,  and  the  fainting- 


DISEASES  OF  THE  STOMACH  679 

fits  succeed  one  another.  You  do  not  dare  to  leave  the  patient,  and  are 
rightly  afraid  of  fatal  syncope.  You  ask  yourself  whether  fatal  haema- 
temesis  may  not  occur  at  any  moment,  and  you  think  of  surgical  intervention. 

The  difficulty  is  great,  for  you  must  now  take  the  responsibility  of 
choosing  the  right  moment  for  surgical  intervention. 

What,  then,  is  the  right  moment  in  the  case  of  severe  hsematemesis 
due  to  exulceratio  simplex  ?  It  is  certainly  true  that  the  above  treatment 
is  of  great  value,  but  it  has  its  limits.  My  first  patient  succumbed,  although 
he  had  received  3  pints  of  serum.  Brault's  patient  succumbed,  though 
large  and  repeated  injections,  including  an  intravenous  one  of  3  pints,  were 
given.  Medical  treatment  is  therefore  at  times  powerless,  and  surgical 
methods  have  a  better  chance  of  success  if  they  are  applied  before  fatal 
syncope  is  imminent.  What,  then,  are  the  indications  showing  that  the 
operation  is  urgent  ?  Is  it  necessary  when  the  number  of  red  corpuscles  has 
been  reduced  to  a  certain  number  ?  Can  it  be  said,  for  example,  that  an 
operation  is  necessary  as  soon  as  the  number  of  red  corpuscles  has  been 
reduced  to  1,200,000  ?  I  do  not  think  that  this  is  the  sole  criterion,  for 
Lepine  and  Bret's  patient  succumbed  when  he  had  1,300,000  corpuscles; 
and,  on  the  other  hand,  one  of  my  patients  at  the  Hotel-Dieu  recovered, 
though  he  had  only  630,000  corpuscles.  These  cases  show  that  a  blood- 
count  alone  is  no  guide. 

I  do  not  know  of  any  exact  §ign  by  which  to  decide  when  operation  is 
urgent.  The  decision  must  rest  upon  a  survey  of  all  the  facts.  Account 
must  be  taken  of  the  state  of  the  pulse,  the  strength  of  the  patient,  and  his 
powers  of  resistance.  In  short,  we  must  not  only  know  when  to  wait,  but 
also  when  to  decide.  I  am  convinced  that  operations  for  haematemesis 
due  to  exulceratio  simplex  will  give  brilliant  results,  for  they  are  infinitely 
more  simple  in  the  case  of  exulceration  than  of  ulcer.  In  the  case  of  ex- 
ulceratio there  are  no  adhesions,  no  perigastric  lesions,  and  no  large  ulcers 
in  the  stomach.  On  the  contrary,  there  is  a  very  hmited  superficial  lesion 
which  lends  itself  to  operation.  The  lesion  is  so  superficial,  and  at  first 
sight  so  little  apparent,  that  it  may  escape  notice  if  previously  unsuspected. 
Remember  what  happened  to  operators  until  the  anatomical  and  cUnical 
history  of  exulceratio  came  to  be  written. 

If  a  patient  was  seized  with  severe  and  repeated  attacks  of  haematemesis, 
he  was  generally  thought  to  be  suffering  from  ulcus  simplex,  and  was  handed 
over  to  the  surgeon.  The  surgeon,  certain  of  finding  an  important  lesion, 
such  as  adhesions,  induration  of  the  walls  of  the  stomach,  or  a  large  tumour 
with  thick  edges,  opened  the  stomach,  and  was  much  surprised  at  the 
absence  of  the  expected  lesion.  He  believed  that  there  had  been  an  error 
in  the  diagnosis,  and  closed  the  stomach,  or  else  performed  gastro-enter- 
ostomy,  without  accounting  for  what  had  really  happened.    A  similar  mistake 


680  TEXT-BOOK  OF  MEDICINE 

has  been  noted  in  several  cases.  Michaux  opened  the  stomach,  with  the 
full  conviction  that  he  would  find  an  ulcer ;  but  he  did  not  find  it,  and  the 
exulceratio  simplex,  which  was  the  cause  of  fatal  haemorrhage,  passed  un- 
noticed, and  the  mistake  was  only  found  at  the  post-mortem  examination. 
Hartmann  opened  the  stomach,  expecting  to  find  an  ulcer,  and  failed  to 
discover  the  exulceratio  simplex  which  gave  rise  to  the  fatal  haemorrhage, 
and  was  only  found  later  at  the  autopsy.  In  the  case  of  the  patient  upon 
whom  Cazan  operated  at  my  request,  the  stomach  was  opened,  and  at  first 
sight  appeared  healthy.  As  I  felt  certain  that  an  exulceratio  simplex  was 
present,  it  was  looked  for,  found,  and  Ugatured,  with  the  result  that  the 
patient  recovered. 

It  must  not  be  said,  as  has  been  incorrectly  advanced,  that  it  is  im- 
possible to  find  an  exulceratio  simplex  at  the  time  of  operation,  and  I  protest 
against  such  an  assertion.  Until  recently  we  were  not  familiar  with  ex- 
ulceratio simplex.  No  monographs  had  been  written,  and  it  liad  attracted 
so  little  attention  that  when  the  stomach  was  opened  it  was  not  seen, 
because  we  had  not  been  taught  how  to  look  for  it.  It  passed  unnoticed, 
because  its  existence  was  unknown.  We  have  therefore  a  new  chapter 
to  add  to  our  accounts  of  ulceration  of  the  stomach.  In  future  the  physician 
will  make  his  diagnosis,  and  when  the  surgeon  has  opened  the  stomach  for 
hsematemesis  due  to  an  exulceration,  he  will  know  that  the  stomach  may 
at  first  sight  appear  perfectly  healthy,  and  that  he  must  look  for  the  ex- 
ulceratio simplex  with  the  most  minute  care.  He  must  examine  the  mucosa, 
cleansing  and  smoothing  it  out,  and,  if  necessary,  using  a  lens,  when  he  will 
find  the  exulceration,  which  may  vary  in  size  from  a  lentil  to  a  shilhng.  He 
will  discover  it  the  more  easily  as  the  exulceration,  no  matter  how  superficial 
it  is,  generally  occupies  a  certain  surface  and  is  sometimes  surrounded  by 
ecchymoses,  which  serve  as  a  guide. 


X.  SIMPLE  ULCER  OF  THE  STOMACH  (CRUVEILHIER'S 

DISEASE). 

Several  questions  concerning  simple  ulcer  have  been  discussed  under  Exulceratio 
Simplex ;  they  will  also  be  mentioned  in  Section  XIII.  I  would  therefore  ask  the 
reader  to  study  these  sections  together. 

History. — We  have  already  seen  that  the  acute  ulcerative  lesions  of  the  stomach  are 
numerous,  and  that  their  origin  is  multiple.  The  present  description  refers  to  a  chronic 
variety  which  has  been  called  simple  ulcsr  (Cruveilhier),  perforating  ulcer  (Rokitansky), 
ulcus  rotundum  (Niemeyer)  ;  it  is  peculiar  to  the  stomach,  oesophagus,  and  duodenum, 
and  was  first  described  by  Cruveilhier. 

In  the  year  1830,  he  described  the  simple  chronic  ulcer,  and  separated  it  from  cancer 
of  the  stomach,  with  which  it  had  previously  been  confounded.  He  completed  his 
work  in  1838,  and  has  left  us  so  complete  a  clinical  and  anatomical  picture  of  the  disease 
that  this  malady  rightly  bears  his  name.     Rokitansky 's  monograph  is  dated  1839.     I 


DISEASES  OF  THE  STOMACH  681 

may  be  permitted  to  state  that  the  clinical  distinction  between  ulcer  and  cancer  of  the 
stomach  is  not  always  absolute.  Cruveilhier  himself  noted  the  coexistence  of  both 
lesions  in  the  same  stomach,  and  during  the  past  few  years  several  cases  have  been 
noted  which  prove  that  gastric  ulcer  is  sometimes  only  the  prelude  of  cancer,  or,  rather, 
cancer  frequently  grafts  itself  on  the  ulcer  or  its  cicatrix. 

The  name  ulcus  rotundum  is  suitable  ;  the  ulcer,  however,  has  not  always  a 
rounded  form,  and  the  name  of  perforating  is  no  better,  because  the  ulcer  does  not 
always  end  in  perforation.     The  name  simple  ulcer  should  therefore  be  preserved. 

Pathological  Anatomy. — According  to  statistics  collected  by  Rosen- 
heim and  Brinton,  the  situation  of  ulcer  is  as  follows  : 

Posterior  wall  of  the  stomach  . .  . .  83 

Pyloric  region  . .  . .  . .  . .  36 

Lesser  curvature     . .  . .  . .  . .  37 

Anterior  wall  .  .  .  .  . .  . .  26 

The  ulcer  is  generally  rounded.  It  has  a  semilunar  or  circular  form 
when  it  embraces  the  pyloric  region,  but  is  large  and  irregular  when  several 
ulcers  have  coalesced. 

The  ulceration  tends  to  destroy  successively  the  mucous,  fibrous,  mus- 
cular, and  peritoneal  coats,  and  the  depth  of  the  ulcer  varies,  therefore, 
according  to  the  coat  destroyed.  As  regards  its  anatomical  course,  the 
simple  ulcer  commences  as  an  erosion,  forms  an  ulceration,  and  ends  by 
cicatrization  or  by  perforation. 

On  the  mucous  aspect,  the  uloer  appears  funnel-shaped,  the  orifice  of 
the  ulcer  being  wider  than  the  bottom.  Its  edges  are  not  ragged,  but  clean- 
cut,  like  a  punch-hole.  On  the  edges  and  the  floor  of  the  ulcer  we  often  find 
arterioles  cut  through,  while  the  lumen  has  been  obhterated  by  a  plug  of 
embryonic  tissue.  When  the  lesion  is  old,  the  edges  of  the  ulcer  may  become 
so  indurated  and  thickened  as  to  simulate  cancer.  The  dimensions  of  the 
ulcer  are  variable.  Some  are  hardly  as  big  as  a  sixpence,  while  others  may 
be  larger  than  a  crown.  The  ulcer  may  be  single  or  multiple.  According 
to  Brinton  it  is  double  once  in  five  times,  while  as  many  as  five  have  been 
found  in  the  same  subject  (Rokitansky).  Post  mortem,  it  is  no  uncommon 
thing  to  discover  the  scars  of  healed  ulcers.  The  mucous  membrane  is 
absent  over  these  areas. 

Recovery  is  frequent,  but  sometimes  occurs  at  the  expense  of  scars, 
which  constrict  the  pylorus  or  produce  an  hour-glass  stomach.  When  the 
ulcer  terminates  in  perforation,  the  peritoneal  opening,  which  varies  in  size, 
is  as  clean-cut  as  the  gastric  opening.  The  perforation  in  some  cases  opens 
into  the  peritoneal  cavity,  and  if  adhesions  are  absent  fatal  peritonitis  is 
the  result,  unless  an  early  operation  is  performed.  In  other  cases  the  per- 
foration is  limited  by  the  adhesions  to  a  neighbouring  organ,  whicli  forms 
a  tampon,  and  in  turn  becomes  ulcerated.  In  this  way  the  floor  of  the 
ulcer  is  formed,  as  the  case  may  be,  by  the  diaphragm,  liver,  spleen,  pancreas, 


682  TEXT-BOOK  OF  MEDICINE 

mesenteric  glands,  or  sternum  (Barth).  In  other  cases  the  perforation 
establishes  a  fistula  between  the  stomach  and  the  duodenum,  colon,  bronchi, 
pericardium,  or  skin.  The  perforation  may  give  rise  to  subphrenic  abscess, 
which  we  shall  study  later.  As  the  ulceration  does  not  spare  the  arteries 
of  the  stomach  (coronary,  splenic,  gastro-epiploic  vessels),  fatal  gastror- 
rhagia  may  result. 

The  ulcer,  even  in  the  absence  of  perforation,  causes  adhesions  between 
the  stomach  and  the  neighbouring  organs.  This  fact  often  comphcates  the 
technique  in  the  case  of  surgical  intervention.  The  microscopic  examina- 
tion of  the  tissues  bounding  the  ulcer  shows  the  lesions  of  gastritis.  The 
glands  show  a  tendency  to  disappear,  the  cells  are  affected  by  fatty  degenera- 
tion, and  masses  of  embryonic  cells  appear  under  the  mucosa  in  the  cellular 
tissue,  while  the  submucous  muscular  tissue  is  broken  and  the  subjacent 
tunicse  musculares  are  invaded. 

etiology — Pathogenesis. — Is  simple  ulcer  of  the  stomach  a  distinct 
morbid  entity,  or  is  it  only  the  end  of  the  various  erosions  and  ulcerations 
which  may  at  a  given  moment  pass  into  simple  ulcer  ?  Both  opinions 
have  been  upheld.  Whichever  be  the  theory  preferred,  how  can  we  explain 
the  process  which  takes  the  chief  part  in  the  formation  of  this  ulcer  ?  It 
has  been  held  that  the  ulceration  at  its  commencement  is  only  an  ecchymotic 
patch  caused  by  blood-stasis,  due  to  fatty  or  atheromatous  degeneration  of 
the  small  vessels.  Superficial  necrobiosis  of  the  mucosa  is  the  result,  and 
the  gastric  juice,  by  digesting  the  walls  of  the  stomach,  becomes  the  chief 
factor  in  the  morbid  process. 

The  action  of  the  gastric  juice  appears  the  more  Hkely  to  many  writers, 
because  patients  suffering  from  simple  ulcer  of  the  stomach,  often  suffer 
from  hyperchlorhydria  or  excess  of  acid,  during  digestion,  and  from  hyper- 
secretion, or  continuous  excess  of  hydrochloric  acid,  even  apart  from  diges- 
tion. It  must  be  admitted  that  hyperchlorhydria,  hypersecretion,  and  ulcer 
of  the  stomach  seem  to  belong  to  the  same  pathological  family.  Patients 
begin  with  hyperchlorhydria  or  hypersecretion  and  end  with  ulcer.  These 
facts  would  decide  in  favour  of  those  who  hold  that  the  gastric  juice  may 
cause  the  ulcer  by  digestion  of  the  tissues  (autodigestion).  On  the  other 
hand,  how  are  we  to  reconcile  this  hypothesis  with  the  fact  that  simple 
ulcer  is  found  in  the  oesophagus — that  is  to  say,  in  a  region  where  the 
gastric  juice  is  absent  ?  and,  above  all,  how  are  we  to  reconcile  this  hypo- 
thesis with  the  fact  that  in  the  same  stomach  two  ulcers  may  run  opposite 
courses,  the  one  burrowing,  thanks  to  the  action  of  the  gastric  juice,  and 
the  other  cicatrizing,  in  spite  of  it  ?  This  fact  is  not  favourable  to  the 
theory. 

The  germ  theory  may  explain  the  formation  of  the  ulcer,  which  is  at  its 
commencement  only  an  exulceration.     As  I  have  discussed  this  question 


DISEASES  OF  THE  STOMACH  683 

under  Exulceratio  Simplex,  I  shall  not  refer  to  it  again.  The  theory  that 
compares  gastric  ulcer  with  perforating  ulcer  of  the  foot  is  ingenious,  but 
not  proven.  Alcoholism  has  been  looked  upon  as  the  chief  cause  of  gastric 
ulcer.  This  view  is  wide  of  the  truth,  as  LetuUe  has  pointed  out,  because 
in  most  cases  the  patients  are  not  alcohoUc  and  the  arteries  of  the  stomach 
are  not  atheromatous. 

According  to  Gilles  de  la  Tourette,  hysteria  has  an  important  place  in 
the  causation  of  ulcer. 

Simple  ulcer  is  fairly  common,  especially  in  England  and  Germany.  It 
is  found  more  frequently  in  women  than  in  men,  and  chiefly  in  young 
adults.  Young  women  of  the  chlorotic  type  are  prone  to  it.  Traumatism 
(blows,  contusions  of  the  epigastrium)  may  perhaps  be  the  cause  in  a  certain 
number  of  cases  (Potain).  In  short,  the  real  cause  of  ulcus  simplex  fre- 
quently escapes  us. 

Symptoms. — In  the  classical  form  the  symptoms  are  as  follows  :  After 
a  varying  period  of  dyspepsia,  and  often  of  hyperchlorhydria,  the  cardinal 
symptoms  of  pain,  vomiting,  and  hsematemesis  appear. 

The  pain,  which  is  generally  hmited  to  the  xiphoid  point,  is  almost  always 
accompanied  by  a  corresponding  pain  in  the  spine,  on  a  level  with  the  first 
lumbar  vertebra  (rachidian  point,  Cruveilhier).  This  gnawing  and  boring 
pain  returns  several  times  a  day,  or  at  more  distant  intervals.  I  have  seen 
patients  in  whom  these  pains,  like  those  of  severe  burns,  were  so  acute  that 
the  relief  could  only  be  obtained  by  the  excessive  use  of  morphia  for  months 
at  a  time.  The  pain  is  increased  by  pressure  or  palpation  of  the  stomach. 
It  is  generally  brought  on  by  the  ingestion  of  food,  and  persists  during  the 
whole  period  of  gastric  digestion,  being  most  severe  at  this  time.  It  must 
not  be  forgotten  that  pain  is  sometimes  absent,  and  that  similar  pain  may 
be  present  in  certain  cases  of  gastralgia,  especially  with  hyperchlorhydria. 
In  some  cases  the  gastric  intolerance  is  absolute,  and  milk  or  even  water  is 
rejected. 

Vomiting  is  frequent.  Vomiting  of  food  takes  place  more  or  less  rapidly 
after  meals  ;  indeed,  the  pain  may  only  cease  with  the  vomiting.  Some 
patients  vomit  phlegm  tinged  with  bile  during  the  day,  and  especially  in  the 
morning.  The  vomit  is  often  very  acid,  because  in  ulcer  of  the  stomach 
the  gastric  juice  usually  contains  hydrochloric  acid  in  excess.  It  is  the 
presence  or  excess  of  hydrochloric  acid  in  the  chyme  which  in  difficult  cases 
is  one  of  the  signs  of  diagnosis,  though  by  no  means  an  absolute  one,  between 
ulcer  and  cancer. 

Vomiting  of  blood  (hsematemesis)  varies  according  to  the  case.  If  the 
liaBmorrhage  into  the  stomach  is  copious,  and  if  the  blood  is  quickly  vomited, 
it  Is  red  and  liquid.  If,  however,  it  has  remained  for  some  time  in  the 
stomach  in  contact  with  the  gastric  juice  or  the  food,  it  is  voided  in  clots, 


684  TEXT-BOOK  OF  MEDICINE 

or  more  usually  in  the  form  of  a  blackish  liquid,  like  coffee-grounds  or  soot 
diluted  with  water.     This  is  called  the  black  vomit. 

Sometimes  a  portion  of  the  blood  passes  from  the  stomach  into  the 
intestine,  and  the  patient  voids  tarry  stools.  This  is  called  melaena.  If 
the  hsemorrhage  is  not  copious,  and  occurs  slowly  in  small  quantities,  the 
blood  may  pass  into  the  intestine,  and  the  meleena  is  then  the  only  sign  of 
the  gastric  haemorrhage. 

Attacks  of  haematemesis  are  also  possible  when  the  ulcer  has  cicatrized, 
and  a  fatal  haemorrhage  takes  place  by  a  fresh  lesion  of  the  cicatrized 
tissue,  as  the  following  case  proves  (Bonnet)  : 

A  woman  who  had  had  no  previous  illness  showed  all  the  symptoms  of  ulcer  of  the 
stomach,  including  xiphoid  and  gjjinal  pains,  increased  by  the  ingestion  of  food  and 
vomiting.  During  the  course  of  the  illness  severe  hsematemesis  supervened,  and  on 
the  following  day  a  second  ha3morrhage,  more  copious  than  the  first  one.  The  patient 
was  put  on  a  rigid  milk  diet,  and  at  the  end  of  nine  months  she  was  completely  cured 
of  her  trouble.  Eight  years  later  the  patient  was  admitted  into  tlie  Croix  Rousse 
Hospital,  having  just  been  seized  with  copious  hsematemesis  and  melaena.  She  com- 
plained of  pains  in  the  pit  of  the  stomach.  She  was  put  on  a  milk  diet,  and  ice-bags 
were  applied  to  the  abdomen.  At  eight  o'clock  in  the  evening  the  pains  increased, 
and  the  patient  was  seized  with  a  terrible  attack  of  hsematemesis,  amounting  to  about 
4  pints  of  blood.  An  injection  of  ergotin  was  given,  then  one  of  serum,  but  the  patient 
died  at  ten  o'clock.  At  the  post-mortem  examination  large  clots  were  found  in  the 
stomach,  and  on  the  small  curvature  there  was  the  cicatrix  of  the  old  ulcer,  in  which 
there  was  seen  a  small  conical  projection,  terminating  in  a  gaping  orifice  ;  the  latter 
was  the  opening  of  an  arteriole,  the  walls  of  which  had  been  attacked.  (It  might  he 
called  an  exvilceration  grafted  on  the  cicati'ix  of  the  ulcer.) 

Dilatation  of  the  stomach  frequently  accompanies  ulcer.  It  is  not  due 
only  to  organic  stricture  of  the  pylorus,  but  is  also  found  associated  with 
ulcers  of  other  regions.  The  spasmodic  reflex  contraction  of  the  pylorus 
is,  without  doubt,  an  important  factor.  This  contracture  is  said  by  Doyen 
to  play  a  considerable  part  in  the  symptoms  of  gastric  ulcer,  and  is  held 
to  be  the  origin  of  the  cramps  in  the  stomach.  It  is  also  said  to  be  one  of 
the  factors  in  the  dilatation  and  vomiting,  as  well  as  an  obstacle  to  the 
heahng  of  the  ulcer  by  provoking  dilatation  of  the  organ  and  consequent 
dragging  on  the  edges  of  the  ulcer. 

Headache  is  a  symptom  which,  I  notice,  is  nowhere  mentioned,  but  which 
I  have  often  met  with  in  gastric  ulcer.  I  am  not  quite  certain  of  the  cause, 
but  from  a  semeiological  point  of  view  I  mention  its  importance.  The  violent 
and  obstinate  headache  is  often  as  distressing  to  the  patient  as  the  epigastric 
pain,  and  seems  to  me  to  be  of  value  in  diagnosis,  for  it  accompanies  ulcer, 
but  not  cancer. 

The  patient  wastes  quickly,  as  the  result  of  the  pain  and  vomiting. 
Dysmenorrhoea  and  amenorrhcea  are  found  in  women.  The  disease  finally 
produces  cachexia. 


DISEASES  OF  THE  STOMACH  6S5 

The  possible  terminations  of  simple  ulcer  are  as  follows  :  complete 
recovery,  recovery  with  cicatrices  or  with  extragastric  adhesions  ;  death 
from  haemorrhage,  perforation,  peritonitis,  collapse,  cachexia,  or  malignant 
change.  Recurrences  are  fairly  frequent,  and  the  symptoms  may  appear 
again  after  some  months  or  years  of  cure.  Fresh  ulceration  sometimes 
appears  in  an  old  cicatrix. 

Complications. — Amongst  the  terrible  and  fatal  complications  let  us 
mention  first  haemorrhage,  which,  Uke  perforation,  may  result  from  a  latent 
ulcer.     I  saw  a  case  of  this  kind  with  Caussade. 

A  woman,  who  had  shown  no  symptoms  of  gastric  ulcer,  was  seized  with  severe 
liaematemesis.  The  bleeding  ceased,  but  she  died,  a  few  weeks  later,  from  perforation. 
In  one  of  Bazy's  cases  the  patient  died  in  a  few  hours  from  haemorrhage,  and  at 
the  post-mortem  examination  three  ulcers  were  found  in  the  lesser  curvature  ;  the 
ulcei'ation  had  destroyed  the  gastric  artery.  In  Caillard's  case  the  patient  was  carried 
off  in  a  few  hours  by  hsemorrhage.  At  the  post-mortem  examination  an  ulcer  of  the 
lesser  curvature,  involving  the  pyloric  artery,  was  found.  In  a  case  reported  by  Litten 
the  patient  died  of  repeated  hfemorrhages  from  the  stomach,  and  post  mortem  a  per- 
foration in  the  middle  of  the  posterior  wall  and  ulceration  of  the  splenic  artery  were 
found. 

Peritonitis. — Perforation  and  acute  general  peritonitis  are  most  com- 
mon in  ulcers  on  the  anterior  surface  of  the  stomach,  because  this  region 
is  more  mobile  and  more  accessible  to  traumatism,  and  because  adhesions 
do  not  form.  The  seat  of  election  differs,  therefore,  in  ulcer  and  in  per- 
foration, the  ulcer  being  more  common  on  the  posterior  surface  of  the 
stomach.  As  regards  statistics,  perforation  is  forty  times  more  common  in 
anterior  ulcer  than  in  posterior  ulcer.  Ulcers  on  the  anterior  wall  are, 
therefore,  of  exceptional  gravity. 

Superacute  peritonitis,  due  to  the  perforation  of  the  stomach,  will  be 
described  in  the  next  section.  This  form  of  peritonitis  is  rapidly  fatal,  unless 
surgical  intervention  is  prompt.  In  the  more  favourable  cases  the  perfora- 
tion causes  partial  or  encysted  peritonitis.  The  adhesions  have  had  time 
to  unite  the  stomach  to  the  diaphragm,  the  abdominal  wall,  the  Uver,  or 
the  transverse  colon,  aiid  enclose  an  anfractuous  abscess  cavity,  which  is 
usually  situated  in  the  epigastric  and  hypochondriac  regions. 

These  perigastric  abscesses  may  be  classified  in  several  categories  : 

The  gastro-splenic  abscess  is  seated  between  the  fundus  of  the  stomach 
and  tlic  splcnu,  in  the  left  hypochondrium,  and  is  due  to  a  perforation  of  the 
greater  curvature  of  the  stomach. 

The  gastro-subhepatic  abscess  extends  towards  the  right  hypochon- 
drium, being  limited  above  by  the  left  lobe  of  the  hver,  below  by  the  lesser 
curvature  of  the  stomach  and  the  pylorus,  and  in  front  by  the  adhesions 
which  unite  the  edge  of  the  liver  to  the  stomach.  It  is  due  to  a  perforation 
in  the  pyloric  region. 


686  TEXT-BOOK  OF  MEDICINE 

The  gastro-abdominal  or  antegastric  abscess  is  placed  between  the  front 
of  the  stomach  and  the  abdominal  wall.  It  may  cause  inflammation  of  the 
anterior  abdominal  wall,  with  gastric  fistula,  and  is  due  to  a  perforation  of 
the  anterior  wall  of  the  stomach. 

Subphrenic  Abscess. — The  gastro-hepato-phrenic  abscess,  called  also 
subphrenic  abscess,  or  subdiaphragmatic  pyopneumothorax,  is  the  most 
common  variety,  and  is  usually  due  to  a  perforation  of  the  posterior  wall 
of  the  stomach.  It  forms  a  subphrenic  empyema,  which,  hke  the  pre- 
ceding varieties,  contains  gas,  putrefying  fragments  of  food,  and  sloughy 
shreds.  From  a  topographical  point  of  view,  the  abscess  is  constituted  in 
the  following  manner  :  Its  superior  wall  is  formed  by  the  diaplu-agm,  which, 
under  the  pressure  of  hquid  and  gas,  may  be  pushed  up  as  high  as  the 
third  intercostal  space.  The  lung  is  in  its  turn  displaced,  and  the  sub- 
phrenic collection,  ascending  into  the  right  or  left  side  of  the  chest,  may 
simulate  pleuritic  effusion  or  pyopneumothorax.  The  inferior  wall  of  the 
abscess  is  formed  by  the  liver,  stomach,  and  transverse  colon,  which  are 
adherent  and  covered  by  false  membranes.  The  right  wall  of  the  abscess  is 
formed  by  the  suspensory  Hgament,  which  joins  the  convex  surface  of  the 
liver  to  the  diaphragm  and  abdominal  wall.  The  left  wall  is  formed  by  the 
spleen  adhering  to  the  stomach  and  by  the  vertical  portion  of  the  diaphragm, 
while  the  posterior  wall  is  formed  by  the  coronary  ligament,  which  extends 
from  the  posterior  edge  of  the  Uver  to  the  corresponding  part  of  the 
diaphragm.  The  abscess,  which  contains  pus  and  gas,  occupies  the  epi- 
gastrium and  the  hypochondria,  especially  the  left.  The  thoracic  organs 
may  be  displaced. 

The  earliest  symptoms  are  often  epigastric  pain  and  vomiting,  but  as 
these  symptoms  much  resemble  those  of  ulcer  the  onset  of  phrenic  abscess 
may  not  be  recognized.  In  other  cases  the  abscess  forms  in  an  insidious 
manner,  and  either  passes  unnoticed  or  is  masked  by  the  urgent  and  painful 
symptoms  of  ulcer.  Some  patients  complain  of  pains  which  radiate  into 
the  shoulder  when  the  abscess  is  forming,  while  others  suffer  from  rigors 
and  fever,  which  indicate  suppuration. 

A  subphrenic  abscess,  when  it  has  formed,  gives  rise  to  abdominal  and 
thoracic  symptoms.  The  abdominal  symptoms  are  pain,  bulging,  and 
deformity  of  the  epigastrium  and  left  hypochondrium.  They  are  localized 
to  the  supra-umbilical  portion  of  the  abdomen,  whilst  the  subumbihcal 
portion  remains  supple,  and  shows  no  abnormahty.  This  point  is  valuable 
in  diagnosis. 

The  thoracic  symptoms  comprise  enlargement  of  the  base  of  the  thorax 
and  signs  of  pleural  effusion  or  of  pyopneumothorax.  As  the  diaphragm 
may  be  pushed  upwards,  the  signs  of  pleural  effusion  and  also  of  pyo- 
pneumothorax are  seen.     The  difficulty  in  diagnosis  is  apparent,  but  I 


DISEASES  OF  THE  STOMACH  687 

think  that  it  may  be  thus  overcome.  Bulging,  deformity,  and  dullness  in 
the  epigastrium  and  the  hypochondria  do  not  exist  in  pleural  effusions  nor 
in  true  pyopneumothorax.  There  are,  however,  cases  in  which  effusion 
into  the  left  pleuja  may  deform  the  left  hypochondrium  and  abohsh  the 
resonance  in  Traube's  space.  This  happens  when  there  is  considerable 
effusion,  amounting  to  3  or  4  pints  at  least.  With  such  an  effusion,  how- 
ever, the  heart  is  displaced  outwards,  and  the  dullness  reaches  the  clavicular 
region,  which  is  not  the  case  in  pseudo-pleural  effusions  of  abdominal 
origin.  There  are  also  cases  in  which  an  effusion  of  the  right  pleura  may 
depress  the  hver  and  cause  bulging  in  the  right  hypochondrium,  but  here 
also  it  is  a  case  of  large  effusions  which  cause  dullness  up  to  the  clavicular 
region.  This  is  not  the  case  in  pseudo-pleural  effusions  of  abdominal 
origin. 

The  peritoneal  abscesses  just  described  may  terminate  in  different  ways  : 
(1)  they  may  bring  about  suppuration  in  the  abdominal  wall,  with  gastro- 
abdominal  fistula  ;  (2)  they  may  empty  into  the  small  intestine  or  into  the 
colon,  causing  fcetid  diarrhoea  and  gastro -intestinal  fistula,  which  may 
close  up  ;  (3)  they  may  open  into  the  peritoneum  and  cause  general  peri- 
tonitis ;  (4)  they  may  perforate  the  diaphragm,  and  open  into  the  peri- 
cardium, pleurae  (causing  empyema  and  pyopneumothorax),  or  into  the 
bronchi  and  lungs  (causing  gangrene  or  bronchopneumonia). 

Latent  Ulcer. — The  description  of  gastric  ulcer,  as  given  above,  holds 
good  in  the  majority  of  cases.  Dyspeptic  troubles  first  appear,  and  are 
followed  by  pain,  vomiting,  and  attacks  of  hsematemesis.  The  disease  may 
last  months  and  years  (two  years  being  the  average),  with  alternate 
improvement  and  relapse,  which,  with  proper  treatment,  often  ends  in  cure. 
The  ulcer  does  )\ot,  however,  always  present  the  same  form.  In  certain 
cases  it  is  latent,  or  only  betrays  itself  by  slight  dyspepsia,  and  an  apparently 
healthy  person  is  suddenly  stricken  with  perforation  of  the  stomach,  acute 
peritonitis,  ulceration  of  a  large  vessel,  or  violent  ha3matemesis,  wliich 
endangers  life  in  a  few  days  (rapid  variety)  or  in  a  few  hours  (fulminant 
variety)  (Jaccoud).  These  terrible  complications  are  found  in  the  ordinary 
chronic  ulcer,  but  then  they  are  foreseen.  I  cannot  lay  too  great  stress 
on  this  latent  form,  which  causes  such  great  surprises.  Fatal  peritonitis 
from  perforation  is  more  common  than  is  generally  supposed  in  cases  where 
the  ulcer  has  made  progress,  although  pain,  hscmorrhage,  and  vomiting  are 
absent  or  almost  latent. 

The  following  cases  will  illustrate  the  point : 

Case  1. — An  anjEinic  girl,  who  had  never  had  stomach  trouble,  was  taken  sucldonly 
ill  during  the  night,  with  violent  epigastric  pain  and  all  the  signs  of  supcracuto  jicri- 
tonitis  except  vomiting.  She  died  in  fifteen  hours  from  peritonitis,  duo  to  perforation 
of  an  ulcer  on  the  anterior  surface  of  the  stomach. 


688  TEXT-BOOK,  OF  MEDICINE 

Case  2. — A  healthy  young  woman  was  suddenly  seized  with  very  sharp  pain  in  the 
left  hypochondrium,  and  the  temperature  fell  to  96°  F.  in  a  few  hours.  The  abdomen 
■vas  distended  and  very  painful.  The  extremities  grew  cold,  and  the  respiration  was 
greatly  quickened ;  the  pulse  could  not  be  counted,  and  the  patient  died  in  twenty- 
four  hours.  At  the  post-mortem  examination  double  perforation  of  the  stomach  was 
found  on  the  anterior  and  posterior  walls,  the  two  perforations  being  almost  opposite 
one  ancthir. 

Case  3. — A  young  girl,  eighteen  years  of  age,  was  suddenly  seized  with  sharp  pains 
in  the  abdomen.  Symptoms  of  general  peritonitis  soon  appeared.  An  operation  was 
performed  on  the  third  day  ;  the  patient  succumbed.  At  the  post-mortem  examination 
an  ulcer  with  a  large  perforation  was  found. 

Case  4. — I  saw,  with  Tisne,  a  young  girl  who  had  been  suddenly  taken  ill  with 
terrible  pain  in  the  abdomen  ;  no  vomiting.  Next  morning  we  diagnosed  peritonitis 
from  perforation,  and  I  sent  the  patient  to  the  Necker  Hospital  for  operation.  Her 
condition  became  so  bad  that  the  operation  was  not  completed  ;  she  died  twenty  hours 
after  the  onset  of  complications.  At  the  post-mortem  examination  we  found  two 
large  rounded  perforations  on  the  anterior  and  posterior  surfaces  of  the  stomach. 
They  were  absolutely  superposable,  as  if  one  ulcer  had  produced  the  other.  The  ulcers 
were  of  the  latent  type.  The  patient  had  never  experienced  any  gastric  symptom.  I 
made  a  minute  inquiry  into  the  case.  On  the  previous  evening  she  had  been  out 
walking,  and  had  made  an  excellent  dinner. 

Case  7. — A  young  woman,  twenty -six  years  of  age,  was  admitted  by  Fernet  for 
superacute  peritonitis,  which  had  come  on  soon  after  a  meal.  The  woman,  who  was  in 
good  health,  had  felt  some  slight  dyspeptic  troubles,  ascribed  to  chlorosis.  She  died 
twenty-four  hours  after  the  onset  of  the  symptoms,  and  at  the  post-mortem  examination 
two  ulcers  were  found  to  have  perforated  through  the  anterior  surface  of  the  stomach. 

These  cases  of  latent  ulcer  allow  me  to  draw  the  following  conclusions  : 
Latent  ulcer  of  the  stomach  is  especially  common  in  young  women,  with  or 
without  chloro-ansemia.  It  is  usually  situated  on  the  anterior  surface  of 
the  stomach.  The  more  latent  the  ulcer  is,  the  more  is  it  to  be  feared, 
because  the  patient  follows  no  treatment,  as  she  has  not  been  warned  by 
any  symptom  of  the  presence  of  the  disease,  which  may  kill  her  as  by  a 
flash  of  lightning. 

Superacute  peritonitis  from  perforation  of  a  simple  ulcer  of  the  stomach 
will  be  discussed  in  the  next  article.  We  shall  see  that,  while  its  symptoms 
are  severe  and  sudden,  they  differ  much  from  those  of  early  appendicitis. 
In  its  suddenness  and  its  immediate  gravity  perforation  of  a  gastric  ulcer 
free  from  adhesions  is  only  comparable  with  that  of  simple  ulcer  of  the 
duodenum. 

Diagnosis. — Violent  pains  at  the  xiphoid  and  spinal  points ;  vomiting, 
with  hyperchlorhydria,  following  more  or  less  quickly  after  taking  food ; 
hsematemesis,  which  is  more  or  less  copious  and  repeated,  with  or  without 
melsena,  and  the  absence  of  an  epigastric  tumour,  are  all  in  favour  of  simple 
ulcer.  These  symptoms  are,  however,  not  always  clearly  marked,  and  some 
of  them  may  be  wanting,  so  that  in  certain  cases  the  diagnosis  is  very 
difficult. 

As  pain  in  the  stomach  may  be  early,  frequent,  and  intense,  thus  form- 


DISEASES  OF  THE  STOMACH  689 

ing  the  chief  symptom  in  simple  ulcer  of  the  stomach,  we  must  review  the 
various  diseases  in  which  attacks  of  pain  may  simulate  ulcei . 

The  pains  of  hepatic  COlic,  from  their  position  and  violence,  may  simulate 
those  of  gastric  ulcer.  In  hepatic  coUc  the  pain  is  independent  of  digestion, 
but  in  ulcer  the  pain  is  at  once  excited  by  food,  and  becomes  most  intense 
two  or  three  hours  after  a  meal,  when  the  quantity  of  free  hydrochloric 
acid  attains  its  maximum.  Hepatic  coUc  provokes  vomiting  of  bile,  while 
ulcer  causes  vomiting  of  food,  mucus,  or  dark  blood.  Hepatic  cohc  is  a 
passing  episode,  often  accompanied  by  jaundice  and  urobihnuria.  Nothing 
of  a  similar  nature  is  seen  in  gastric  ulcer. 

The  gastric  crises  of  tabes  may,  from  their  situation  and  intensity, 
simulate  the  pains  of  ulcer  ;  the  hkeness  is  the  greater  as  the  crises  in  tabes 
may  be  accompanied  by  hyperchlorhydria  and  bloody  vomit.  In  the  tabetic 
patient,  even  in  the  pre-ataxic  stage,  some  stigmata  of  tabes  will  always  be 
found  if  carefully  looked  for — lightning  pains  in  the  legs,  retardation  of 
sensibihty,  abolition  of  the  patellar  reflexes  ;  eye  troubles,  ptosis,  strabismus  ; 
urinary  troubles,  Romberg's  sign.  Finally,  in  the  intervals  between  the 
gastric  crises  the  stomach  performs  its  function  well,  without  dyspepsia 
and  hyperchlorhydria. 

Gastric  uraemia,  with  its  gastralgia,  intolerance  of  food,  repeated  and 
at  times  blood-stained  vomit,  may  simulate  simple  ulcer  of  the  stomach. 
The  vomit  in  uraemia  is  very  rarely  acid,  and  frequently  contains  urea  and 
carbonate  of  ammonia,  while  the  patient  usually  has  albuminuria,  and 
always  shows  signs  of  Brightism  or  of  confirmed  Bright' s  disease. 

Hysteria  simulates  gastric  ulcer.  Acute  gastralgia,  intolerance,  vomiting, 
hyperchlorhydria,  and  hsematemesis  may  be  present,  so  that  it  is  only  by 
careful  search  for  the  stigmata  of  hysteria,  such  as  pharyngeal  anaesthesia, 
hemianaesthesia,  ovarian  pain,  contraction  of  the  field  of  vision,  hystero- 
geneous  zones,  etc.,  that  it  will  be  possible  to  make  a  diagnosis. 

The  diagnosis  of  ulcer  from  hyperchlorhydria  is  very  difficult,  because 
in  both  cases  the  pains  caused  by  digestion  reach  their  maximum  two  or 
three  hours  after  a  meal ;  but  the  pyrosis  and  acid  regurgitation  in  hyper- 
chlorhydria are  not  usually  accompanied  by  vomiting  of  food.  Hyper- 
secretion and  ulcer  have  as  common  symptoms  paroxysmal  and  continuous 
pains,  but  nocturnal  vomiting  of  several  ounces  of  liquid  and  the  presence  of 
hydrochloric  acid  in  the  stomach,  apart  from  digestion,  are  special  to  hyper- 
secretion. The  diagnosis  of  ulcer  and  cancer  will  be  discussed  under  Cancer 
of  the  Stomach. 

The  diagnosis  of  the  site  of  the  ulcer  is  of  importance.  The  anterior 
ulcer,  which  most  often  leads  to  perforation,  causes  pain  towards  the  left 
hypochoudrium.  It  is  made  worse  by  the  prone  position  and  relieved  by  the 
supine   posture.     The   posterior   ulcer,    which   causes   severe   lia;niorrhage 

U 


690  TEXT-BOOK  OF  MEDICINE 

(splenic  artery),  gives  rise  to  great  pain,  which  is  especially  acute  in  the 
spinal  region.  The  pain  is  reUeved  by  the  prone  position.  The  pyloric 
ulcer  has  its  centre  of  pain  to  the  right  of  the  median  hne. 

The  prognosis  is  always  grave,  even  when  the  disease  has  a  benign 
appearance.  It  is  grave  because  the  ulcer  exposes  the  patient  to  attacks 
of  hsemorrhage,  perforation,  peritonitis,  or  stenosis  of  the  stomach,  and 
also  because  the  ulcer  is  sometimes  rebelhous  to  treatment  and  subject  to 
return.  Finally,  the  prognosis  is  grave  because  cancer  may  graft  itself 
on  ulcer. 

Treatment. — The  patient  must  take  milk,  fresh  or  boiled,  hot  or  cold, 
according  to  taste,  at  equal  intervals — every  two  hours,  for  instance — so 
as  to  make  up  3  or  4  pints  in  the  twenty-four  hours. 

I  had  in  the  Hotel-Dieu  a  young  woman  suffering  from  ulcer  of  the 
stomach,  with  hsematemesis,  acute  pain,  uncontrollable  vomiting,  and 
loss  of  flesh.  The  intolerance  of  the  stomach  was  such  that  cow's  milk, 
even  in  very  small  doses,  was  immediately  vomited.  I  therefore  prescribed 
ass's  milk.  In  two  months  she  gained  25  pounds  in  weight,  and  was  quite 
restored  to  health. 

The  milk  diet,  in  order  to  be  efficacious,  must  be  as  rigid  as  possible. 
At  first,  if  the  milk  does  not  agree  well,  each  glass  is  mixed  with  a  table- 
spoonful  of  lime-water,  to  which  small  doses  of  morphia  and  cocaine  are 
added.  Lime-water,  with  the  addition  of  very  small  doses  of  morphia 
and  cocaine,  is,  in  my  opinion,  an  excellent  remedy  in  all  diseases  where 
the  abnormal  excitabihty  of  the  stomach  provokes-  pain  and  vomiting. 
Injections,  of  morphia  should  be  reserved  for  cases  in  which  the  gastralgia 
is  acute  aud  obstinate.  Nitrate  of  silver,  in  doses  of  ^  grain  or  more  daily, 
with  opium  and  subnitrate  of  bismuth,  or  alkalis  in  large  doses  (Debove), 
is  of  service.  Haemorrhage  must  be  treated  with  perchloride  of  iron,  ergotin, 
and  iced  drinks.  The  continuous  appUcation  of  an  ice-bag  to  the  epigastric 
region  is  excellent,  both  for  haemorrhage  and  also  for  the  pain  and  vomiting. 
In  severe  heematemesis  I  advise  large  subcutaneous  injections  of  artificial 
serum,  repeated  several  times  a  day. 

If  the  ulcer  be  situated  on  the  anterior  surface  of  the  stomach,  I  would 
advise  absolute  rest  in  bed,  in  the  dorsal  position.  The  convalescence  must 
be  carefully  watched,  and  we  must  not  forget  that  the  disease  may  recur. 

In  some  cases  medical  treatment  fails.  If  the  haemorrhage,  pain,  and 
vomiting  are  persistent  (in  the  absence  of  syphihs),  recourse  must  be  had 
to  surgical  treatment. 

Marion  sums  up  the  question  as  follows  :  The  reports  of  intervention 
for  haemorrhage  are  still  too  few  to  give  exact  information  as  to  surgical 
treatment.  Gannat,  who  operated  upon  a  patient  for  hajmatemesis,  was 
alarmed  by  the  perigastric  adhesions,  and  closed  the  abdomen.     The  post- 


DISEASES  OF  THE  STOMACH  691 

mortem  examination  revealed  the  presence  of  a  simple  ulcer,  which  involved 
the  pancreatico-duodenal  artery. 

Mikulicz  operated  four  times  for  haematemesis.  In  the  first  case  he 
cauterized  the  ulcer,  but  the  patient  died  of  collapse  fifty  hours  after  opera- 
tion. In  the  second  case  he  attempted  to  suture  the  bleeding  area,  but  the 
patient  died  from  collapse  the  same  evening.  In  the  case  of  a  woman 
he  curetted  the  ulcer  and  perforated  the  wall  of  the  stomach,  which  he 
sutured.  The  patient  recovered.  Finally,  in  the  fourth  case  he  sutured 
the  stomach  at  the  bleeding  spot,  and  in  the  evening  death  supervened  from 
collapse.  Kiister  operated  on  a  young  girl  for  haematemesis.  He  cauterized 
the  ulcer,  and  completed  the  operation  by  gastro-enterostomy,  to  obviate 
any  ulterior  contraction  of  the  pylorus  due  to  cicatrix  of  the  ulcer.  The 
patient  recovered.  Roux  performed  partial  gastrectomy,  followed  by 
suture  of  the  three  layers,  in  a  patient  with  haematemesis  following  simple 
ulcer  which  had  eroded  the  gastric  artery.  The  double  ligature  of  this 
artery,  with  the  excision  of  the  ulcerated  portion,  saved  the  patient. 

In  cases  other  than  those  of  haemorrhage  numerous  and  important 
successes  have  been  recorded  (Doyen).  If  an  ulcer  reveals  itself  by  frequent 
and  repeated  attacks  of  haematemesis,  incessant  vomiting,  symptoms  of 
spasm  or  pyloric  constriction,  or  signs  of  cachexia,  as  these  cases  resist 
medical  treatment,  gastro-enterostomy  should  be  done.  Each  operator 
modifies  the  procedure  according  to  his  hking,  and  according  to  the  adhesions, 
the  dimensions,  the  extent,  the  depth,  and  the  situation  of  the  ulcer. 

XI.  PERFORATION  OF  SIMPLE  ULCER  OF  THE  STOMACH— 
SUPERACUTE  PERITONITIS. 

In  the  preceding  section  I  described  the  consequences  of  perforation  of 
the  ulcer  when  adhesions  limit  the  lesion.  I  shall  now  consider  perforation 
followed  by  superacute  peritonitis.  As  a  type,  I  will  quote  the  following 
case,  taken  from  oiu;  of  my  clinical  lectures  :  * 

One  morning,  at  the  Hdtel-Dieu,  I  saw  a  boy  whose  pale  face  expressed  the  most 
intense  sufTering.  He  walked  with  diftieulty,  his  back  bent  and  his  stomatli  nitracted, 
while  liis  hanils  were  lield  forward,  as  if  to  protect  Ihe  abdomen  and  avoid  contact 
with  anythinii  wliich  migiit  increase  the  pain.  He  was  sufTering,  so  he  told  us,  from 
terrible  pains  in  the  belly  ;  they  eanio  on  sudth'idy  in  tiie  morning  at  six  o'clock,  "  as 
if  the  intestines  wore  being  torn."  'I'liesf;  awful  pains  were  followed  neither  by  vomiting 
nor  by  hiccough.  Tlio  belly  was  Hat,  the  pulse  OS,  and  the  temperature  OS-S"  F.  He 
Invd  only  one  symptom — j)ain.  I  formed  a  bad  impression  of  tlie  case,  the  features  being 
drawn  and  the  nose  pinched.  It  was  necessary  to  decide  the  question  of  immediate 
surgical  intervention.     Was  the  pain  due  to  appendicitis  or  peritonitis  from  perforation 


•  "  Perforation  de  I'lJIccre  Simple  de  i'EBtomac  :  Peritonito  Suraiguc  "  (Ctinique 
Medicate  de  rHStelDieu,l898,  5""  le^on). 

44—2 


692  TEXT-BOOK  OF  MEDICINE 

of  an  ulcer  of  the  stomach  or  duodenum  ?  Had  we  to  do  with  internal  strangulation 
or  acute  entero-colitis  ?  Was  it  a  case  of  renal,  hepatic,  or  lead  colic  ?  In  such  cases  an 
exact  diagnosis  can  only  be  made  by  careful  consideration  of  the  signs  and  symptoms. 

Pain  was  here  the  chief  symptom,  and  therefore  demanded  prompt  investigation. 
The  pain  commenced  at  six  o'clock  in  the  morning,  being  sudden  and  acute  from  the 
first.  It  was  unexpected,  the  patient  having  gone  to  bed  the  previous  evening  feeling 
quite  well.  The  suddenness  and  intensity  of  the  pain  recalled  in  every  point  what  I 
have  named  "  the  peritoneal  dagger-thrust,"  or  the  special  symptom  of  perforation  of  a 
gastric  or  duodenal  ulcer.  The  sudden  onset  eliminated  the  idea  of  appendicitis.  We 
no  longer  admit  the  erroneous  idea  that  appendicitis  can  commence  suddenly  with 
terrible  pain  due  to  perforation.  At  the  risk  of  repetition,  I  must  again  state  that 
in  appendicitis  (if  we  look  closely)  events  do  not  run  this  course.  No  matter  how 
painful  the  onset  of  appendicitis  may  be,-  the  pains  increase  gradually.  Question  your 
patients  carefully,  and  try  to  obtain  from  them  precise  answers,  and  you  will  be  con- 
vinced that  it  is  only  after  one  or  several  hours  that  the  pain  reaches  its  maximum,  and 
even  then  it  is  very  rarely  excessive.  In  peritonitis  from  perforation  the  pain  is  as 
sudden  as  it  is  violent,  and  the  comparison  with  the  peritoneal  dagger-thrust,  which  is 
here  correct,  is  not  applicable  to  appendicitis.  In  short,  the  onset  of  perforation  bears 
little  or  no  resemblance  to  that  of  appendicitis. 

Furthermore,  the  localization  of  the  pain  is  important  in  diagnosis,  and,  even  sup- 
posing that  the  entire  belly  be  painful,  you  can  still,  by  methodical  examination,  locate 
the  region  in  which  the  pain  began  and  the  spot  where  it  became  most  acute.  In 
appendicitis  (even  if  the  pains  extend  elsewhere)  this  spot  occupies  the  centre  of  a  line 
drawn  from  the  umbilicus  to  the  right  an tero -superior  spine  of  the  ilium.  It  is  at 
McBurney's  point  that  the  pain  of  appendicitis  commences.  On  palpation,  you  will 
find  the  greatest  tenderness  there,  and  the  defensive  contraction  of  the  underlying 
muscle.  Finally,  gentle  stroking  of  the  skin  in  that  region  will  reveal  hyperaesthesia, 
shown  by  reflex  movements  in  the  belly  wall  and  the  neighbouring  parts. 

In  my  patient,  examination  of  the  belly  showed  the  principal  point  of  pain  was  not 
in  the  appendicular  region.  The  whole  belly  was  painful,  but  the  spontaneous  pain  of 
the  onset,  the  tenderness  on  palpation  and  percussion,  the  defensive  contraction,  and 
the  hyperaesthesia  had  their  maximum  of  intensity,  not  in  the  appendicular  region,  but 
in  the  subhepato-gastric  region  above  and  a  little  to  the  right  of  the  umbilicus. 

The  lesion,  therefore,  was  in  this  region,  where  only  three  organs  are  liable  to  per- 
foration— the  gall-bladder,  duodenum,  and  stomach.  There  was  no  question  here  of 
the  gall-bladder,  because  he  had  never  had  any  symptoms  of  gall-stones.  T  therefore 
made  the  following  diagnosis  :  perforation  of  a  latent  ulcer  of  the  pylorus  or  duodenum, 
the  signs  and  symptoms  of  perforation  being  identical  in  the  two  cases. 

Although  the  peritonitis  had  only  existed  four  hours,  his  complexion  was  already 
becoming  ashen.  He  had  the  peritoneal  facies,  which  is  an  important  index  in  diag- 
nosis. I  diagnosed  superacute  peritonitis,  due  to  perforation,  though  he  was  free  from 
fever,  acceleration  of  the  pulse,  vomiting,  hiccough,  and  ballooning  of  the  belly, 
which  are  the  classical  signs  of  acute  peritonitis.  I  had  also  to  admit  a  latent  ulcer, 
as  the  patient  had,  prior  to  the  perforation,  never  shown  any  symptom  of  ulcer.  There 
was  not  a  moment,  then,  to  be  lost,  for  perforation  with  general  peritonitis  is  always 
fatal,  and  the  only  chance  o'f  recovery  lies  in  immediate  operation.  The  peritoneal 
cavity  was  opened  by  a  median  incision.  Peritonitis  was  at  once  evident ;  the  coils  of 
bowel  were  injected,  and  brownish  liquid  came  out  from  the  wound.  A  sponge  intro- 
duced into  the  upper  portion  of  the  incision  towards  the  stomach  was,  on  withdrawal, 
soaked  with  puriform  fluid.  No  trace  of  food.  The  sponge  had  therefore  been  in  the 
neighbourhood  of  the  lesion.  The  lower  edge  of  the  liver  was  pulled  upwards  and  out- 
wards, so  as  to  expose  the  pylorus.  About  an  inch  from  the  pylorus,  on  the  anterior 
surface  of  the  stomach,  a  circular  punched-out  opening  of  the  size  of  a  lentil  was  found. 


DISEASES  OF  THE  STOMACH  693 

His  condition  was  satisfactory  until  the  next  day,  when  two  attacks  of  vomiting 
occurred,  and  he  became  very  collapsed.  He  became  worse  on  the  third  day  :  the 
pulse  was  116,  the  temperature  rose  to  104°  F.,  the  vomit  was  porraceous,  and  the  eyes 
were  sunken.  He  became  rapidly  worse,  and  died.  At  the  post-mortem  examination 
the  sutures  employed  to  close  the  perforation  were  in  exact  apposition.  Death  was 
caused  by  the  general  suppurative  peritonitis. 

Analysis  of  the  Symptoms. — On  admission,  the  peritonitis,  which 
was  but  four  hours  old,  presented  certain  pecuharities.  To  begin  with,  the 
belly  was  flat  and  fairly  hard,  and  tympanites  was  not  present.  Tympanites 
is  generally  given  as  one  of  the  symptoms  of  peritonitis  caused  by  perfora- 
tion, but  it  may  be  absent.  It  is  absent  in  cases  of  perforation  when  the 
peritonitis  from  the  first  produces  such  reflex  contraction  of  the  abdominal 
muscles  that  the  belly  is  flat,  hard,  and  retracted,  instead  of  being  tym- 
panitic. The  abdomen  was  flat  and  hard  in  a  young  girl  whom  I  saw  with 
Tisne,  although  two  symmetrical  ulcers  of  the  stomach  had  just  perforated. 
The  abdomen  was  tight,  "  flat,  and  as  hard  as  a  board,"  in  a  case  reported 
by  Utudjian.  We  shall  see  later  that  the  same  remark  applies  to  super- 
acute  peritonitis  following  perforation  of  a  duodenal  ulcer. 

We  are  too  apt  to  think  that  peritonitis  caused  by  perforation  is  followed 
by  meteorism  from  intestinal  paralysis  or  the  passage  of  gas  tlirough  the 
perforation.  This  is  not  always  the  case,  and  it  would  be  quite  wrong  to 
exclude  peritonitis  because  the  abdomen  is  flat  and  hard.  These  two 
conditions  may,  however,  follow"  one  another.  A  patient,  for  instance, 
whose  abdomen  is  flat  and  hard  shortly  after  the  perforation  will  very  likely 
show  tympanites  on  the  next  day.  The  tympanites  may  be  so  marked  in 
the  symptom-complex  that  perforation  of  the  stomach  is  wrongly  taken  for 
obstruction  of  the  gut.  I  am  acquainted  with  several  cases  in  which  the 
surgeon  operated  for  strangulation  and  found  peritonitis.  It  seems  to  me 
that  this  error  might  have  been  avoided,  for  pain  is  always  a  marked  symp- 
tom, and  should  lead  to  a  correct  diagnosis.  I  know  that,  if  the  abdomen 
is  tympanitic  in  consequence  of  a  perforation  of  the  stomach,  sensibility 
is  sometimes  dulled,  and  that  all  the  desired  information  cannot  be  obtained 
from  the  patient.  If,  however,  the  commencement  of  the  complication 
be  stated  precisely,  it  will  be  seen  that  the  perforation  was  ushered  in  by 
sudden  severe  pain  in  a  person  who  had  passed  a  free  motion  the  night  before. 
Intestinal  occlusion  docs  not  begin  in  this  manner.  Its  symptoms,  including 
meteorism,  come  on  more  slowly,  and  "  the  peritoneal  dagger-thrust," 
which  points  to  gastric  or  duodenal  perforation,  never  marks  the  commence- 
ment of  intestinal  occlusion,  wliatcivcr  be  its  cause. 

Our  patient  had  neither  hiccough  nor  vomiting,  two  signs  which 
occupy  an  important  part  in  the  general  description  of  acute  peritonitis. 
These  two  signs  are  often  wanting  in  peritonitis  from  perforation  of  a 
gastric  or  duodenal  ulcer,  especially  in  the  period  following  the  perforation. 


094  TEXT-BOOK  OF  MEDICINE 

A  fantastic  theory  has  been  put  forward  that  the  patient  does  not  vomit 
because  the  contents  of  the  stomach  pass  into  the  peritoneum  through  the 
perforation.  Another  unexpected  fact  for  those  not  well  acquainted  with 
the  question  is  that  the  pulse  was  normal  and  the  temperature  only  99°  F. 
It  seems  surprising  that  a  patient  suffering  from  superacute  peritonitis 
of  four  hours'  duration  should  have  no  increase  in  the  pulse-rate  and  no 
rise  or  fall  of  temperature.  Nothing  of  the  kind  occurred  in  the  case  before 
us,  and  similar  facts  have  been  noticed  by  other  writers.  My  patient, 
therefore,  had  not  tympanites,  fever,  vomiting,  or  hiccough,  in  spite  of 
superacute  peritonitis  from  perforation  of  the  stomach.  No  previous  gastric 
symptoms  were  present  as  a  guide,  and  yet  it  was  possible  to  make  an 
accurate  diagnosis.  In  speaking  thus,  I  only  wish  to  prove  the  importance 
of  a  well-conducted  semeiology.  One  sign  carefully  examined — viz.,  pain — 
was  sufficient  to  lead  to  the  diagnosis. 

We  see,  too,  that  the  old  description  of  acute  peritonitis  must  be  re- 
modelled. It  is  impossible  to  give  a  dogmatic  description  of  peritonitis, 
for  the  same  symptoms  are  far  from  being  applicable  to  all  cases.  Thus 
peritonitis  in  typhoid  fever  does  not  resemble  that  due  to  perforation  of 
an  ulcer  of  the  stomach  or  the  duodenum  ;  the  latter  form  does  not  resemble 
appendicular  peritonitis,  which,  again,  is  quite  different  to  primary  pneumo- 
coccal peritonitis,  etc.  It  may  be  said  that  the  researches  of  recent  years 
have  quite  changed  the  description  of  the  medico-chirurgical  diseases  of 
the  abdomen. 

Treatment  here  is  purely  surgical.  In  superacute  peritonitis  following 
on  ulcer  of  the  stomach,  operation  is  imperative.  We  must,  however,  decide 
and  act  promptly,  for  the  chances  of  success  are  the  greater  the  sooner  the 
operation  is  performed. 

In  a  communication  on  perforations  of  ulcer  of  the  stomach,  Le  Dentu 
has  entered  into  minute  details,  and  collected  the  following  statistics  con- 
cerning the  results  of  operation  : 

Michaux's  statistics  for  the  year  1894  :  In  25  cases,  5  cures  and  20  deaths. 

Chapt's  statistics  for  the  year  1895  :  In  27  cases,  6  cures  and  21  deaths. 

Chapt  and  Mauclaire's  combined  statistics  :  In  45  cases,  15  cures  and 
30  deaths. 

Houze's  statistics  for  the  year  1895  :  In  67  cases,  20  cures  and  47  deaths. 

Parisier's  statistics  :  In  99  cases,  33  cures  and  66  deaths. 

These  figures  show  recovery  in  a  third  of  the  cases,  a  good  result  in  a 
disease  which  is  fatal  in  the  absence  of  surgical  intervention.  Further- 
more, it  may  be  laid  down  as  an  axiom  that  the  earlier  the  operation,  the 
more  certain  the  cure.  Out  of  nineteen  cures  reported  by  Comte, 
eleven  were  due  to  the  fact  that  the  operation  was  performed  within 
ten  hours  of  the  perforation.     Out  of  Parisier's  thirty-three  cures,  twenty- 


DISEASES  OF  THE  STOMACH  695 

three  were  due  to  the  fact  that  operation  was  performed  ten  to  fifteen 
hours  after  the  perforation.  On  the  other  hand,  the  chance  of  recovery 
decreases  in  proportion  as  the  operation  is  performed  at  longer  intervals 
after  the  perforation. 


XII.  PERFORATING  ULCERS  OF  THE  STOMACH  AND  DUODENUM 
CONSECUTIVE  TO  APPENDICITIS. 

In  Section  IX.  I  described  the  erosions  and  the  exulcerations  of  the 
stomach  consecutive  to  appendicitis.  I  shall  now  prove  that  the  appen- 
dicular infection  may  also  give  rise  to  deep  ulcers  of  the  stomach  and  the 
duodenum,  which  run  a  rapid  course  and  end  in  perforation.  This  question 
is  discussed  in  a  clinical  lecture  I  have  recently  delivered  upon  perforating 
ulcers  consecutive  to  appendicitis.     To  quote  examples  : 

Clinical  Cases. — An  enfeebled  man,  about  sixty  years  of  age,  was  admitted  on 
January  16,  1905.  His  history  was  so  vague  that  accurate  diagnosis  was  not  possible. 
Abdomen  somewhat  swollen  ;  diffuse  dullness  in  the  right  iliac  fossa,  and  acute  tender- 
ness on  deep  pressure  in  the  right  hypochondrium. 

He  died  next  day,  and  his  wife  gave  the  following  information  :  for  some  time  he 
liad  had  pain  in  the  belly ;  acute  pain  then  appeared  suddenly  in  the  region  of  tbe 
stomach,  and  he  decided  to  come  to  hospital. 

Post-mortem  results  :  peritoneal  adhesions  in  the  right  flank,  circumscribing  a 
retrocaecal  abscess  of  appendicular  origin. 

On  opening  the  stomach,  numerous^  capillary  haemorrhages  were  found,  chiefly  at 
the  cardiac  end.  The  duodenum  showed  an  unexpected  lesion :  on  the  posterior  wall 
of  the  first  portion  an  ulcer  had  perforated  the  gut ;  it  was  the  size  of  a  shilling,  and 
evidently  of  recent  date,  because  the  edges  were  not  indurated,  as  in  a  classical  ulcer. 
Itwasal>out  ^  inch  from  the  pylorus  and  rested  against  the  posterior. abdominal  wall, 
wliich  formed  the  floor  and  acted  as  a  tampon,  preventing  general  peritonitis. 

In  short,  he  had  had  subacute  appendicitis,  with  retrocaecal  abscess  and  adhesions  ; 
the  infection  had  led  to  hsemorrhagic  erosions  in  the  stomach,  and  to  an  acute  per- 
forating ulcer  in  the  duodenum. 

Lediard  and  Sedgmck's  Case. — A  man  aged  fifty-six  was  taken  ill  with  j)ains  in  the 
right  iliac  fossa.  One  year  later  they  came  back  over  the  appendix.  In  April,  1904, 
a  fresh  attack.  Diagnosis  :  appendicitis.  Operation  on  May  8.  On  opening  the 
belly,  the  appendix  was  found  to  bo  large  and  covered  with  old  exudate.  It  was  re- 
moved and  the  M'ound  was  closed.  During  the  next  few  days  there  was  no  fever. 
Slight  jaundice  of  the  skin  and  conjunctiva;.  Ho  then  passed  bloody  stools.  On 
dressing  the  wound,  the  stitches  were  found  to  bo  loose  ;  foul-smelling  pus  flowed  out 
of  the  wound.  A  week  after  the  operation  more  and  more  blood  appeared  in  the  stools, 
the  pulse  became  intermittent,  and  tlie  general  pallor  indicated  abundant  loss  of  blood. 
What  was  the  cause  and  the  seat  of  the  blooding  ?  H.omatomesis  was  also  present,  and 
death  occurred  on  June  29.  The  autopsy  was  made  on  tiie  same  day.  On  ojiening 
the  abdomen,  no  peritonitis  ;  the  stomach  M'as  healthy.  On  the  second  part  of  the 
duodenum,  near  the  ampidla  of  Vater,  there  was  an  oval,  crateriform,  perforating 
ulcer,  that  was  1  inch  in  length  and  i  inch  in  breadth  ;  its  long  axis  was  parallel  to 
that  of  the  bowel ;  the  edges  of  the  ulcer  were  smooth,  and  the  floor  was  obliterated 
by  the  pancreas,  which  formed  a  tampon,  preventing  acute  peritonitis,  which  would 
otherwise  have  followed  the  perforation. 


696  TEXT-BOOK  OF  MEDICINE 

The  pancreatic  tissue  showed  early  ulceration  ;  two  open  vessels  (probably  branches 
of  the  inferior  pancreatico -duodenal  artery)  had  given  rise  to  the  fatal  intestinal 
haemorrhage.  A  section  through  the  edge  of  the  ulcer  and  the  adherent  pancreatic 
tissue  showed  complete  destruction  of  the  bowel  wall,  and  also  of  the  adjacent  pancreatic 
tissue. 

Milward's  Case. — A  girl  aged  seven  years  had  been  ill  for  two  weeks.  On  admission 
the  right  iliac  fossa  was  painful  and  the  abdomen  distended.  Operation :  On  opening 
the  belly  in  the  appendicular  region,  2  ounces  of  pus  flowed  out  from  a  cavity  external  to 
the  caecum  and  shut  oflE  from  the  general  peritoneum  by  adhesions.  The  appendix 
was  not  found  ;  possibly  it  was  destroyed  or  buried  under  the  adhesions.  After  the 
operation,  rapid  pulse,  high  temperature,  and  diarrhoea.  On  the  eighth  day  bulging  in 
the  epigastric  region,  which  was  resonant.  The  bulging  increased  slowly,  and  appeared 
to  vary  with  the  condition  of  the  intestines,  being  more  marked  when  the  patient  was 
constipated. 

The  tumour  became  so  large  on  the  twenty-fifth  day  that  an  operation  was  decided 
upon.  The  epigastrium  was  incised,  and  the  operator  found  near  the  stomach  a 
cavity  containing  gas,  pus,  and  gastric  contents.  It  was  shut  off  from  the  peritoneal 
cavity  by  adliesions,  which  fixed  the  stomach  to  the  abdominal  wall.  The  anterior 
siwface  of  the  stomach  showed  a  perforating  ulcer  of  the  size  of  a  threepenny-piece. 
The  perforation  and  the  abdominal  wound  were  sutured,  but  feeding  became  more 
difficult,  the  situation  grew  worse,  and  the  patient  died  five  days  after  the  operation. 

The  autopsy  showed  that  the  iliac  and  epigastric  lesions  were  independent.  The 
course  of  the  disease  had  been  as  follows  :  Appendicitis  of  a  fortnight's  duration,  with 
encysted  pericsecal  abscess.  Acute  ulceration  of  the  stomach,  and  formation  of 
adhesions  between  the  stomach  and  abdominal  wall.  The  perigastritis  had  prevented 
the  onset  of  acute  peritonitis.  The  gas,  which  made  its  way  through  the  perforation, 
caused  bulging  of  the  epigastric  region. 

Warren  Low's  Case. — On  April  14,  1904,  a  girl  of  sixteen  was  admitted  to  St.  Mary's 
Hospital.  She  appeared  to  be  suffering  from  general  peritonitis,  and  was  very  weak. 
Her  history  was  as  follows  :  On  the  evening  of  April  9  she  felt  pain  in  the  right  iliac 
fossa.  Next  day  she  remained  in  bed.  On  April  12  pain  in  the  epigastric  region. 
Next  evening  at  five  o'clock  she  was  taken  ill  with  vomiting  and  very  acute  pain  in  the 
region  of  the  appendix.  On  admission  she  was  collapsed,  with  pale  and  drawn  face. 
Abdomen  distended  and  sensitive  ;  pain  on  palpation  over  the  lower  part  of  the  belly, 
especially  on  the  right  side.  The  collapse  improved  with  the  aid  of  warmth  and  stimu- 
lants. Next  morning  an  incision  was  made  over  the  appendix  ;  some  odourless  pus 
came  out.  The  appendix  was  removed ;  it  contained  two  calculi,  and  extravasated 
blood  was  present  in  its  walls.  The  case  seemed  to  belong  to  the  relapsing  type. 
A  median  incision  above  the  umbilicus  revealed  adhesive  peritonitis  above  the  trans- 
verse colon.  A  perforation  as  large  as  a  crown  was  exposed  ;  it  involved  the  front  of 
the  lesser  curvature  of  the  stomach,  near  the  cardiac  end.  The  ulcer  was  sutured  ;  both 
wounds  in  the  abdominal  wall  were  drained.     Recovery. 

Cheyne  and  Haydock  Wilbe's  Case. — A  boy  aged  thirteen  years  complained  of  pain 
in  the  stomach.  Next  day  the  pain  was  more  severe  and  extensive.  Dr.  Wilbe,  who 
saw  the  child  in  the  afternoon,  found  him  much  collapsed.  He  found  muscular  rigidity 
and  general  hypersesthesia  ;  the  pain  was  most  marked  in  the  right  ihac  fossa. 

Mr.  Watson  Cheyne  saw  him  the  same  day.  The  abdomen  was  hard,  distended, 
and  tympanitic  ;  the  hypersesthesia  was  general,  and  the  pain  most  marked  to  the  right 
and  above.  Perforation  of  the  appendix  was  diagnosed,  and  an  operation  performed. 
An  incision  was  made  over  the  appendix.  As  soon  as  the  peritoneum  was  opened, 
an  escape  of  gas  indicated  perforation  of  the  aUmentary  canal.  Serous  fluid  was 
present  in  the  peritoneal  cavity.  The  caecum  and  the  appendix  were  examined.  The 
latter  was  long  and  inflamed,  and  contained  a  calculus.     The  operator  felt  sure  that 


DISEASES  OF  THE  STOMACH  697 

some  other  lesion  was  also  present.  As  no  faeces  were  free  in  the  peritoneal  cavity,  and 
there  was  no  intestinal  perforation,  a  fresh  incision  was  made  in  the  epigastric  region. 
Turbid  fluid  and  bubbles  of  gas  were  seen  over  the  front  of  the  stomach  near  the  cardiac 
end.  A  rounded  perforation  was  sho\ra  up  by  reflected  light  about  1  inch  from  the 
cardiac  end  of  the  stomach  ;  fluid  and  gas  were  escaping  from  it.  The  perforation  was 
about  as  big  as  a  lead-pencil ;  its  edges  were  not  thickened.  No  other  lesions  in  the 
vicinity.  The  edges  of  the  ulcer  were  sutured.  Rapid  improvement  followed,  and  the 
patient  was  discharged  cured. 

PfihVs  Case. — A  boy  was  taken  ill  with  appendicitis.  At  the  operation  a  few  days 
later  a  pericaecal  abscess  was  opened,  but  the  appendix  was  not  found.  He  died  from 
profuse  haematemesis  twenty-three  days  after  the  operation.  The  autopsy  showed  a 
perforating  ulcer  on  the  anterior  surface  of  the  stomach  four  fingers'  breadth  from  the 
pylorus  ;  the  perforation  was  circular,  punched  out,  and  as  large  as  a  sixpence. 

Discussion. — In  each  of  these  six  cases  a  perforating  ulcer  of  the 
stomach  or  duodenum  was  ass6ciated  with  appendicitis.  Careful  study 
shows  the  order  in  which  the  lesions  appeared.  Appendicitis  preceded  by 
a  more  or  less  lengthy  period  the  symptoms  of  ulcer. 

In  these  cases  there  is  no  suggestion  that  the  appendicitis  was  preceded 
by  the  classical  signs  of  ulcer— epigastric  and  spinal  pain,  vomiting, 
hsematemesis,  and  melaena.  On  the  contrary,  the  scene  opened  with 
appendicitis. 

We  find  in  each  case  that  acute,  subacute,  or  relapsing  appendicitis 
was  in  progress  when  the  gastric  or  duodenal  complication  appeared  sud- 
denly, and  ended  in  perforation/  When  we  consider  the  chronological 
order  of  the  different  lesions,  we  may  justly  admit  that  the  ulcer  was 
secondary  to  the  appendicitis. 

Does  this  chronological  order  justify  the  view  that  the  perforating 
ulcer  is  dependent  upon  the  appendicitis  ?  We  know  that  the  duodenum, 
and  especially  the  stomach,  may  in  the  course  of  appendicitis  be  attacked 
hy  erosions,  exidcerations,  and  perforating  ulcer. 

We  have  seen  in  Section  VIII.  that  erosions  and  exulcerations  occur  in 
the  stomach.  In  the  following  case,  quoted  by  Dupont,  deep  ulceration, 
with  acute  necrosis  of  the  gastric  mucous  membrane,  was  present. 

In  November,  1904,  a  soldier  was  taken  ill  with  toxic  appendicitis.  The  prognosis 
rapidly  became  grave:  tlie  heart  was  iiTcgular,  tlic  Ijrcathing  was  jerky,  the  nose  pini'hed, 
and  the  eyes  hollow.  Tlic  patient  did  not  consent  to  operation  till  the  fourth  day  of  the 
disease.  Naturally  no  improvement  resulted,  and  he  vomited  ilark  blood  on  two 
occasions.  Vomito  negro  is  nearly  always  of  evil  omen.  During  the  next  few  days 
restlessness  and  delirium  set  in,  and  he  died  in  coma. 

Post  mortem  :  On  opening  the  stomach,  ecchj-moses  of  variable  size  were  foimd  in 
the  greater  curvature  and  the  pyloric  region  ;  at  the  pylorus,  two  ulcerations  of  the 
size  of  a  lentil  ;  in  their  centre  the  mucous  membrane  was  raised  up  around  a  crater 
as  big  as  a  ])in's  liead.  Nattan-Larrier's  examination  revealed  the  course  of  the  lesion. 
He  found  coagulation  necrosis  of  the  cells,  converting  the  tissue?  into  a  hyaline  nuisa 
and  alTccting  tlie  glands  in  an  irregular  way,  so  that  normal  and  degenerated  ghuuls 
W(>re  found  side  by  side.     The  necrosis  was  sot  up  by  the  ai)pendicular  toxincs. 


698  TEXT-BOOK  OF  MEDICINE 

Experimental  research  also  gives  us  information  regarding  the  patho- 
genesis of  gastric  and  duodenal  ulcers  resulting  from  appendicitis.  Talma's 
experiments  on  simple  ulcer  of  the  stomach  show  the  action  of  intestinal 
strangulation  in  causing  gastric  erosions  and  ulcerations.  He  ligatured 
a  loop  of  bowel,  and  found  among  the  lesions  present  hsemorrhagic  erosions 
and  ulcerations  of  the  stomach. 

Roger  has  shown  that  experimental  infections  of  the  caecum  produce  in 
the  stomach  ecchymoses  like  those  of  purpura.  "  It  is  difficult  to  explain," 
says  he,  "  how  the  caecal  affection  can  react  upon  the  stomach.  The  fact 
has  none  the  less  a  certain  importance,  especially  if  we  consider  it  in  relation 
with  Dieulafoy's  observations,  which  show  clearly  the  existence  of  gastric 
haemorrhages  due  to  appendicitis.  Experimental  pathology,  therefore, 
confirms  clinical  observation." 

Nattan-Larrier  and  Loevy  have  made  the  following  experiments :  In  two  dogs  an 
inch  of  small  intestine  was  shut  off  by  two  ligatures.  The  animals  died  in  five  days 
from  acute  peritonitis.  A  small  quantity  of  the  fluid  from  the  ligatured  loop  and  from 
the  peritoneum  was  injected  into  a  ligatured  loop  in  two  other  dogs.  They  died  in 
three  days  from  acute  peritonitis.  A  small  quantity  of  fluid  (taken  as  before)  was  then 
injected  into  a  fifth  dog,  which  died  in  forty-eight  hours  without  any  trace  of  peri- 
tonitis. Its  stomach,  however,  contained  two  spoonfuls  of  blackish  fluid  (gastrorrhagia) ; 
two  clean-cut  exulcerations  were  found,  involving  the  mucous  membrane  and  the  sub- 
mucous tissue.  One  of  the  exulcerations  was  on  the  greater  curvature,  the  other  on 
the  first  part  of  the  duodenum. 

The  urine  contained  bile  pigment,  albumin,  and  fatty  casts.  The  cells  in  Henle's 
loops  took  the  stain  badly,  and  were  studded  with  fine  fatty  granules,  the  nuclei  being 
indistinct.  In  the  liver  the  cells  took  the  stain  better,  although  they  showed  fatty 
degeneration.  Three  inoculations  in  series,  therefore,  modified  the  results.  In  the  first 
two  series  ligature  of  a  segment  of  gut  simply  gave  rise  to  septic  troubles,  but  in  the 
third  inoculation  the  animal  showed  toxsemia,  with  gastro- duodenal,  hepatic,  and 
renal  lesions. 

These  lesions,  produced  experimentally,  confirm  the  views  I  expressed 
at  the  Academic  de  Medecine  regarding  the  toxicity  of  appendicitis.  Prior 
to  this  occasion,  appendicitis  was  considered  to  be  simply  an  infective 
focus.  I  have  shown,  however,  that  poison  is  manufactured  in  this  focus, 
and  thence  invades  the  economy.  We  have,  therefore,  a  new  variety  of 
appendicitis,  which  gives  rise  to  toxaemia  ;  and  I  have  called  this  condition 
"  appendicsemia."  We  have  also  seen  that  the  appendicular  poison  has  a 
marked  preference  for  the  stomach,  liver,  and  kidney. 

In  the  kidney  the  toxic  nephritis  excites  albuminuria,  hsematuria, 
oliguria,  anuria,  and  at  times  symptoms  of  uraemia.  In  the  liver  the 
lesions  cause  jaundice,  urobilinuria,  and  in  some  cases  symptoms  of  icterus 
gravis.  In  the  stomach  the  erosions  and  exulcerations  give  rise  to  haemor- 
rhage, which  may  be  fulminant. 

In  some  cases  of  appendicitis  the  ulcers  in  the  stomach  and  duodenum 


DISEASES  OF  THE  STOMACH  699 

run  a  rapid  course,  ending  in  perforation  ;  in  other  cases  the  ulcers  are 
accompanied  by  erosions  and  ecchynioses  in  the  neighbourhood  of  the 
ulcers.  In  my  patient  the  stomach  was  the  seat  of  capillary  haemorrhages, 
while  a  perforating  ulcer  was  present  in  the  duodenum.  As  a  general  rule, 
it  seems  that  the  stomach  and  duodenum  are  organs  prone  to  ulceration  and 
perforation.  This  fact  is  shown  by  the  pneumococcal  erosions,  the  exulcera- 
tions,  and  thesimple  ulcer.  The  appendicular  toxines  play  a  large  part  in  this 
ulcerative  process,  which  may  end  in  erosion,  exulceration,  or  perforation. 
While  it  may  be  hard  to  distinguish  between  appendicitis  and  perforating 
ulcer  of  the  stomach  or  duodenum,  the  distinction  is  much  more  difficult  if 
the  two  lesions  succeed  one  another  and  exist  together.  The  diffuse  pain 
from  two  separate  foci,  and  the  possible  existence  of  acute  peritonitis,  so 
complicate  the  situation  that  a  diagnosis  may  be  almost  impossible.  The 
surgeon  must  discover  both  foci,  and  act  accordingly.  In  the  cases  quoted 
two  patients  were  saved  by  a  double  operation,  which  involved  the  appendix 
and  the  gastric  ulcer.  Similar  operations  are  described  later,  under  the 
Association  of  Appendicitis  and  Cholecystitis. 

XIII.  TRANSFORMATION  OF  SIMPLE  ULCER  OF  THE  STOMACH 

INTO  CANCER. 

The  transformation  of  ulcer  of  thfe  stomach  into  cancer  is  not  uncommon. 
Cruveilhier,  in  his  excellent  work  on  simple  ulcer  of  the  stomach,  deserves 
great  credit  for  elucidating  a  question  which  was  previously  obscure.  IJlcer 
and  cancer  were  confounded,  and  the  simple  ulcer,  which  is  rightly  called 
"  Cruveilhier's  disease,"  had  not  become  a  morbid  entity.  After  Cruveil- 
hier, people  perhaps  went  too  far ;  the  division  between  ulcer  and  cancer 
was  too  absolute,  and  the  fact,  that  Cruveilhier  himself  had  noted  the  co- 
existence of  the  two  lesions  in  the  stomach,  was  forgotten. 

This  coexistence  of  carcinoma  and  ulcer,  says  Rokitansky,  leads  to  the 
supposition  that  the  former  supervenes  on  the  latter.  Dittrich,  of  Prague, 
states  positively  the  termination  of  ulcer  in  cancer.  In  1848  he  published 
the  statistics  of  160  cases,  in  which  ulcer  of  the  stomach- was  eight  times  asso- 
ciated with  cancer.  Sometimes  both  ulcer  and  cancer  were  present  in  the 
same  stomach,  but  at  other  times  the  cancer  was  grafted  on  a  healed  or 
an  active  ulcer.  Lebert  considers  tliat  in  100  cases  of  cancer  of  the  stomach, 
nine  are  preceded  by  ulcer.  In  1882  Hanscr  studied  histologically  the  lesions 
of  the  mucous  membrane  in  the  vicinity  of  the  ulcer.  He  noted  the  develop- 
ment of  adenomatous  tissue,  and  the  tendency  for  cylindrical  cells  to  take 
the  place  of  the  glandular  epithelium.  This  was  the  first  stage,  which  ended 
later  in  the  invasion  of  the  muscularis  mucosa)  and  tunica  muscularis. 
Rosenheim  admits  that  ulcer  is  complicated  with  cancer  in  the  proportion 


700  TEXT-BOOK  OF  MEDICINE 

of  6  per  cent.,  and  Sonicksen  found  that  in  156  cases  of  cancer  of  the  stomach, 
examined  in  the  Kiel  Institute,  ulcer  had  preceded  cancer  in  the  proportion 
of  14  per  cent.  Pignal  has  collected  several  cases  of  the  transformation  of 
ulcer  into  cancer,  observed  by  Bouveret  and  Lepine.  Mathieu  has  published 
three  cases. 

I  have  devoted  a  clinical  lecture*  to  this  question.  The  following  case 
will  serve  as  an  example  : 

A  man  came  under  my  care  for  cancer  of  the  stomach.  Cachexia,  marked  loss  of 
flesh,  and  straw-coloured  complexion  justified  the  diagnosis  of  cancer  at  first  sight. 
I  questioned  him,  and  learnt  that  the  disease  had  made  its  appearance  fifteen  months 
previously,  with  pains  and  vomiting,  which  had  since  been  the  chief  symptoms.  During 
this  period  he  had  had  one  attack  of  haematemesis  and  several  of  malsena.  On  ex- 
amining the  epigastric  region,  I  was  surprised  to  find  that  the  slightest  pressure  was 
so  painful  as  to  prevent  a  complete  examination.  He  had  not  only  deep-seated  pain, 
but  also  acute  cutaneous  hypersesthesia.  He  then  described  his  pains.  From  the 
commencement  of  the  disease  they  supervened  after  meals,  persisted  during  digestion, 
and  did  not  cease  when  the  stomach  was  empty.  They  were  sometimes  tearing  in 
character,  and  were  seated  principally  in  the  pit  of  the  stomach,  but  they  also  radiated 
towards  the  spine.  The  fits  of  vomiting  were  frequent,  and  the  vomit  was  so  acid 
as  to  cause  a  lasting  taste  of  vinegar  in  the  mouth.  It  was  evidently  a  case  of  hyper- 
chlorhydria.  The  stomach,  which  did  not  appear  to  be  dilated,  was  so  intolerant 
that  water  and  milk  were  at  once  vomited. 

The  severity  of  these  symptoms  led  me  to  doubt  the  diagnosis  of  cancer.  Cancer 
of  the  stomach  is  not,  as  a  rule,  accompanied  by  such  acute  pains  and  uncontrollable 
vomiting.  Although  pain,  dyspepsia,  and  vomiting  occupy  a  most  important  place 
in  cancer  of  the  stomach,  I  have  not  seen  a  case  in  which  they  were  so  severe  ;  the  symp- 
toms belong  especially  to  simple  ulcer. 

I  had  the  vomit  examined  by  Du  Pasquier,  and  instead  of  finding  hyperchlorhydria, 
which  must  have  been  present  before  when  the  vomit  was  as  acid  as  vinegar,  he  found 
marked  hypochlorhydria.  The  hydrochloric  acid  was  present  in  the  proportion  of 
0-18  instead  of  1-74  per  1,000.  The  results  obtained  after  a  test  meal  were  practically 
the  same. 

The  diagnosis,  therefore,  was  difficult.  The  violence  of  the  pain  and  the  frequent 
vomiting,  with  the  intolerance  of  the  stomach  and  the  previous  acidity,  were  all  in 
favour  of  simple  ulcer.  On  the  other  hand,  the  actual  hypochlorhydria  and  progressive 
emaciation  of  the  patient,  his  cachectic  look,  and  the  presence  of  inguinal  glands,  were 
in  favour  of  cancer.  Exploration  of  the  epigastric  region  did  not  settle  the  question, 
for  there  was  neither  tumour  nor  induration  ;  moreover,  the  presence  of  induration  is 
of  little  value,  for  the  tumour  may  escape  notice,  and  also  an  ulcer,  if  surrounded  by 
indurated  tissues,  may  resemble  cancer. 

My  previous  experience,  combined  with  the  course  of  the  symptoms,  led  me  to  think 
that  the  patient  had  originally  had  an  ulcer  of  the  stomach  on  which  cancer  bad  been 
grafted. 

As  it  was  necessary  to  relieve,  if  not  to  cure,  him,  I  ordered  the  following  mixture, 
which  I  recommend  in  all  cases  of  painful  dyspepsia  : 

Lime-water       .  .  . .  . .  . .  . .     giii. 

Cocaine  hydrochlorate    , .  . .  . .  "     S^-  i 

Morphia  hydrochlorate  . .  . .  . .  . .     gr.  J 

*  "  Transformation  de  I'Ulcere  Stomacal  en  Cancer  "  {Clinique  Medicate  de  r Hotel- 
Dieu,  1897,  13""'  leyon). 


DISEASES  OF  THE  STOMACH  701 

A  tablespoonful  of  milk  with  a  teaspoonful  of  the  mixture  was  administered  every 
hour.  An  ice-bag  was  placed  on  the  pit  of  the  stomach.  Next  day  the  pain  in  the 
stomach  had  diminished.  The  milk  and  lime-water  were  then  increased.  In  about 
a  fortnight  the  pains  had  almost  disappeared  and  he  took  daily  3  pints  milk  without 
vomiting.  His  general  condition  improved,  sleep  returned,  the  loss  of  flesh  was  less 
marked,  the  weight  even  increased  a  little,  so  that  the  patient  became  hopeful,  and  I 
was  asked  if  the  diagnosis  of  cancer  was  not  wrong,  and  if  it  was  not  necessary  to 
substitute  the  diagnosis  of  simple  ulcer. 

Although  true  improvement  is  rare  in  cancer  of  the  stomach,  it  is  not  imcommon 
to  see  a  period  of  arrest  in  the  course  of  the  disease.  Early  lavage  may  cause  an  im- 
provement, which  does  not  suffice  to  exclude  the  primary  idea  of  cancer.  I  did  not,  there- 
fore, modify  the  diagnosis.  The  course  of  events  justified  my  prophecy.  After  a  month 
of  relative  improvement,  the  pains  again  became  so  severe  as  to  demand  frequent 
injections  of  morphia.     He  refused  food,  and  died  from  cachexia. 

This  mode  of  death  occurs  chiefly  in  cancer.  Ulcer  of  the  stomach  kills  by  peri- 
tonitis, haemorrhage,  or  by  secondary  peritoneal  abscess,  while  cancer  kills  slowly  and 
progressively  by  cachexia,  and  probably  by  its  toxine. 

The  post-mortem  examination  showed  that  it  was  a  case  of  cancer  grafted  on  ulcer. 
The  lesion  comprised  a  huge  ulcer,  perpendicular  to  the  long  axis  of  the  stomach. 


Fig.  46. — Ulcer:  Flook  fui^a^.u  liv  the  Liver. 
u.  Indurated  flat  edge  ;  c,  raised  edge  showing  malignant  change. 

The  ulcer  measured  2  and  4  inches  it  its  two  diameters.  It  occupied  the  lesser  curva- 
ture and  encroached  on  the  anterior  and  posterior  surfaces  of  the  stomach.  To  the 
left  it  extended  to  within  2  inches  of  the  oesophagus,  and  to  the  right  it  was  bounded  by 
the  pylorus.     It  was  a  metatypical  epithehoma. 

In  a  general  way,  ulcer  and  cancer  of  the  stomach  may  coexist  in  different 
combinations.  The  most  frequent  combination  is  that  seen  in  my  patient — 
the  cancerous  degeneration  occurring  whilst  the  ulceration  is  active.  In 
other  cases  the  cicatrix  of  a  healed  ulcer  becomes  the  starting-point  of  the 
cancerous  change  ;  and  in  other  cases,  again,  we  find  cancer  and  ulcer  clearly 
di-stinct,  which  leads  to  the  belief  that  the  cancer  has  arisen  in  a  former 
ulcer.  The  varieties  met  with  include  cylindrical  epithelioma,  meta- 
typical epithelioma,  encephaloidal  carcinoma,  scirrhous  and  colloid  cancer. 
Of  the  different  varieties,  the  metatypical  epithelioma  seems  to  be  the  most 
frecjnent. 

The  transformation  of  ulcer  of  the  stomach  into  cancer  is  comparable 


702 


TEXT-BOOK  OF  MEDICINE 


with  the  change  seen  elsewhere  in  cicatrices.  Chaintre  has  collected  a 
number  of  cases — Poncet :  epithelioma  in  the  scar  of  an  amputation  stump  ; 
Molliere  and  Laroyenne  :  epithelioma  in  the  cicatrix  of  an  old  cautery- 
wound  in  the  deltoid  region  ;  Marcin  :  cancerous  change  in  the  scar  of  a 
burn  on  the  lower  part  of  the  thigh  ;  Poncet :  epithelioma  in  a  urinary 
fistula  ;  Jansion  :  epithelioma  grafted  on  old  ulcers  of  the  leg,  etc. 

Epithelioma  may  appear  in  a  patch  of  buccal,  labial,  or  lingual  leuko- 
keratosis,  or  in  the  cicatrix  of  patches  of  leukokeratosis  which  have  been 
operated  upon.  If,  in  the  present  state  of  our  knowledge,  and  in  spite  of 
its  frequency,  the  epitheliomatous  change  is  not  considered  as  an  inevitable 


Fig.  47.— Section  through  (Fig.  46). 

Malignant  vegetation  ;  cs,  culs-de-sac  of  the  glands  ;  m,  muscularis  mucosae  ; 
s,  submucosa  ;  cm,  muscular  layers  ;  a,  discs  of  cancer  cells  ;  /,  floor  of  ulcer  ; 
2,  zone  of  transition  between  growth  and  healthy  parts  ;  e,  healthy  mucosa  ; 
p,  thickened  peritoneum.     The  lighter  half  of  the  figure  is  healthy  tissue. 


phase  of  the  disease,  it  must  be  held  that  the  change  is  determined  by  an 
inherent  predisposition  in  the  leukokeratosis  itself  (Le  Dentu). 

Analysis  of  the  Symptoms.— It  has  been  shown  that  ulcer  of  the 
stomach  undergoes  cancerous  degeneration  in  relatively  numerous  cases, 
especially  when  heredity  is  concerned.  The  following  problem  has,  then,  to 
be  solved  :  How  are  we  to  teU  whether  ulcer  of  the  stomach,  which  is  often 
curable,  is  undergoing  malignant  change,  which  is  always  fatal  ? 

Several  forms  may  j)resent  themselves.  In  one  case  the  symptoms  of 
ulcer  are  so  pronounced  that  diagnosis  is  impossible,  and  the  presence  of 
the  cancer  is  unnoticed.  A  patient  with  the  classical  signs  of  ulcer  is  taken 
ill  with  perforation  of  the  stomach,  acute  peritonitis,  and  fatal  haemorrhage. 


DISEASES  OF  THE  STOMACH 


703 


The  post-mortem  examination  reveals  an  ulcer,  and  also  a  malignant  growth, 
which  has  not  yet  had  time  to  leave  its  mark  on  the  affection. 

On  the  other  hand,  a  patient  shows  signs  of  malignant  cachexia — loss 
of  flesh,  anorexia,  pallor  of  the  sldn,  hypochlorhydria,  and  enlarged  glands 
in  the  groin  or  in  the  clavicular  region,  pointing  to  cancer  of  the  stomach. 
What  signs  will  show  that  the  cancer  is  grafted  on  an  ulcer — or,  rather, 
what  signs  will  help  us  to  eliminate  the  hypothesis  of  cancer,  and  retain 


Fio.  48. — Section  theough  A  (Fig.  47) ;  Coil  op  Canceb  Cells. 

that  of  ulcer  ?  Cancer  and  ulcer  of  the  stomach  do  not  run  the  same 
course.  It  is  not  sufiicient  to  make  a  thorough  examination  of  the  patient  ; 
we  must  also  review  his  past,  and  study  the  onset  and  import  of  each 
symptom.  The  general  rule  is  :  Violent  pain  in  the  stomach  and  profuse 
haematemesis  are  found,  not  in  cancer,  but  in  ulcer.  An  individual  who 
has  the  appearance  of  cancerous  cachexia,  and  suffers,  or  has  at  some  period 
of  his  illness  suffered,  from  acute  gastric  and  intrascapular  pains,  which  are 
increased  by  the  ingestion  and  digestion  of  food,  has  perhaps  a  cancer 


r^^^x-S^^ 


:,^ 


Fig.  49.— Section  throigii  Coils  op  Canckr  Cells  at  Z  (Fig.  47). 

grafted  on  the  ulcer,  but  he  certainly  has  an  ulcer ;  indeed,  there  may  be 
only  an  ulcer,  and  no  cancer, 

A  similar  argument  is  applicaljle  to  vomiting  of  blood.  Some  cancers 
of  the  stomach  give  rise  to  haematemesis  and  mela;na.  Tliis  cancerous 
gastrorrhagia,  even  thooigh  it  may  bo  profuse,  is  not  comparable  with  the 
vomiting  of  blootl  seen  in  ulcer.  An  individual  who  has  the  apjunirance  of 
cancerous  cachexia,  and  suffers,  or  has  suffered  during  some  period  of  his 


704  TEXT-BOOK  OF  MEDICINE 

illness,  from  repeated  and  profuse  haematemesis,  has  perhaps  a  cancer 
grafted  on  the  ulcer.     He  certainly  has  an  ulcer,  and  cancer  may  be  absent. 

On  reading  again  the  cases  mentioned  by  Trousseau  in  his  lectures  on 
the  diagnosis  of  cancer  and  ulcer  of  the  stomach,  it  seems  to  me  that  two 
of  the  patients  whom  he  considered  to  be  suffering  from  cancer  had  really 
an  ulcer  on  which  the  cancer  was  grafted. 

I  believe  that,  had  Trousseau  known  of  the  coexistence  of  cancer  and 
ulcer,  he  would  perhaps  have  modified  his  opinion.  One  of  his  patients 
in  whom  the  gastric  lesions  had  been  present  for  seven  years — a  very  long 
period  for  cancer — had  had  the  cardinal  symptoms  of  ulcer :  acute  pains 
in  the  stomach  and  profuse  vomiting  of  blood.  Furthermore,  the  man, 
whose  mother  had  cancer,  had,  I  believe,  grafted  on  his  ulcer  a  cancer, 
which  formed  in  the  anterior  wall  of  the  stomach. 

The  statement  regarding  the  acute  pain  and  profuse  haematemesis 
accompanying  ulcer,  with  or  without  cancerous  degeneration,  is  also  appli- 
cable to  suppurative  perigastritis,  which  has  often  been  set  down  to  cancer. 
Feulard  and  Brechoteau  have  collected  cases  of  anterior  phlegmonous  peri- 
gastritis, periumbilical  phlegmon,  and  umbilical  and  gastro-cutaneous  fistulae, 
resulting  from  cancer  of  the  stomach.  Fournier  enunciates  the  opinion  that 
suppurative  perigastritis,  if  closely  looked  into,  is  attributable,  not  to  cancer, 
but  to  ulcer — or,  at  least,  to  an  ulcer  on  which  a  cancer  has  been  grafted. 

"  In  cancer  of  the  stomach,  suppurative  anterior  perigastritis  commonly 
assumes  the  form  of  periumbilical  phlegmon  followed  by  gastro-cutaneous 
or  gastro-colic  fistula,  and  is  a  complication  which'  is  almost  exclusively 
seen  when  the  cancer  develops  in  an  ulcer.  Everything  seems  to  confirm 
Bouveret's  opinion  that  perforation  of  the  stomach  is  more  common  when  the 
cancer  is  grafted  on  an  ulcer.  It  is  especially  when  the  cancer  is  developed 
in  an  ulcer  that  it  tends  to  grow  larger  and  to  invade  the  neighbouring 
organs "  (Fournier).  These  assertions  seem  to  be  absolutely  justified. 
It  is  the  ulcer,  and  not  the  cancer,  which  eats  away  and  perforates  the 
stomach.  A  cancer  that  destroys  the  stomach  to  such  an  extent  as  to 
take  the  liver  and  tJie  pancreas  for  its  walls,  or  provokes  phlegmonous  peri- 
gastritis, is  almost  certainly  associated  with  a  perforating  ulcer.  Every 
individual,  therefore,  who  has  gastric  troubles,  with  cancerous  cachexia, 
and  also  suppurative  perigastritis,  which  may  or  may  not  involve  the 
abdominal  wall  and  cause  gastro-cutaneous  fistula,  has  perhaps  a  cancer 
grafted  on  an  ulcer,  but  he  certainly  has  an  ulcer.  It  is  possible  that  there 
is  only  an  ulcer,  and  not  a  cancer. 

It  follows,  therefore,  that  it  is  generally  possible  to  diagnose  ulcer,  but 
that  it  is  at  times  difficult  to  diagnose  the  transformation  of  ulcer  into 
cancer  ;  and  yet  this  diagnosis  is  of  the  greatest  importance,  for  the  question 
of  cancer  decides  the  prognosis  as  to  death  or  recovery.     I  do  not  know, 


DISEASES  OF  THE  STOMACH  705 

however,  of  any  signs  or  symptoms  which  in  difficult  cases  will  absolutely 
confirm  the  hypothesis  of  cancer.  In  many  cases  a  confident  diagnosis 
of  cancer  has  been  proved  erroneous  by  laparotomy.  Hypochlorhydria 
and  anachlorhydria,  though  signs  of  some  value  in  the  case  of  cancer,  are 
here  of  less  importance,  for  the  presence  of  an  ulcer  seems  sufficient  to 
increase  the  amount  of  hydrochloric  acid.  The  presence  of  induration  in 
the  epigastric  region  has  by  no  means  the  value  which  might  be  supposed, 
because  in  non-cancerous  ulcers  the  indurated  tissues  may  feel  like  a  tumour, 
and,  on  the  other  hand,  some  cancers  of  the  stomach  cannot  bo  felt,  or  do 
not  form  tumours.  This  view  also  applies  to  the  other  signs,  including  the 
transitory  improvement  which  treatment  may  cause  in  the  progress  of  the 
cancerous  cachexia.  Finally,  the  diagnosis  is  complicated  by  the  fact  that 
in  some  patients  apparently  cancerous  cachexia  is  really  the  result  of  ulcer. 
This  study  adds  to  the  gravity  of  the  prognosis  in  ulcer  of  the  stomach. 
An  ulcer  is  serious  by  reason  of  the  pain  and  vomiting,  which  may  induce 
loss  of  strength  ;  it  is  serious,  too,  because  of  such  complications  as  ful- 
minant hsemorrhage,  perforation,  frequency  of  recurrence,  and  the  possi- 
bility of  malignant  changes. 

XIV.  GASTRIC  POLYADENOMA. 

The  growth  formerly  called  gastric  polypus,  or  polypous  gastritis,  is 
now  more  correctly  termed  an  adenoma.  And  as  gastric  adenomata  are 
multiple  (we  may  find  from  thirty  to  several  hundred),  Brissaud  has  pro- 
posed the  term  gastric  polyadenoma.  The  question  of  the  gastric  poly- 
adenoma  is  entirely  anatomical,  for  the  a3tiological  conditions  are  still 
unknown,  and  the  affection  has  practically  no  symptoms. 

On  opening  the  stomach,  the  adenomata  are  seen  chiefly  in  the  pepsino- 
genous regions,  such  as  the  great  cul-de-sac,  inferior  border,  and  greater 
curvature.  They  may  be  as  large  as  a  lentil,  pea,  cherry,  or  hazel-nut,  and 
the  remarkable  thing  is  the  polypi  are  of  the  same  size.  It  seems  as  if  it 
were  a  case  of  an  eruption,  in  which  all  the  elements  are  of  the  same  age 
and  at  the  same  stage  of  growth.  At  the  commencement  the  growth  is 
formed  by  a  simple  elevation  of  the  mucous  membrane  ;  later  it  tends  to 
become  pedunculated.  The  growths  are  mobile,  like  the  mucous  mem- 
brane itself,  and  never  extend  beyond  its  deep  layers. 

In  other  cases  the  adenoma  assumes  the  form  of  mammilla?,  which  are 
disposed  in  linos,  and  somewhat  resemble  the  convolutions  of  the  brain. 

The  adenoma  is  of  glandular  origin.  It  is  met  with  in  chronic  gastritis, 
ulcer  of  the  stomach,  and  cancer.  It  may,  indeed,  be  asked  whether  the 
adenoma  and  the  polyadenoma  are  not  intermediate  between  chronic 
gastritis  and  cancer. 

45 


706  TEXT-BOOK  OF  MEDICINE 

XV.  CANCER  OF  THE  STOMACH. 

Note. — In  order  to  avoid  repetition,  I  would  ask  the  reader  to  study  this  section 
in  conjunction  with  the  two  preceding  sections.  These  three  sections  are  complemen- 
tary to  each  other.  Pathological  anatomy,  semeiology,  and  diagnosis  are  there  treated 
from  slightly  different  points  of  view. 

etiology. — In  point  of  frequency,  cancer  of  the  stomacli  ranks  first 
with  cancer  of  the  breast  and  uterus.  It  is  hereditary  in  one-sixth  of  the 
cases,  more  frequent  in  men  than  in  women,  and  usually  appears  between 
fifty  and  sixty-five  years.  The  growth  is  generally  primary,  unlike  cancer 
of  the  liver,  which  is  almost  always  secondary.  It  has  been  asserted  that 
grief,  arthritism,  and  herpetism  have  some  influence  on  its  development, 
but  these  hypotheses  do  not  appear  likely.  Chronic  gastritis,  ulcer  of  the 
stomach,  and  cancer,  have  such  close  connections,  that  the  cancer  seems 
in  certain  cases  to  graft  itself  on  the  other  lesions  of  the  stomach.  This 
question  has  been  discussed  in  the  preceding  section. 

Pathological  Anatomy.— The  most  common  varieties  are  the  cylin- 
drical-celled epithelioma,  and  the  encephaloid,  scirrhous,  and  colloid  cancers. 
The  pylorus  and  the  lesser  curvature  are  usually  affected,  and  the  posterior 
wall  is  more  frequently  invaded  than  the  anterior  wall.  On  opening  the 
stomach,  we  must  not  always  expect  to  find  a  tumour ;  we  may  find  an 
ulceration,  patch,  or  ring. 

The  cancerous  tumours  form  in  the  interior  of  the  stomach  a  projection 
like  a  donkey's  back,  which  becomes  more  marked  as  it  extends  in  area. 
These  solitary  or  multiple  tumours  are  larger,  more  fungus-like,  softer,  more 
vascular,  and  richer  in  milky  juice  in  the  encephaloid  than  in  the  scirrhous 
variety.  The  mucous  membrane  which  covers  them  is  thickened  or 
ulcerated.  The  ulcerations  are  of  variable  size  ;  they  may  occupy  the  whole 
lesser  curvature  of  the  stomach,  and  surround  the  pylorus  in  the  form  of 
a  ring.  The  ulcer  in  encephaloid  cancer  is  fungating,  with  everted  edges, 
and  made  up  of  a  rose-coloured  tissue,  which  is  soft  and  rich  in  milky  juice. 
In  certain  cases  the  floor  of  the  ulcer  is  bleeding  and  fungous,  or  else,  if 
the  whole  cancerous  growth  is  deeply  destroyed,  the  tunica  muscularis 
appears  denuded,  and  in  part  destroyed.  There  may  even  be  a  perforation. 
These  cases  resemble  at  first  sight  the  simple  ulcer,  and  caused  confusion 
prior  to  the  researches  of  Cruveilhier.  Cancer  en  cuirasse  spreads  in  the 
thickness  of  the  coats  of  the  stomach,  without  forming  a  tumour.  The 
annular  cancer  occupies  the  pylorus  or  the  cardiac  end  ;  in  the  former  case 
it  has  little  tendency  to  spread  to  the  intestine,  but  is  often  accompanied  by 
dilatation  of  the  stomach ;  in  the  latter  case  it  almost  always  attacks  the 
oesophagus,  and  as  a  rule  causes  contraction  of  the  stomach.  The  pylorus  is 
by  far  the  most  common  seat  of  cancer,  and  then  come  the  lesser  curvature, 
the  cardiac  end,  the  anterior  and  posterior  surfaces. 


DISEASES  OF  THE  STOMACH  707 

Perforation  of  the  stomach,  acute  peritonitis,  adhesions,  local  peritonitis, 
fistulae,  and  ulceration  of  the  vessels,  are  far  less  common  in  cancer  than 
simple  ulcer.  Cancer  readily  spreads  from  the  stomach  to  the  neighbouring 
organs,  the  dissemination  taking  jjlace  through  the  subserous  tissue,  blood- 
vessels, or  lymphatics.  The  peritoneum,  the  glands  in  the  gastro-hepatic 
omentum,  great  omentum,  and  mesentery,  the  liver  (according  to  Brinton, 
in  one-fourth  of  the  cases),  lungs,  kidneys,  sternum,  and  vertebrae,  may  be 
the  seat  of  secondary  growths.  In  some  cases  adhesions  are  formed  between 
the  stomach  and  the  abdominal  wall,  and  a  phlegmon  develops  in  the 
umbilical  region.  The  abscess  often  communicates  with  the  cavity  of  the 
stomach  and  with  the  exterior  by  means  of  an  umbilical  fistula.  In  some 
cases,  however,  we  find  that  the  abscess  communicates  only  with  the 
exterior  (cutaneous  fistula).  It  is  a  very  rare  complication  in  cancer  of 
the  stomach,  and  Feulard  has  only  been  able  to  collect  fourteen  cases. 

Cancer  of  the  stomach  commences  in  the  submucous  tissue  and  in  the 
glandular  layer.  The  glands  undergo  a  lengthening,  which  is  due  to  the 
growth  of  the  connective  tissue  between  them.  The  muscular  coat  of  the 
stomach  is  always  hypertrophied  in  the  neighbourhood  of  the  cancer,  and 
the  hypertrophy  may  become  general.  The  hypertrophied  muscular  coat 
owes  its  size  to  the  thick  lamellae  of  connective  tissue  that  divide  the 
muscular  bundles.  These  changes  in.  the  glands  and  muscular  tissue  are  not 
peculiar  to  cancer,  but  are  also  met  with  in  chronic  gastritis. 

Symptoms. — Cancer  of  the  stomach  begins,  as  a  rule,  with  slight  and 
intermittent  dyspepsia  ;  true  anorexia  is  seen  rather  at  a  more  advanced 
stage.  It  commences  in  some  cases  with  persistent  pains  in  the  epigastric 
region,  so  that  in  the  first  period,  which  may  last  for  months,  it  is  difficult 
to  say  whether  the  case  is  one  of  painful  dyspepsia  or  early  cancer.  If  the 
dyspepsia  is,  however,  obstinate,  or  accompanied  by  rapid  loss  of  flesh  and 
pallor  of  the  skin,  or  if  it  supervenes  in  an  old  person,  especially  one  born 
of  cancerous  stock,  the  prognosis  is  serious,  even  before  the  appearance  of 
other  symptoms. 

Pain,  either  early  or  late,  is  seldom  absent  in  cancer  of  the  stomach, 
but  it  is  less  severe  than  in  simple  ulcer,  and  has  not  a  predilection  for 
the  xiphoid  and  spinal  regions.  It  is  more  diffuse,  and  tends  to  radiate 
towards  the  hypochondria.  Vomiting  appears  in  some  cases  from  the  first, 
together  with  the  other  dyspeptic  troubles.  It  may  be  present  throughout 
the  entire  disease,  but  at  other  times  it  shows  itself  only  in  the  last  stage, 
or  may  bo  completely  absent.  The  vomited  matter  is  of  all  kinds  :  it  may 
be  mucous,  almost  watery,  or,  very  rarely,  bilious,  and  may  be  rejected  in 
the  morning,  whilst  fasting,  or  in  the  daytime.  It  may  consist  of  food- 
stuffs. The  vomiting  follows  soon  after  the  ingestion  of  food  if  the  cancer 
is  at  the  cardia,  but  later  if  the  growth  is  at  the  pylorus.     The  vomit  often 

45—2 


708  TEXT-BOOK  OF  MEDICINE 

contains  fragments  of  food  and  undigested  meat,  because  the  hydrochloric 
acid  is  deficient  both  in  quantity  and  in  quality.  There  is  but  little 
combined  hydrochloric  acid,  and  no  free  acid.  Butyric  fermentation 
gives  an  odour  of  rancid  butter  to  the  vomit,  while  putrid  fermen- 
tation, due  to  insufficient  digestion  of  the  proteids,  gives  an  odour  of 
putrefaction. 

Vomiting  of  blood  (hsematemesis)  is  of  great  importance,  being  fre- 
quent (42  per  cent.,  according  to  Brinton),  and  showing  itself  under  divers 
aspects.  Rejection  of  pure  blood  is  less  common  than  in  simple  ulcer,  and 
the  vomited  matter  is  generally  blackish,  like  coffee-grounds  or  soot  diluted 
with  water.  The  colour  results  from  the  contact  of  the  blood  with  the 
acids  of  the  stomach  and  with  the  food-stuffs.  In  some  cases  the  hsema- 
temesis is  so  slight  that  it  may  pass  unnoticed  unless  the  vomit  is  carefully 
examined.  If  the  blood  passes  into  the  intestine,  it  is  voided  in  the  stools 
in  the  form  of  meleena.  In  a  fair  number  of  cases  haemorrhage  from  the 
stomach  is  revealed  by  melsena  without  ha^matemesis.  Gastrorrhagia  is 
usually  a  late  symptom  ;  it  is  due  to  the  ulceration  and  softening  which 
invades  the  vessels  of  the  cancerous  mass.  "  The  degeneration  and  destruc- 
tion are  often  complicated  by  the  presence  of  excrescences  and  of  fungoid 
growths,  which  increase  still  more  the  quantity  of  blood  su23plied."  More 
rarely  the  haemorrhage  is  caused  by  ulceration  of  large  vessels  in  the  walls 
of  the  stomach. 

In  addition  to  late  gastrorrhagia,  we  sometimes  see  early  haemorrhage, 
which  supervenes  during  good  health  "  as  the  first  symptom  of  a  malady 
which  will  certainly  carry  the  individual  to  his  grave  "  (Trousseau).  I 
think  that  these  early  and  profuse  attacks  of  gastrorrhagia  are  rather  the 
result  of  an  iilcer  on  which  cancer  has  been  grafted. 

At  some  period  of  its  development  (80  per  cent.,  according  to  Brinton) 
cancer  of  the  stomach  forms  a  tumour,  which  is  more  or  less  easily  dis- 
cerned, according  to  its  situation.  The  growth  is  easy  to  feel  when  it 
occupies  the  anterior  surface,  the  greater  curvature,  and  the  pylorus,  but 
difficult  when  it  is  situated  at  the  cardia,  or  on  the  posterior  surface  and 
lesser  curvature.  Tumours  of  the  greater  curvature  are  seated  to  the  left 
of  the  median  line,  while  a  growth  of  the  pylorus  is  felt  to  the  right,  near 
the  umbilicus.  The  stomach  is  sometimes  so  dilated  and  drawn  down  that 
the  tumour  is  situated  at  or  below  the  umbilicus. 

In  some  cases  the  cancer  infiltrates  the  coats  of  the  stomach  without 
forming  a  tumour  (cancer  en  cuirasse),  and  there  is  then  a  feeling  of  diffuse 
induration.  Sometimes,  too,  neither  induration  nor  tumour  can  be  felt. 
The  exploration  of  the  abdomen  for  a  tumour  may  be  rendered  difficult  by 
the  contraction  of  the  recti  muscles,  which  may  hide  a  tumour  lying  beneath, 
or  cause  a  phantom  tumour.     For  this  reason  it  is  necessary  to  relax  the 


DISEASES  OF  THE  STOMACH  709 

muscles,  and  the  patient  must  flex  the  thighs  and  breathe  with  the  mouth 
wide  open. 

The  cancerous  tumour,  although  but  little  painful  to  the  touch,  is  never- 
theless more  sensitive  than  the  neighbouring  parts.  When  the  growth 
constricts  the  pyloric  orifice,  it  causes  dilatation  Of  the  stomach  and 
exaggerated  resonance  in  the  epigastric  region. 

The  tumour  may  vary  in  position,  according  as  the  stomach  is  full  or 
empty.  On  abdominal  palpation  the  tumour  most  often  appears  mobile, 
but  this  apparent  mobility  cannot  be  relied  upon,  for  cancer  of  the  posterior 
surface  may  be  adherent  to  the  pancreas,  and  a  growth  in  the  anterior 
surface  may  be  fixed  to  the  abdominal  wall.  Cancer  of  the  pylorus  often 
adheres  to  the  pancreas,  gall-bladder,  duodenum,  small  omentum,  liver,  or 
glands.  In  300  cases  of  laparotomy  for  cancer  of  the  stomach,  the  growth, 
when  pyloric,  was  free  from  adhesions  in  only  fourteen  cases.  When,  there- 
fore, a  cancer  of  the  stomach  is  explored  and  thought  to  be  mobile,  the 
mass  which  moves  includes  both  the  cancer  and  its  adhesions.  It  is  im- 
portant to  remember  these  facts  from  the  point  of  view  of  operation. 

Enlarged  glands  are  more  common  in  cancer  of  the  stomach  than  in  cancer 
of  other  viscera,  not  only  in  the  subclavicular  triangle,  but  also  in  the  groin 
and  axilla.     The  glands  are  hard,  painless,  and  movable. 

The  general  symptoms,  which  are  not  pronounced  at  the  commence 
ment  of  the  disease,  become  characteristic.  Pallor  of  the  skin  is  followed 
by  a  straw-coloured  tint ;  the  patient  shows  a  dislike  for  food ;  the  strength 
fails,  and  diarrhoea  is  frequent.  Fever  is  often  seen  ;  the  loss  of  flesh 
becomes  extreme  ;  the  voice  grows  weak ;  the  skin  becomes  dry  and  cracks, 
and  the  stage  of  cachexia  appears.  During  this  stage  the  intellectual 
faculties  remain  intact,  and  the  patient  is  conscious  of  his  decay.  CEdema 
and  dropsy  appear ;  the  feet  and  legs  become  infiltrated,  and  the  infiltration 
reaches  the  thighs,  scrotum,  and  sometimes  the  hands  and  face,  thougli 
there  is,  as  a  rule,  no  trace  of  albumin  in  the  urine.  This  general  oedema 
must  not  be  confounded  witli  tlic  local  and  sometimes  early  oedema  due  to 
venous  thrombosis  (phlegmasia  alba  dolens).  Trousseau  was  the  first  to 
note  the  relation  between  obliterating  phlebitis  and  cancer.  Wo  shall 
refer  to  tliis  point  under  Diagnosis. 

Complications.— Certain  complications,  though  frequent  in  ulcer,  are 
exceedingly  rare  in  cancer.  We  find  fatal  haimorrhages  are  exceptional, 
whilst  they  are  relatively  frequent  in  ulcer.  Perforation  of  the  stomach 
and  supcracute  peritonitis  are  practically  unknown  in  cancer,  whilst  they  are 
far  from  being  rare  in  ulcer.  Cancer,  like  ulcer,  may  cause  purulent  and 
gangrenous  fistuhc.  Adhesions  are  formed  in  the  region  of  a  cancerous 
ulceration,  which  sometimes  results  in  perforation  and  local  peritonitis. 
The  peritoneal  fistula  thus  formed  may  open  into  the  colon  (ga.stro-colio 


710  TEXT-BOOK  OF  MEDICINE 

fistula),    or    may  involve    the    umbilical   region,   as    I    have   previously 
remarked. 

Amongst  the  complications  secondary  deposits  in  other  organs  must  be 
noted.  Sometimes  they  result  from  direct  propagation,  and  it  is  through 
adhesions  that  the  cancer  attacks  the  liver,  glands,  spleen,  pancreas,  intes- 
tine, and  abdominal  wall.  Sometimes  there  is  general  cancerous  infiltration 
in  the  true  sense  of  the  word,  by  means  of  the  lymphatics  or  bloodvessels. 

Diagnosis. — I  have  just  described  the  usual  course  of  cancer  of  the 
stomach,  with  its  insidious  onset,  accompanied  by  dyspeptic  troubles, 
gradual  wasting,  vomiting,  heematemesis,  and  anorexia,  as  well  as  the 
appearance  of  the  tumour  and  the  cachectic  stage.  Cancer  of  the  stomach, 
however,  does  not  always  run  such  a  regular  course.  In  one  case  the  usual 
signs  are  absent,  and  the  disease  is  latent.  We  find  neither  vomiting, 
hsematemesis,  nor  tumour.  The  patient  has  malignant  cachexia,  but  the 
seat  of  the  lesion  is  undecided.  Or,  again,  we  may  find  a  tumour,  but  no 
symptoms  of  cancer.  In  another  case,  while  the  cancer  of  the  stomach 
is  at  an  early  stage  of  its  evolution,  secondary  deposits  in  the  liver  attract 
attention,  and  carry  off  the  patient,  masking  the  lesion  in  the  stomach. 
In  some  cases  the  patient  has  anorexia,  haematemesis,  cachexia,  and  epi- 
gastric tumour,  so  that  the  diagnosis  points  to  cancer  of  the  stomach ;  but 
in  a  few  months  recovery  gives  the  lie  to  the  diagnosis.  In  the  preceding 
section  I  have  dwelt  on  this  point  in  diagnosis  at  some  length. 

The  following  summary  shows  the  errors  which  may  occur  in  regard  to 
cancer  of  the  stomach  : 

Vomiting,  hsematemesis,  tumour,  and  cachexia  are  the  classical  signs 
of  cancer  of  the  stomach  ;  but  they  may  be  due  to  extensive  ulcers,  with 
thick,  indurated  edges.  This  fact  holds  good  both  in  simple  (Trousseau's 
and  Rommelaere's  cases)  and  in  tubercular  ulcers  (Brechemin's  case).* 

The  above  signs,  though  classical  of  cancer,  may  exist  in  chronic 
gastritis,  with  thickening  of  the  walls  (hypertrophic  submucous  sclerosis), 
as  in  a  remarkable  case  reported  by  Trousseau,  where  chronic  gastritis  was 
mistaken  for  cancer. 

Vomiting,  hsematemesis,  and  cachexia,  may  exist  in  dilatation  of  the 
stomach,  and  cause  an  erroneous  belief  in  the  existence  of  cancer  (Dujardin- 
Beaumetz). 

Vomiting,  haematemesis,  epigastric  tumour,  and  cachexia,  may  exist 
when  the  stomach  is  healthy.  In  such  a  case  the  tumour  is  formed  by  a 
cancer  of  the  omentum,  pancreas,  or  mesenteric  glands,  or  by  a  peritoneal 
thickening  (Leube).  The  cachexia  is  due  to  cancer  in  one  of  the  above- 
*  Whilst  I  was  house-physician  to  Potain,  one  of  his  patients  had  haemate- 
mesis,  progressive  cachexia,  and  a  tumour  in  the  epigastric  region.  The  diagnosis 
pointed  to  cancer  of  the  stomach.  At  the  post-mortem  examination  we  found  cancer  in 
the  glands.     He  had  been  operated  on  two  years  previously  for  cancer  of  the  left  testicle. 


DISEASES  OF  THE  STOMACH  711 

mentioned  regions,  and  the  haematemesis  proceeds  from  the  stasis  in  the 
gastric  circulation,  caused  by  compression  of  the  gastric  veins. 

Doubt  may  also  exist  in  certain  periumbilical  phlegmons,  as  mentioned 
under  the  pathological  anatomy.  In  the  case  quoted*  the  phlegmon  was 
evident,  when  the  symptoms  of  cancer  were  not  appreciable. 

This  list  proves  how  difficult — I  might  almost  say  impossible — it  is 
in  some  cases  to  diagnose  cancer  of  the  stomach.  Let  us  consider  the  signs 
of  cancer  of  the  stomach  one  by  one,  and  see  what  is  their  respective  value 
in  diagnosis. 

Acute  epigastric  pain,  which  pierces  the  patient  through  and  through 
(xiphoid  and  spinal  points),  and  comes  on  in  paroxysms  after  meals  or  during 
digestion  is  caused  by  ulcer  of  the  stomach.  It  may  also  be  seen  in  cases 
of  acid  dyspepsia.  The  pain  is  less  common  in  cancer  ;  it  is  also  less  acute, 
more  diffuse,  and  appears  later. 

Vomiting  of  bright  or  dark  blood,  with  or  without  melaena,  after  a  longer 
or  shorter  period  of  gastralgia,  is  caused  rather  by  ulcer  than  by  cancer ; 
but  haematemesis  is  of  all  the  symptoms  the  most  uncertain  in  diagnosis. 
Haematemesis  in  cancer  is,  it  is  true,  less  common  and  less  profuse,  and  the 
blood  is  more  mixed  with  food,  and  more  of  a  "  coffee-ground  colour  " 
than  in  ulcer  ;  but  these  signs  are  inconstant,  and  in  ulcer,  gastritis,  or 
dilatation  of  the  stomach,  attacks  of  haematemesis  may  supervene,  and  be 
exactly  alike  in  character. 

If  we  find  epigastric  swelling  or  induration  in  a  patient  who  has  vomiting, 
haematemesis,  loss  of  flesh,  and  cachexia,  the  tumour  is,  as  a  rule,  considered 
the  most  important  point  in  the  diagnosis  of  cancer.  And  yet  I  do  not 
hesitate  to  say  that  the  tumour  most  often  causes  the  error  in  diagnosis. 
As  long  as  the  patient,  though  suffering  from  other  symptoms,  has  no 
tumour,  we  think  of  ulcer ;  when  the  tumour  appears,  cancer  is  diagnosed. 
The  following  cases  are  a  sufficient  proof : 

In  1888  Kolatschewsky  performed  pylorectoray  on  a  boy  with  a  hard,  movable 
tumour  of  the  pylorus,  which  was  as  large  as  an  apple,  and  was  looked  upon  as  can- 
cerous. The  operation  revealed  a  healed  gastro -duodenal  ulcer,  surrounded  by  glands. 
The  patient  recovered.  Billroth  diagnosed  cancer  of  the  pylorus,  and  performed 
pylorectomy.  Salzer,  who  reported  the  case  to  the  Medical  Society  of  Vienna,  in 
December,  1887,  proved  that  it  was  a  case  of  ulcer  of  the  stomach.  Orthmann  diag- 
nosed cancer  of  the  pylorus  in  a  woman  forty  years  of  age.  He  performed  pylorectomy 
on  May  17,  1889.  The  operation  revealed  a  cicatrized  ulcer,  with  indurated  edges. 
In  Juno,  1884,  Southa  operated  for  cancer  on  a  patient,  who  presented  a  hard  and 
mobile  tumoxir  in  the  neigh bourliood  of  the  umbilicus,  with  all  the  symptoms  of  cancer. 
The  patient  succumlwd,  and  a  fibrous  constriction  of  the  pylorus  Mas  found,  but  not 
a  trace  of  cancer. 

In  one  of  Chaput's  cases  the  patient  showed  symptoms  wliicli  miglii  liave  been 
due  to  ulcer  or  cancer  of  the  stomach.    Brissaud  thought,  from  the  epigastric  tumour, 


Dieulafoy,  "  Diagnostic  du  Cancer  do  I'Estomac,"  Sem.  Med.,  January  4,  1888. 


712  TEXT-BOOK  OF  MEDICINE 

that  it  was  a  case  of  cancer,  and  the  patient  was  operated  upon.  It  was  then  found 
that  the  tumour  was  due  to  an  abscess  of  the  pancreas,  following  a  perforating  ulcer 
of  the  stomach. 

A  woman  came  under  tlie  care  of  Terrier  for  gastric  trouble,  which  presented  the 
complete  picture  of  cancer  of  the  stomach,  with  epigastric  tumour.  Terrier  performed 
laparotomy,  and  found  adhesions  between  the  stomach,  liver,  and  anterior  wall  of 
the  abdomen,  but  not  cancer.  These  adhesions  (probably  due  to  ulcer  of  the  stomach) 
were  broken  down,  and  the  patient  recovered.  On  this  point  Terrier  states  that 
Landerer  has  published  three  cases  of  laparotomy  for  cancer  of  the  stomach.  The  opera- 
tion showed  that  the  tumours  were  due,  not  to  cancer,  but  to  adhesions,  the  excision 
of  which  brought  about  a  cure.  Doyen  has  reported  several  cases  in  which  an  ulcer 
with  adhesions  has  been  taken  for  a  cancerous  tumour. 

This  series  of  cases  shows,  I  think,  that  the  presence  of  an  epigastric 
tumour  is  often  a  cause  of  error  in  diagnosis. 

Progressive  cachexia,  with  loss  of  appetite,  straw-coloured  complexion, 
and  oedema  of  the  legs,  is  caused  by  cancer  of  the  stomach.  Similar  symp- 
toms, however,  may  be  present  with  ulcer,  gastritis,  and  dilatation  of  the 
stomach,  with  or  without  spasmodic  contraction  of  the  pylorus,  in  which 
case  the  cachexia  is  caused  by  the  haematemesis  and  vomiting  of  food,  with 
consequent  malnutrition. 

Phlebitis  obliterans  is  a  valuable  sign  noticed  by  Trousseau.  "  When 
you  are  in  doul)t  between  chronic  gastritis,  simple  ulcer,  or  carcinoma  of 
the  stomach,  phlegmasia  alba  dolens  of  the  leg  or  arm  is  a  positive  indica- 
tion in  favour  of  cancer."  Trousseau  later  proved  this  fact  in  his  own  case ; 
indeed,  the  appearance  of  phlegmasia  in  the  leg  led  my  venerated  master 
to  afhrm  the  existence  of  cancer  of  the  stomach,  from  which  he  died  eight 
months  later.  Although  phlegmasia  has  been  found  by  Bouchard  in 
dilatation  of  the  stomach,  it  remains,  none  the  less,  one  of  the  most  valuable 
signs  of  distinction  between  cancer  and  ulcer. 

Rommelaere  believed  that  it  was  possible  to  base  a  diagnosis  of  cancer 
on  the  diminution  of  the  urea.  The  amount  of  urea  is  lowered  in  cancer, 
but  as  similar  diminution  exists  in  many  disorders  of  nutrition,  this  sign 
loses  its  value. 

Enlarged  glands  above  the  clavicle  are  common  in  abdominal  cancer, 
and  notably  in  cancer  of  the  stomach.  They  are  found  on  the  left  side 
five  times  as  often  as  on  the  right  side.  Whatever  explanation  is  given 
for  this  distant  metastasis  of  the  primary  lesion,  it  is  none  the  less  true  that 
this  sign  is  of  value.  In  a  doubtful  case,  however,  it  does  not  prove  the 
existence  of  cancer  of  the  stomach,  because  enlargement  of  these  glands 
has  been  found  in  ulcer  of  the  stomach. 

It  has  been  suggested  that  examination  of  the  chyme,  taken  during 
digestion,  might  furnish  useful  information ;  and  at  the  present  time  this 
analysis  is  commonly  made,  but  it  has  not  led  to  any  fixed  results. 

The  amount  of  hydrochloric  acid  is  of  great  value  in  diagnosis.     It  is 


DISEASES  OF  THE  STOMACH  713 

present  normally  in  the  gastric  juice  in  the  proportion  of  r74  per  1,000, 
but  it  is  absent  when  the  stomach  is  at  rest.  The  other  acids  of  the  gastric 
juice,  and  amongst  them  lactic  acid,  are  formed  from  the  food-stuffs.  Regard- 
ing their  forniation,  Ewald  divides  the  process  of  digestion  into  three  stages  : 
In  the  first  stage,  which  lasts  from  ten  to  thirty  minutes,  lactic  acid  is 
found  in  the  stomach  ;  in  the  second  stage,  free  hydrochloric  acid  exists 
side  by  side  with  the  lactic  acid  ;  but  in  the  third  stage,  which  commences  half 
or  three-quarters  of  an  hour  after  the  beginning  of  digestion,  the  lactic 
acid  has  generally  disappeared,  and  hydrochloric  acid  alone  is  found.  The 
hydrochloric  acid  must  therefore  be  looked  for  during  this  stage. 

The  method  requires  care.  The  patient  is  first  given  a  test  meal, 
consisting  of  two  small  rolls  and  a  cup  of  tea,  without  sugar  or  milk,  taken 
when  the  stomach  is  empty.  An  hour  or  an  hour  and  a  quarter  later  the 
chyme  is  withdrawn  by  means  of  Debove's  tube,  or  the  siphon-tube  may 
be  first  filled  with  a  little  water,  and  the  hydrochloric  acid  is  tested  for  in 
the  chyme  thus  withdrawn.  The  acid  may  be  detected  by  various  reagents, 
such  as  methyl- violet  or  Congo  red,  which  changes  to  a  blue  colour.  Lepine 
prefers  vert  brilliant.*  This  stain,  diluted  with  water,  loses  its  greenish 
colour  and  becomes  blue.  If  2  or  3  drops  of  a  concentrated  solution  of 
vert  brilliant  be  mixed  with  a  few  centimetres  of  filtered  chyme  containing 
hydrochloric  acid,  the  mixture  changes  from  blue  to  green,  if  the  proportion 
of  hydrochloric  acid  be  from  0"18  to  0'19  per  1,000.  The  mixture  becomes 
yellow,  if  the  proportion  of  hydrochloric  acid  be  from  0"19  to  1  per  1,000. 
This  reaction  is  important,  because  lactic  acid  has  practically  no  action  on 
vert  brilliant. 

To  have  its  full  value,  the  test  should  be  followed  by  a  quantitative 
estimation  of  the  free  hydrochloric  acid  and  other  elements  (acids  of  fer- 
mentation, combined  chlorine),  as  well  as  of  the  pej)sin  and  rennet  ferment. 

From  our  ])resent  point  of  view,  hypersecretion  of  the  hydrochloric 
acid,  which  may  amount  to  3  and  -lo  per  1,000,  instead  of  TT,  occurs  in 
simple  ulcer,  in  the  gastric  crises  of  ataxia,  and  in  certain  cases  of  hyperchlor- 
hydric  dyspepsia.  It  is  never  seen  in  cancer  of  the  stomach,  unless  a  cancer 
is  grafted  on  an  ulcer.  Diminution  or  disappearance  of  the  hydrochloric 
acid  has  been  found  in  amyloid  degeneration  of  the  vessels  of  the  gastric 
mucosa,  chlorosis,  most  cachectic  conditions,  and  alcoholic  gastritis ;  but  it 
is  in  cancer  of  the  stomach  that  the  disappearance  of  hydrochloric  acid 
is  almost  the  rule.  This  disappearance  is  ]»r()bably  due  to  cilaIlg(^s  in  the 
gastric  juice,  caused  by  the  cancerous  secretion  (Riogel's  ex[)erimeuts). 

Those  facts  do  not  show  that  the  absence  of  hydrochloric  acid  excludes 
cancer  al)solutely,  for  the  acid  has  been  found  in  cancer.  Neverthe- 
less, the  numerous  cases   in  which   the   absence   of   hydrochloric   acid   has 

*   \'(it  l)rilliant  is  prohiihly  idonticiil  witli  omoralil,  smaragd  or  malachite  greon. 


714  TEXT-BOOK  OF  MEDICINE 

prevented  errors  in  diagnosis  prove  that  the  estimation  of  hydrochloric 
acid  is  a  valuable  method.  To  differentiate  between  the  anachlorhydria 
of  cancer  and  that  of  chronic  gastritis  it  is  important  to  test  for  the  ferments. 
Total  disappearance  of  the  pepsin  and  rennin  point  rather  to  chronic  gas- 
tritis ;  the  disappearance  of  the  pepsin  alone  would  be  in  favour  of  cancer. 

Examination  of  the  blood  and  diminution  in  the  colour  index  in 
cancerous  patients  have  not  yet  given  definite  results. 

I  have  tried  to  show  in  this  detailed  and  critical  survey  the  extreme 
difficulty  at  times  experienced  in  making  a  diagnosis  of  cancer  of  the  stomach, 
and  I  cannot  dismiss  the  question  without  mentioning  dyspepsia  in  neuras- 
thenic patients.  We  have  all  seen  neurasthenic  patients  who  suffer  from  dys- 
pepsia or  gastralgia,  with  or  without  hyperchlorhydria  or  hypochlorhydria. 
They  lose  their  appetite,  vomit,  grow  thin,  and  are  firmly  convinced  that 
they  have  cancer  of  the  stomach.  Careful  examination  of  the  neurasthenic 
symptoms  will  eliminate  the  idea  of  cancer. 

The  diagnosis  of  the  situation  of  the  cancer  must  now  occupy  our 
attention.  Cancer  of  the  cardiac  orifice  is  generally  confounded  with  cancer 
of  the  oesophagus,  because  the  growth  is  rarely  limited  to  the  cardiac  orifice. 
The  food  is  arrested  at  the  constriction,  and  is  rejected  soon  after  ingestion. 
Exploration  with  the  bougie  shows  the  seat  and  extent  of  the  constriction. 
Cancers  of  the  cardiac  orifice  and  of  the  lesser  curvature  are  very  difficult  to 
palpate.  Cancer  of  the  pylorus  often  causes  stricture  and  secondary  dilata- 
tion of  the  stomach.  The  vomiting  comes  on  some  time  after  meals  ;  the 
loss  of  flesh  is  rapid,  and  the  cachexia  appears  early.  The  tumour,  which 
can  be  felt,  remains  fixed  in  the  same  region.  Cancers  of  the  curvatures 
and  surfaces  of  the  stomach  are  less  rapid  in  their  progress  than  those  of 
the  orifices,  because  they  do  not  affect  the  passage  of  food.  Vomiting  is 
not  so  common,  loss  of  flesh  occurs  late,  and  cachexia  is  slow  to  appear. 
Cancer  of  the  greater  curvature  is  remarkable  for  its  mobility,  and  alters  its 
position  according  as  the  stomach  is  full  or  empty.  If  the  stomach  is  much 
distended,  the  tumour  may  occupy  the  most  varied  positions  in  the  abdomen. 

Duration. — Cancer  of  the  stomach  has  an  average  duration  of  some 
twelve  to  eighteen  months,  but  it  may  last  even  longer  if  it  does  not 
involve  the  orifices,  and  allows  the  passage  of  food.  In  young  subjects — 
under  thirty  years  of  age — its  course  is  usually  rapid.  Death  is  the  ter- 
mination of  cancer,  and  is  due  to  cachexia,  repeated  hsematemesis,  or 
secondary  growths.  Perforation  of  the  stomach  and  peritonitis,  which  are 
relatively  frequent  in  ulcer,  are  exceptional  in  cancer. 

Treatment. — We  now  come  to  the  treatment.  The  early  dyspepsia  must 
be  treated  with  alkalis,  lime-water,  Vichy  water,  and  prepared  chalk.  Milk 
diet,  associated  with  easily  digested  food,  is  indicated  in  the  early  stages. 
Vanilla  and  coffee  ices,  or  ices  containing  2  ounces  of  meat- juice,  agree  well. 


DISEASES  OF  THE  STOMACH  715 

The  vomiting  and  pain  may  be  checked  by  small  doses  of  morphia  and  cocaine 
in  solution.  H  the  pain  does  not  }aeld,  it  must  be  quieted  with  injections 
of  morphia.  Haemorrhage  is  treated  with  astringents,  perchloride  of  iron, 
and  iced  drinks.  Careful  lavage  is  of  service  by  preventing  decomposition, 
and  favouring  the  tolerance  of  the  organ  for  food.  The  stomach  is  washed 
out  every  morning  with  luke-warm  water,  to  which  bicarbonate  of  soda  has 
been  added.  AVhen  the  fluids  in  the  stomach  undergo  decomposition,  a 
solution  of  choral  (5  to  10  parts  per  1,000)  may  be  employed.  If  the  stomach 
perform  its  functions  badly,  and  if  anorexia  or  a  tendency  to  vomiting  be 
present,  meat-powders,  mixed  with  milk  or  chocolate,  may  be  given.  This 
latter  operation  may  be  performed  by  means  of  a  tube,  shorter  than  the 
one  used  for  lavage,  because  there  is  no  need  for  it  to  pass  into  the 
stomach.  When  feeding  by  the  stomach  becomes  impossible,  either  from 
intolerance  or  from  constriction  of  the  cardiac  or  pyloric  orifice,  nutrient 
enemata  should  be  given.  One  glass  of  milk,  with  the  yolk  of  an  egg, 
2  spoonfuls  of  liquid  peptone,  5  drops  of  laudanum,  and  15  grains  of  bicar- 
bonate of  soda  (Dujardin-Beaumetz),  make  an  excellent  formula. 

The  surgical  treatment  of  cancer  of  the  stomach  gives  fairly  satisfactory 
results.  It  consists  in  performing  partial  or  entire  resection  of  the  organ. 
The  object  of  gastro-enterostomy  is  to  unite  a  portion  of  the  posterior 
surface  of  the  stomach  near  the  pylorus  to  the  first  part  of  the  jejunum. 
In  order  to  be  efficacious,  surgical  treatment  must  be  early. 

The  surgical  treatment  varies  according  to  the  case.  If  the  lesion  is 
not  very  extensive,  and  especially  if  it  occupies  the  pylorus,  and  has  not 
invaded  the  neighbouring  organs,  pylorectomy  should  be  performed.  The 
earlier  the  operation  is  done,  the  better  the  chance  of  success.  Statistics 
show  that  many  patients  have  enjoyed  excellent  health  for  several  years 
after  operation  :  Wolfler's  cases,  four,  five,  and  seven  years  ;  Lobker's 
cases,  five  and  seven  years  ;  Hahn's  cases,  four  and  seven  years.  These 
facts  are  encouraging,  and  prove  that  excellent  results  may  follow  operative 
measures  in  cancer  of  the  stomach. 

When  resection  is  not  possible,  we  must  be  content  with  gastro-enter- 
ostomy (Roux's  method).  The  jejunum  is  cut  through,  about  3  inches  from 
the  duodeno- jejunal  angle;  the  lower  end  is  joined  to  the  posterior  surface 
of  the  stomach  through  an  opening  in  the  transverse  mesocolon ;  and  the 
upper  end  of  the  cut  jejunum  is  then  joined  to  the  intestinal  loop  about 
2  inches  below  the  anastomosis  with  the  stomach.  By  this  means  the  food 
passes  from  the  stomach  into  the  jejunum,  and,  on  the  other  hand,  the 
bile  and  pancreatic  juice  pass  from  the  duodenum  into  the  jejunum.  There 
is  no  risk  of  a  vicious  circle.  The  peptic  ulcer  of  the  jejunum  which  some- 
times follows  in  gastro-entero.stomy  has  never  been  seen  in  gastro-enter- 
ostomy for  cancer  of  the  stomach. 


716  TEXT-BOOK  OF  MEDICINE 

XVI.  SYPHILIS  OF  THE  STOMACH. 
The  following  case  from  my  clinical  lectures*  is  typical : 

A  man  had  suffered  for  eighteen  months  with  the  classical  signs  of  gastric  ulcer. 
He  complained  of  pains  in  the  epigastrium  and  spine,  which  became  more  severe  after 
meals,  and  were  frequently  followed  by  vomiting  of  food.  He  was  thought  to  be  suffer- 
ing from  ulcus  simplex,  and  strict  milk  diet  was  prescribed.  Milk,  kephir,  ice,  and 
morphia  were  given,  while  cupping  and  the  actual  cautery  were  applied  to  the  epigas- 
trium. A  few  weeks  afterwards  the  patient,  as  he  did  not  improve,  left  the  hospital. 
The  pain,  however,  being  just  as  bad,  he  soon  sought  further  advice.  The  symptoms 
had  not  changed.  He  suffered  from  the  same  epigastric  and  spinal  pains,  gastric 
intolerance,  and  vomiting  of  food.  He  was  again  treated  for  ulcus  simplex  with  milk 
diet,  alkalis,  bicarbonate  of  soda,  counter  -  irritants,  and  frequent  cuppings  to  the 
epigastric  region  and  to  the  back.  After  treatment  extending  over  a  period  of  three 
months,  he  left  the  hospital  without  appreciable  improvement,  but  soon  came  back, 
because  the  gastric  pain  was  more  severe,  and  the  vomiting  of  food  was  frequent.  One 
night  he  had  a  profuse  hasmatemesis,  the  clots  being  so  large  that  he  pulled  them  out 
of  his  mouth  with  his  fingers. 

During  the  eight  months  that  he  was  in  hospital,  he  had  most  careful  treatment. 
Milk  diet  and  alkalis  were  again  tried,  but  as  this  regime  did  not  give  the  expected 
results,  a  diet  composed  partly  of  eggs  and  partly  of  meat-powder  was  prescribed. 
The  stomach  was  washed  out  every  day  for  three  months,  and  counter-irritation  was 
applied  in  various  forms,  including  dry-  and  wet-cuppings,  tincture  of  iodine,  five  blisters, 
and  many  appUcations  of  actual  cautery.  As  the  disease  was  so  stubborn,  the  question 
of  neurosis  was  raised,  although  the  patient  did  not  show  a  single  sign  of  hysteria. 
Douches,  medicated  baths,  and  electrical  treatment  were  also  prescribed,  but  all  the 
remedies  made  no  difference. 

He  left  the  hospital,  but  soon  came  back  under  another  physician  in  the  annex  of 
the  Hotel-Dieu.  He  still  showed  all  the  symptoms  of  ulcus  simplex,  and  a  second 
haematemesis,  more  profuse  than  the  first,  occurred.  He  wasted,  suffered  continually, 
and  got  no  sleep.  As  the  means  hitherto  employed  had  failed,  and  the  ulcer  was  so 
rebellious  to  treatment,  he  was  advised  to  submit  to  surgical  treatment. 

He  now  came  under  my  care.  I  found  him  squatting  on  his  bed,  stupefied  by  pain, 
his  eye  wan  and  his  expression  dull.  The  symptoms  left  no  doubt  as  to  the  diagnosis 
of  ulcus  simplex.  The  pain  was  clearly  marked  at  the  xiphoid  and  spinal  points.  He  said 
that  this  pain  stabbed  him  through  and  through,  and  deprived  him  of  rest.  It  was 
most  severe  after  meals,  and  came  on  even  after  drinking  a  Uttle  milk.  The  stomach 
was  so  intolerant  that  milk  and  food  were  rejected  half  an  hour  later.  I  could  find  no 
dilatation,  but  the  pit  of  the  stomach  was  very  tender  on  pressure,  and  the  patient 
obtained  sUght  relief  only  when  lying  on  his  right  side.  During  my  examination  I 
noticed  on  the  legs  some  scars  suggestive  of  syphihdes.  He  stated  that  he  had  had 
syphilis  three  years  previously.  He  was  at  that  time  in  the  St.  Louis  Hospital,  under 
Fournier,  for  syphilides  of  the  skin,  mucosae,  scrotum,  and  mouth,  and  ulcerated 
syphihdes  of  the  legs.  He  remained  only  a  fortnight  under  Fournier,  and  it  was  ten 
months  after  these  syphilitic  lesions  that  the  fii'st  symptoms  of  gastric  ulcer  appeared. 
It  was  therefore  reasonable  to  suppose  that  the  gastric  symptoms  were  of  a  syphihtic 
nature.  This  hypothesis,  already  put  forward  by  Kahn,  Avas  the  more  hkely  as 
the  milk  diet  and  other  measures  which  generally  improve  or  cure  ulcus  simplex,  had 
given  in  this  case  no  result  after  a  year  and  a  half. 

Before  prescribing  specific  treatment,  I  wished  to  satisfy  myself  as  to  the  condition 

*  "  Syphilis  de  I'Estomac  "  {Clinique  Medicate  de  V Hotel-Dieu,  1898,  4  ^  Lecon). 


DISEASES  OF  THE  STOMACH  717 

of  the  patient.  I  therefore  ordered  milk  diet,  but  no  medicine.  The  pains  in  the  stomach 
and  the  vomiting  continued  as  before,  and  the  milk  was  vomited  in  a  liquid  state  or 
in  clots.  I  then  ordered  a  daily  injection  of  biniodide  of  mercury.  The  symptoms 
persisted  for  five  days,  but  after  the  sixth  injection  the  pains  diminished  ;  after  about 
a  dozen  injections  the  pain  and  the  vomiting  disappeared.  The  patient  slept,  although 
his  insomnia  had  been  of  such  long  duration.  His  features  changed  from  day  to  day. 
To  prove  how  much  better  he  felt,  he  hit  his  stomach  and  turned  in  his  bed  without 
feeling  the  least  pain.  He  was  now  able  to  take  4  or  5  pints  of  milk  without  vomiting, 
and  his  health  was  much  better  than  it  had  been  for  the  past  eighteen  months. 

A  few  days  later  I  added  iodide  of  potassium  to  the  mercurial  injections.  The 
pain  in  the  stomach  and  the  vomiting  reappeared  no  more.  The  patient  could  not 
satisfy  his  hunger,  and  besides  his  usual  four  meals,  he  asked  for  extra  rations.  He 
put  on  flesh  so  quickly  that  he  gained  10  pounds  in  five  weeks.  His  recovery  was 
complete. 

This  therapeutic  success  is  attributable,  in  my  opinion,  to  the  specific  treatment 
adopted.  For  a  year  and  a  half  milk  and  kephir  had  been  administered  without  result ; 
alkalis  in  large  doses  had  been  given  in  vain,  and  daily  lavage  of  the  stomach  for  three 
months  at  a  stretch  had  done  no  good.  Counter-irritants  had  been  employed,  douches 
had  been  used,  and  a  prolonged  course  of  baths  had  been  tried,  as  well  as  electrical 
treatment,  without  changing  the  condition  of  the  patient.  The  violent  pain,  insomnia, 
vomiting,  hsematemesis,  and  the  loss  of  flesh  resisted  every  measure  employed  ;  surgical 
intervention  seemed  to  be  the  only  hope,  and  was  all  but  put  into  execution.  Mercurial 
injections,  however,  changed  the  situation  completely,  and  brought  about  what  a  year 
and  a  half's  treatment  for  the  so-called  ulcus  simplex  was  unable  to  accomplish.  Under 
the  influence  of  the  specific  treatment  the  improvement  was  rapid,  and  the  person  most 
astonished  was  the  patient.  In  such  a  case  it  is  probable  that  the  process  of  repair  in 
the  lesion  is  similar  to  that  which  we  can  observe  in  ulcerating  gummata  which  are 
accessible  to  view. 

I  had  the  opportunity  of  observing  a  similar  case  at  the  Hotel-Dieu  :* 

A  man  was  seized  one  day  with  profuse  haematemesis  without  any  apparent  reason. 
Ho  went  to  bed  and  took  ergotin,  but  on  the  following  day  he  had  several  attacks 
of  hsematemesis,  one  after  the  other.  He  reckoned  the  total  loss  of  blood  to  be  about 
3  pints.  He  then  came  into  the  Hotel-Dieu.  He  had  had  syphihs ;  the  testes  had 
been  involved,  and  he  had  at  the  time  suppurating  gummata  on  his  neck.  All  these 
complications  gave  way  to  mercurial  treatment.  They  returned  and  ceased  anew  with 
such  regularity  that  the  same  origin  was  evident  in  each  one. 

Furthermore,  syphilis  of  the  stomach  is  not  so  rare  as  was  formerly 
believed,  as  the  following  cases  prove  : 

Anatomical  Cases.  —  Gailliard  borrows  the  following  case  from 
Murchison  : 

A  man  who  had  contracted  syphilis  was  seized  five  years  later  with  attacks  of  nausea, 
profuse  haematemesis,  and  melaena.  Ho  died,  and  the  liver  was  cirrhotic  and  nodular. 
An  ulcer  was  found  in  the  stomach,  and  in  the  centre  of  the  ulcer  an  artery  had  been 
opened. 

Cornil  has  recorded  the  following  case  : 

A  woman  who  had  pain  in  the  stomach  and  wa.s  unable  to  digest  food,  died  from 
pulmonary  complications.    Post  mortem,  gummata  were  found  in  the  stomach  and  liver. 


Journal  de  Medecine  et  de  Chirurgie  Pratiques,  December  10,  1902. 


718  TEXT-BOOK  OF  MEDICINE 

Along  the  lesser  curvature  and  in  the  neighbourhood  of  the  pylorus  several  dark  tumours 
stood  out  in  relief  under  the  mucous  membrane,  which  was  thinned  and  adlierent. 
The  gummata  were  situated  in  the  glandular  layer  of  the  mucous  membrane. 

In  Klebs's  case  it  was  a  question  of  syphilitic  ulceration  of  the  stomach 
in  a  man  who  had  syphilitic  ulcers  of  the  skin  and  throat,  with  syphilomata 
of  the  tongue,  liver,  and  intestine.  A  rounded  ulceration,  as  large  as  a 
shilling,  was  seen  on  the  mucosa,  and  the  other  layers  of  the  wall  of  the 
stomach  were  thickened.  The  base  and  edges  of  the  ulcer  had  a  gummatous 
structure. 

Weichselbaum's  case  : 

A  man,  aged  twenty-five,  died  of  facial  erysipelas.  He  had  syphihtic  lesions 
of  the  skull,  pharynx,  nose,  larynx,  and  liver.  The  stomach  showed  a  radiating 
white  cicatrix  and  two  ulcers,  the  base  of  which  wa,?  formed  by  a  cicatricial  tissue, 
evidently  of  gummatous  origin. 

Birch- Hirschf eld  has  reported  three  cases  of  syphilis  of  the  stomach  : 

(1)  A  new-born  child  h!i.d  cutaneous  syphilides  and  gummatous  nodules  in  the  Uver 
and  lungs,  as  well  as  a  gummatous  patch  at  the  pylorus.  (2)  A  woman,  forty-five 
years  of  age,  died,  after  suffering  for  four  years  from  gastric  trouble.  The  post-mortem 
examination  revealed  on  the  left  lobe  of  the  liver  a  gumma  of  the  size  of  an  apple,  and 
on  the  right  anterior  wall  of  the  stomach,  in  the  pyloric  region,  a  slightly  ulcerated 
gummatous  patch.  (3)  In  a  man  gummatous  patches  were  found  in  the  intestines, 
the  oesophagus,  and  the  stomach. 

Wagner  has  reported  the  case  of  a  man  of  fifty-eight,  in  whom  at  the 
autopsy  syphilitic  lesions  of  the  larynx  and  of  the  stomach  were  found. 

Chiari  systematically  examined  the  stomach  in  243  cases  of  syphilis,. 
In  145  cases  the  disease  was  hereditary,  and  in  98  cases  it  was  acquired. 
He  often  noticed  such  lesions  of  the  stomach  as  ecchymoses,  haemorrhagic 
erosions,  cicatrices  of  ulcers,  and  ulcers  in  active  progress.  An  ulcer  was 
found  in  a  man  of  forty-six  years  of  age  who  had  had  syphilis,  and  died  of 
an  attack  of  hsematemesis.     The  coronary  artery  was  eroded  by  an  ulcer. 

Frankel  has  reported  a  very  interesting  case  : 

A  man  who  had  had  syphilis  was  attacked  by  a  gummatous  ulceration,  which  per- 
forated the  stomach  and  caused  fatal  peritonitis.  This  case  proves  that  syphilitic 
ulceration  can  produce  peritonitis.  At  the  post-mortem  examination  gummata  were 
found  in  the  stomach  and  intestines. 

Clinical  Cases. — Two  clear  cases  of  syphilis  of  the  stomach  are  found  in 
Andral's  "  Clinical  Medicine  "  : 

Case  1. — A  woman  was  taken  ill  with  acute  gastric  symptoms  ;  the  pain  and  vomiting 
were  incessant,  and,  in  spite  of  all  treatment,  the  disease  made  rapid  progress.  Andral 
almost  gave  up  hope,  but  one  day  the  patient  complained  of  diiiiculty  in  swallowing. 
He  discovered  on  the  jiosterior  wall  of  the  pharynx  an  ulcer  which  appeared  to  be 
syphilitic.  It  was,  therefore,  a  question  whether  the  affection  of  the  stomach  which 
was  killing  the  patient  was  not  due  to  syphilis.  Andral  ordered  mercury,  and  im- 
provement was  soon  manifest.     He  then  prescribed  mercurial  inunctions.     "  After  the 


DISEASES  OF  THE  STOMACH  719 

twelfth  rubbing  the  condition  of  the  patient  was  no  longer  recognizable."  Recovery 
was  rapidly  effected.  It  is  evident  that  this  was  a  case  of  syphiUtic  lesions  of  the 
stomach. 

Case  2. — A  patient  had  had  the  following  syjjhilitic  troubles  :  j^eriosteal  nodes, 
osteoskopic  pains,  and  cutaneous  pustules.  He  was  subsequently  taken  ill  with  symp- 
toms of  phthisis  and  gastritis,  frequent  cough,  hoarseness,  pain  in  the  pharynx,  short 
and  hurried  breathing,  anorexia,  pain  in  the  epigastrium,  and  frequent  vomiting. 
SyphiUtic  periostitis  of  the  tibia  supervened,  and  it  was  a  question  whether  the  other 
complications  were  npt  also  syphiUtic.  Mercurial  inunction  was  i^rescribed,  and 
recovery  followed. 

In  this  case,  too,  we  must  admit  the  syphilitic  nature  of  the  lesions  in  the  stomach, 
for  the  gastritis  and  vomiting  yielded  to  mercurial  treatment. 

Fournier  communicated  to  the  Academie  the  following  cases,  of  which 
I  give  a  resume  : 

Some  thirty  years  ago  I  attended  a  beautiful  girl  suffering  from  syphilitic  rupia 
of  the  back.  She  recovered  rapidly.  Ten  years  afterwards  she  sent  for  me,  and  I 
found  her  moribund.  By  her  side  was  a  basin  full  of  blood.  For  the  past  three  or 
four  months  she  liad  been  vomiting  blood,  in  spite  of  all  the  usual  remedies.  I  pre- 
scribed iodide  of  potassium.  A  dramatic  change  took  place  and  recovery  was  rapid. 
Six  or  seven  years  after  this  a  veritable  spectre  came  into  my  consulting-room.  It 
was  this  woman.  She  had  just  come  from  Italy,  where  she  had  been  seized  Avith  fresli 
attacks  of  hajmatemesis.  She  asked  for  iodide  of  potassium,  which  the  doctors  decUned 
to  administer.     I  prescribed  it,  and  witnessed  a  resm-rection. 

Fournier's  second  case  is  similai  to  the  first : 

A  Russian  suffering  from  severe  syphiUs  was  taken  ill  with  vomiting  of  blood, 
which  was  cured  by  specific  treatment.  He  left  off  treatment,  and  then  suffered  from 
rupia  and  haematomesis,  which  yielded  to  iodide  of  potassium. 

The  following  is  a  resume  of  Dubuc's  case,  in  which  syphilis  of  the  stomach 
simulated  cancer  : 

A  man  contracted  a  hard  chancre,  followed  by  roseola  and  tubercular  syphilides. 
Ten  years  later  Dubuc  noticed  in  the  epigastric  region  an  indurated  projection  of  the 
size  of  a  pigeon's  egg.  There  was  not  the  slightest  doubt  tliat  the  tumour  was  in  the 
wall  of  the  stomach.  He  grew  thinner,  digestion  was  retarded,  and  there  was  dull 
pain  in  the  affected  region.  It  was  difficult  not  to  think  of  the  possibility  of  cancer, 
in  con.sequencc,  however,  of  the  antecedent  syphiUs,  treatment  with  mercury  and 
iodide  was  prescribed  and  brought  about  recovery. 

General  Considerations. — Anatomically,  the  syphilitic  lesions  of  the 
.stomach  are  :  erosions,  ccchymoses,  gummata,  gummatous  infiltration  and 
ulceration,  and  cicatrices.  Clinically,  these  lesions  show  themselves  by 
symptoms  which,  according  to  their  nature  and  grouping,  resemble  dys- 
pepsia, gastralgia,  ulcer,  and  cancer  of  the  stomach.  One  patient  has 
dyspepsia,  and  is  sent  to  Vichy,  Pouges,  or  Capvern,  when  the  proper 
treatment  is  injection  of  biniodide  of  mercury. 

Another  patient,  suffering  from  less  of  ajipc^tite,  retching,  vomiting  of 
mucus,  and  gastric  intolerance,  is  wrongly  looked  upon  as  alcoholic,  in 


720  TEXT-BOOK  OF  MEDICINE 

spite  of  every  assurance  that  he  has  always  been  temperate.  Sometimes, 
as  in  one  of  my  cases,  there  is  a  group  of  symptoms  which  so  clearly 
counterfeits  ulcus  simplex  as  to  cause  mistakes.  Sharp  pains  in  the  stomach, 
which  is  worse  during  the  process  of  digestion,  localization  of  pain  to  the 
xiphoid  and  spinal  points,  intolerance  of  the  stomach,  vomiting  of  food, 
and  hsematemesis  are  present.  Moreover,  hsematemesis  is  not  uncommon 
in  syphilis  of  the  stomach.  My  patient  had  two  severe  attacks  of  hsema- 
temesis,  and  Fournier's  patients  had  similar  attacks,  which  yielded  to  specific 
treatment. 

In  some  cases  the  lesion  assumes  the  mask  of  exulceratio  simplex. 
The  patient  is  seized  with  fulminating  hsematemesis,  and  dies  without  having 
shown  gastric  symptoms.  At  the  post-mortem  examination  an  arteriole 
is  found  open  in  the  exulceration  (Murchison). 

Finally,  the  patient  suffers  from  gastric  troubles,  with  loss  of  flesh,  and 
has  also  an  epigastric  tumour,  which  is  thought  to  be  cancerous.  As  the 
patient  is  syphilitic,  specific  treatment  is  administered,  and  a  cure  is  effected 
(Dubuc). 

This  polymorphism  of  syphilis  of  the  stomach  proves  that  there  are  no 
signs  and  symptoms  which  allow  us  to  make  a  positive  diagnosis.  We 
must,  however,  remember  that,  in  a  patient  suffering  from  the  gastric  troubles 
which  we  have  just  discussed,  syphilis  must  always  be  looked  for.  When 
it  is  evident  that  the  patient  has  had  syphilis,  and  even  more  so  when  it  is 
possible  to  reconstruct  the  various  stages  of  syphilis  which  has  caused  trouble 
for  several  years,  we  must  at  once  prescribe  specific  treatment.  It  is  the 
more  necessary  to  arrive  at  a  diagnosis  because  we  must  not  send  to  the 
surgeon  a  patient  suffering  from  stomach  trouble  which  is  rebellious  to  all 
ordinary  medical  means,  but  which  is  at  once  cured  by  specific  treatment. 

This  treatment  must  consist  in  the  combination  of  mercury  and  iodine, 
and  I  would  add  the  former  is  more  important  than  the  latter.  I  give  the 
preference  to  injections  of  an  aqueous  solution  ofj  biniodide  of  mercury, 
in  doses  of  |  grain  per  diem. 

XVII.  DILATATION  OF  THE  STOMACH. 

Pathogenesis. — Dilatation  is  a  morbid  condition,  met  with  in  many 
affections  of  the  stomach.  It  is  sometimes  mechanical,  and  results  from  a 
constriction  of  the  pyloric  orifice  (cancer,  cicatrices  following  on  simple 
ulcer,  spasm  of  the  pylorus),  but  in  this  case  it  is  rather  a  question  of  dis- 
tension than  dilatation.  Sometimes  it  follows  atony  of  the  muscular  fibres 
(chronic  catarrh,  neurosis,  neurasthenia,  tuberculosis,  general  exhaustion, 
and  typhoid  fever). 

Dilatation  is  frequent  in  large  eaters  and  heavy  drinkers.     According  to 


DISEASES  OF  THE  STOMACH  721 

Bouchard,  dilatation  of  the  stomach  is  not  simply  a  symptom  of  various 
pathological  conditions,  but  a  morbid  entity,  the  stomach  allowing  itself 
to  be  distended  because  its  resistance  is  unequal  to  the  obstacle  which  it  has 
to  surmount.  Although  dyspepsia  and  dilatation  of  the  stomach  are  always 
associated,  the  dilatation  is  the  cause  more  often  than  the  result  of  the 
dyspepsia. 

Pathological  Anatomy. — The  dilated  stomach  does  not  always  preserve 
its  normal  form  (stomach  en  hissac)  ;  its  capacity  is  such  that  it  may  contain 
as  much  as  10,  20,  or  40  pints  of  fluid.  The  increase  in  size  always  takes 
place  at  the  expense  of  the  greater  curvature,  which  is  depressed. 

The  lesions  of  the  muscular  layer  are  very  variable,  and  there  may  be 
hypertrophy  or  atrophy.  Amyloid  degeneration  has  been  noticed.  The 
mucous  membrane  generally  shows  chronic  inflammatory  changes.  Amongst 
the  elements  contained  in  the  stomach  there  is  frequently  a  cryptogram, 
known  under  the  name  of  sarcina. 

Symptoms. — The  appetite  may  be  diminished  or  increased,  and  the 
thirst  is  intense.  Constipation  is  the  rule,  while  digestion  is  delayed,  painful, 
and  frequently  accompanied  by  vomiting. 

The  vomited  matter  may  amount  to  several  pints  daily.  This  enormous 
loss  of  fluid  naturally  diminishes  the  amount  of  urine  (Kussmaul).  The 
vomited  matter  is  generally  mucous,  coloured,  of  foetid  odour  and  bitter 
taste.  The  food  in  the  vomit  has  been  ingested,  as  a  rule,  two  or  three 
days  previously.  In  a  few  exceptional  cases  true  attacks  of  haematemesis 
have  been  noticed.  Constipation  is  followed  by  attacks  of  profuse  diarrhoea. 
The  patient  rarely  complains  of  sharp  pains. 

The  dilated  stomach  often  forms  a  tumour  in  the  epigastric  region. 
Percussion,  which  should  be  carried  out  when  the  stomach  is  empty,  reveals 
extensive  hyperresonance,  while  gentle  tapping  in  the  epiga,stric  region 
yields  a  splashing  sound,  which  is  more  marked  if  the  patient  swallows  a 
glass  of  water.  The  succussion  splash,  which  is  produced  on  shaking  the 
patient,  is  similar  in  nature.  Nodules  are  sometimes  seen  on  the  second 
joints  of  the  fingers  ;  they  are  evidence  of  the  rheumatic  diathesis,  so  common 
in  persons  suffering  from  dilatation  of  the  stomach  (Bouchard).  When 
the  dilatation  is  of  recent  date  and  of  moderate  extent,  we  do  not  find  the 
symptoms  just  enumerated.  As  the  disease  progresses,  the  dyspepsia, 
vomiting,  and  malnutrition  cause  loss  of  flesh  and  cachexia,  so  that  it  is 
often  difficult  to  distinguish  between  simple  dilatation  and  cancer  of  the 
stomach. 

\n  some  individuals  we  see  a  series  of  complications,  amongst  which  I 
may  mention  hypochondria,  vertigo,  palpitation,  cardiac  intermittence,  and 
angina  pcftoris.  I  would  also  mention  cramp,  contraction  of  the  flexor 
muscles  of  the  fingers,  and  epileptiform  fits,  complications  comparable  to 

46 


722  TEXT-BOOK  OF  MEDICINE 

those  of  uraemia,  and  resulting,  according  to  Bouchard,  from  the  absorption 
of  toxic  substances  produced  by  abnormal  fermentation  in  the  dilated 
stomach.  Paralyses,  either  alone  or  associated  with  convulsions,  have  also 
been  noted. 

According  to  Bouchard,  primary  dilatation  of  the  stomach,  with  food 
stasis  and  consequent  fermentation,  is  of  considerable  importance.  In 
such  a  case  it  is  not  simply  a  question  of  an  individual  having  a  very  dilated 
stomach,  as  in  most  cases  the  dilatation  is  only  very  slightly  pronounced. 
Fermentation  in  the  dilated  stomach  (flatulence)  is  usually  due  to  diminution 
of  the  hydrochloric  acid,  which  under  normal  conditions  has  an  antiseptic 
action.  In  these  patients  gastric  trouble,  accompanied  with  fever,  is 
common.  In  other  words,  the  description  and  treatment  of  dyspepsia  in 
general,  and  gastritis  in  particular,  blend  with  dilatation  of  the  stomach. 
In  other  cases  there  is  gastric  insufficiency  (Ewald). 

As  regards  treatment,  excellent  results  are  obtained  from  lavage.  The 
remedies  advised  for  dyspepsia  are  suitable  in  dilatation  of  the  stomach. 
The  reader  is  therefore  requested  to  refer  to  the  chapter  on  Dyspepsia. 
Milk  diet  or  dry  diet  should  be  prescribed,  according  to  the  particular  case. 


XVIII.  GASTRORRHAGIA— HiEMATEMESIS. 

Note. — As  I  am  anxious  to  avoid  repetition,  I  would  ask  the  reader  to  refer  to  the 
sections  on  acute  ulceration  and  cancer  of  the  stomach,  where  gastrorrhagia  and  hjema- 
temesis  are  discussed  in  detail. 

Definition. — The  words  haematemesis  and  gastrorrhagia  must  not  be 
confounded.  Gastrorrhagia  is  bleeding  from  the  surface  of  the  mucous 
membrane,  or  from  the  wall  of  the  stomach,  the  blood  being  dis- 
charged subsequently  into  its  cavity,  whilst  hsematemesis  simply  denotes 
the  vomiting  of  blood  which  comes  from  the  stomach,  or  has  been  discharged 
into  the  stomach  after  coming  from  a  neighbouring  region.  It  is  clear, 
therefore,  that  haematemesis  and  gastrorrhagia  are  not  always  associated. 
Either  may  occur  alone,  as  in  the  following  examples :  An  individual 
vomits  blood,  which  has  entered  the  stomach  in  consequence  of  epistaxis 
or  profuse  haemoptysis  :  in  this  case  there  is  haematemesis  without  gastror- 
rhagia. Another  individual,  suffering  from  cancer  or  ulcer  of  the  stomach, 
has  an  attack  of  haemorrhage  from  the  stomach,  but  the  bleeding  is  not 
followed  by  vomiting,  and  the  blood  passes  from  the  stomach  into  the 
intestine,  giving  rise  to  melaena :  this  is  an  example  of  gastrorrhagia  without 
haematemesis. 

etiology. — Gastrorrhagia  arises  from  many  causes — to  wit,  lesions  of 
the  stomach,  traumatism,  contusion,  chronic  gastritis,  cancer  of  the 
stomach,  and  especially  simple  ulcer  and  acute  ulcerations,  pneumococcal 


DISEASES  OF  THE  STOMACH  723 

or  appendicular  erosions,  and  exulceratio  simplex.  In  three  of  the  preceding 
sections  I  have  discussed  the  bleeding  which  accompanies  hgemorrhagic 
necrosis  of  the  mucosa,  destruction  of  the  mucous  membrane  and  of  the 
muscularis  mucosse,  erosion  of  the  arterioles  under  the  muscularis,  etc. 
Further  reference  is,  therefore,  superfluous. 

Lesions  obstructing  the  portal  circulation  cause  stasis,  with  or  without 
gastric  erosions,  sometimes  followed  by  haemorrhage.  Atrophic  cirrhosis 
of  the  liver  causes  varices  of  the  stomach  (Letulle),  and  especially  of  the 
oesophagus,  which  may  rupture  and  lead  to  profuse  hsematemesis.  This 
point  will  be  discussed  under  Laennec's  Cirrhosis. 

In  the  three  cases  quoted  by  Gailliard  fulminant  hgematemesis  was  caused 
by  the  rupture  of  miliary  aneurysms.  Active  congestion  of  the  stomach 
accounts  for  the  so-called  nervous  (hysteria)  and  supplementary  (suppres- 
sion of  the  menses,  haemorrhoids)  gastrorrhagia.  Attacks  of  gastrorrhagia 
which  supervene  in  black  variola,  typhus,  icterus  gravis,  yellow  fever,  etc., 
are  due  to  changes  in  the  blood  and  capillaries. 

Symptoms. — Gastrorrhagia  is  not  always  preceded  by  prodromata. 
Rigors,  pallor,  fainting-fits,  which  accompany  profuse  haemorrhage  from  the 
stomach,  are  not  prodromata,  but  symptoms  associated  with  gastrorrhagia. 
They  are  the  consequence  thereof,  and  sometimes,  when  haematemesis  is 
absent,  they  are  the  sole  index  of  haemorrhage  from  the  stomach.  The  cases 
of  gastrorrhagia  without  haematemesis  are  worthy  of  recognition,  and 
often  pass  unnoticed,  though  they  are  more  frequent  than  is  generally 
believed.  It  may  be  the  first  symptom  of  ulcer  or  cancer  of  the  stomach. 
"  People  in  good  health,"  says  Trousseau,  "  are  suddenly  taken  ill  with  a 
vague  feeling  of  malaise  ;  they  grow  pale,  and  suffer  from  syncope.  A  few 
hours  later,  on  going  to  stool,  they  pass  faeces  as  black  as  pitch,  and  for  some 
time  they  remain  weak,  and  suffer  from  loss  of  appetite,  with  pallor  of  the 
skin,  and  then  health  returns.  These  troubles  may  recur  at  longer  or 
shorter  intervals,  and  are  often  mistaken,  not  only  by  the  patient,  but  also 
by  the  physician." 

In  this  first  class  of  cases,  gastrorrhagia,  whether  accompanied  or  not  by 
pallor,  fainting-fits,  or  syncope,  is  not  followed  by  haematemesis.  These 
cases  are  fairly  frequent.  Although  many  people  with  cancer  never  vomit 
during  the  whole  course  of  the  disease,  yet  if  their  stools  are  carefully 
examined,  pitchy  faeces  will  be  found  (melaena),  indicative  of  gastric 
heemorrhage. 

Gastrorrhagia  is  generally  followed  by  haematemesis.  The  vomiting  of 
blood  shows  itself  in  different  forms. 

The  quantity  of  blood  vomited  may  be  large  or  small.  Slight  haema- 
temesis may  pass  unnoticed.  Vomiting  of  food  is  frequent  in  ulcer  and 
cancer  of  the  stomach.     On  careful  examination  of  the  vomit,  collected  in 

46—2 


724  TEXT-BOOK  OF  MEDICINE 

a  basin,  a  blackish  dust,  like  cojffee-grounds,  is  seen  on  the  surface  of  the 
liquid  or  on  the  sides  of  the  vessel.  This  dust  is  due  to  slight  hsematemesis, 
and  the  microscope  will  confirm  the  diagnosis. 

In  severe  hsematemesis  the  blood  is  rarely  red  ;  most  often  the  vomited 
blood  is  blackish,  like  soot  dissolved  in  water.  Blackish  clots  of  the  size 
of  a  nut,  a  small  pear,  or  even  larger,  are  mixed  with  the  fluid.  Under 
Acute  Ulceration  of  the  Stomach  I  have  mentioned  several  cases  in  which 
the  vomit  contained  some  3  pints  of  blood,  either  liquid  or  in  clots.  Some- 
times the  hsematemesis  is  fulminant,  and  due  to  the  opening  of  an  arteriole, 
which  causes  death  from  hsemorrhage.  Every  intermediate  degree  is  seen 
between  the  slight  hsematemesis,  in  which  a  blackish  dust  floats  in  the 
mucous  or  viscid  fluid,  and  the  fulminant  hsematemesis. 

Diagnosis. — The  diagnosis  of  gastrorrhagia  rests  upon  the  existence  of 
hsematemesis  and  melsena,  but  care  must  be  exercised  to  make  sure  that  the 
blood  really  comes  from  the  stomach,  as  it  is  well  known  that  the  blood  in 
profuse  epistaxis  may  pass  into  the  stomach,  and  be  got  rid  of  later  in  the 
vomit  or  the  stools. 

We  must  next  diagnose  the  cause.  Is  the  gastrorrhagia  due  to  a  lesion 
of  the  stomach,  such  as  acute  ulcerations,  ulcer,  or  cancer  ?  and  even  if 
the  subject  is  in  good  health,  is  it  not  an  early  warning  of  cancer  ?  Is  it 
the  result  of  a  lesion  in  the  liver  (atrophic  cirrhosis),  or  is  it  caused  by 
gastric  congestion  (hysteria,  supplementary  hsemorrhage)  ?  A  reply  can 
only  be  given  to  these  various  questions  by  carefully  studying  the  past 
history  of  the  patient  and  the  symptoms  preceding  the  gastrorrhagia.  The 
diagnostic  value  of  hsematemesis  has  been  discussed  at  length  in  the  pre- 
ceding sections,  and  especially  under  Exulceratio  Simplex. 

Treatment. — On  the  question  of  treatment  I  would  refer  the  reader 
to  the  section  on  Exulceratio  Simplex.  Every  patient  suffering  from 
gastrorrhagia  must  be  put  on  starvation  diet,  and  given  large  injections  of 
artificial  serum.  Rectal  feeding  is  necessary  (nutrient  enemata,  peptones, 
lactose,  eggs,  etc.). 

XIX.  VISCERAL  PTOSES. 

The  abdominal  viscera  may  undergo  displacement  from  stretching  of 
their  suspensory  ligaments.  The  interesting  study  of  visceral  ptoses  was 
first  undertaken  by  F.  Glenard.  The  heart  even  is  not  exempt  from  ptosis 
(Rummo).  As  I  shall  devote  a  special  section  to  Floating  Kidney,  I  shall 
now  mention  only  the  ptoses  of  the  stomach,  intestines,  liver,  and  spleen. 

Gastroptosis  is  downward  displacement  of  the  stomach.  It  shows  itself 
by  abnormal  prominences  in  front  of  the  vertebral  column  (prominence  of 
the  pancreas,  of  the  superior  fold  of  the  stomach,  and  of  the  stenosed  trans- 


DISEASES  OF  THE  STOMACH  725 

verse  colon),  and  causes  gastric  succussion  and  downward  displacement  of 
the  lesser  curvature  of  the  stomach,  which  is  well  marked  after  the  in- 
sufflation of  the  organ.  Gastroptosis  must  not  be  confounded  with  dilata- 
tion of  the  stomach,  with  which  it  has  many  symptoms  (F.  Glenard)  in 
common. 

Enteroptosis  is  prolapse  of  the  intestine.  It  is  characterized  by  relaxa- 
tion of  the  abdominal  walls  and  flattening  of  the  epigastric  region,  where 
the  pulsation  of  the  aorta  may  be  seen  and  felt.  The  patient  experiences  a 
feeling  of  relief  when  the  abdominal  wall  is  lifted  upwards  and  backwards 
by  a  person  standing  behind  him. 

Hepatoptosis  is  downward  displacement  of  the  liver,  which  is  felt 
below  the  false  ribs,  while  the  upper  limit  of  the  hepatic  dullness  is  lowered. 

Splenoptosis  is  do\vnward  displacement  of  the  spleen.  It  includes  the 
classical  mobile  spleen,  which  is  always  enlarged,  as  well  as  true  spleno- 
ptosis, which  is  always  accompanied  by  hepatoptosis,  and  sometimes  by 
nephroptosis. 

Visceral  ptoses  are  rarely  isolated ;  as  a  rule,  several  organs  are  affected. 
The  functional  signs,  which  vary  slightly,  according  to  the  organ  affected, 
are  chiefly  of  the  neuropathic  kind — asthenia,  dyspepsia,  twitching  and 
sensations  of  weight  and  emptiness,  to  which  vertigo,  insomnia,  headache, 
and  nervous  instability  are  added.  The  aetiology  of  visceral  ptoses  depends, 
according  to  Glenard,  on  hepatisiil,  or  the  hepatic  diathesis,  which  pro- 
duces more  or  less  marked  functional  weakness.  Support  of  the  organs  by 
special  belts  forms  the  basis  of  treatment,  though  surgical  intervention  is 
necessary  in  obstinate  cases.  In  hepatoptosis  it  has  given  splendid  results 
(rUenard,  Marchant). 


CHAPTER  V 
DISEASES  OF  THE  INTESTINE 

I.  ACUTE  ENTERITIS 

Definition. — Enteritis  is  inflammation  of  the  mucous  membrane  of  the 
intestine.  When  the  stomach  takes  part  in  the  inflammation,  there  is 
gastro-enteritis.  The  word  "  enteritis "  refers  to  inflammation  of  the 
small  intestine.  If  the  large  intestine  is  also  inflamed,  there  is  entero- 
colitis. Inflammation  of  a  portion  of  the  intestine  is  called,  according 
to  circumstances,  duodenitis  (duodenum),  typhlitis  (caecum),  or  rectitis 
(rectum). 

Before  describing  enteritis,  it  will  be  useful  to  see  what  we  mean  by 
the  term  employed.  It  is  essential  not  to  confound  enteritis  with  one  of 
its  usual  symptoms — diarrhoea — since  these  different  morbid  states  lead 
to  different  therapeutic  indications.  And  yet  confusion  is  frequent.  We 
are  too  prone  to  speak  of  acute  or  chronic  enteritis  -^hen  the  case  is  one  of 
simple  non-inflammatory  diarrhoea.  Diarrhoea  is  often  associated  with 
intestinal  infection,  and  from  slight  catarrh  to  grave  enteritis  it  constitutes 
an  important  symptom.  In  other  cases,  however,  it  has  nothing  to  do 
with  enteritis,  being  of  different  origin.  To  this  latter  category  belong  : 
(1)  sudoral  diarrhoea,  which  is  caused  by  a  disturbance  of  the  functions 
of  the  skin  (sudden  suppression  of  perspiration)  ;  (2)  nervous  diarrhoea, 
which  arises  from  mental  emotions,  and  constitutes  one  of  the  disorders 
of  secretion  in  tabes  dorsalis  and  exophthalmic  goitre ;  (3)  diarrhoea 
caused  by  irritation,  consequent  on  abnormal  excitement  of  the  glandular 
adnexa  (liver,  pancreas),  and  on  the  ingestion  of  certain  foods  and  drinks. 
These  are  all  simple  secretory  troubles,  and  must  be  distinguished  from 
acute  enteritis. 

etiology. — Acute  enteritis  is  a  disease  of  all  ages,  and  in  young  children 
has  a  special  importance,  which  I  shall  discuss  in  the  next  section.  It  is 
more  frequent  in  warm  weather,  and  is  often  brought  on  by  a  chiU.  Chill 
is  well  known  as  an  exciting  cause  producing  enteritis  in  some  persons 
and  bronchitis  in  others.  If  the  primary  cause  of  enteritis  is  carefully 
sought  for,  it  will  be  seen  that  the  disease  may  be  of  infectious  or  toxic 

726 


DISEASES  OF  THE  INTESTINE  727 

origin.  There  is  no  need  for  me  to  speak  here  of  certain  specific  microbes 
(typhoid  fever,  tuberculosis,  cholera),  which  provoke  specific  catarrhs.  I 
allude  to  those  microbes  which  usually  inhabit  the  intestine,  and  become 
pathogenic  in  certain  conditions :  such  are  the  Coli  bacillus,  the  Bacterium 
aceti,  amoebge,  etc.  Other  microbes  ingested  with  the  food  pass  from  the 
stomach  into  the  intestine,  but  in  order  to  do  this  the  putrefying  food  must 
find  an  insufficient  antiseptic  in  the  hydrochloric  acid.  The  toxic  sub- 
stances capable  of  causing  acute  enteritis  are  in  some  cases  elaborated  by 
microbes,  in  others  taken  into  the  stomach,  or,  lastly,  are  manufactured 
by  the  patient,  who  is  already  ill  (uric  acid  in  gout,  carbonate  of  ammonia 
in  uraemia,  changes  in  the  bile). 

Certain  individuals  are  predisposed  to  enteritis,  and  the  influence  of  the 
season  produces  epidemic  enteritis. 

Symptoms. — Enteritis  is  accompanied  by  intestinal  fermentation, 
which  causes  the  absorption  of  toxic  products,  with  the  phenomena  of  auto- 
infection,  so  carefully  described  by  Bouchard. 

Slight  enteritis  is  not  febrile,  but  the  same  cannot  be  said  of  severe 
enteritis.  Colic  and  diarrhoea  are  the  first  symptoms,  and  the  pain  is 
especially  severe  at  the  umbilicus,  whence  it  radiates.  Colic  sometimes 
occurs  in  fits,  which  may  be  very  painful,  accompanied  by  borborygmi, 
and  followed  by  loose  stools.  The  evacuations,  which  are  more  or  less 
fluid,  are  formed  at  first  of  the  contents  of  the  intestine  ;  later  they 
become  liquid,  yellowish,  and  composed  of  serous  fluid,  mucus,  and 
bile.  The  appetite  is  diminished  or  absent ;  thirst  is  great.  The  tongue  is 
coated,  the  belly  distended  and  painful.  In  slight  cases  these  symptoms 
improve  rapidly,  and  the  disease  ends  in  a  few  days  ;  in  severe  cases  the 
evacuations  are  frequent  and  copious,  the  enteritis  is  choleriform,  the  loss 
of  strength  is  rapid,  and  the  prognosis  in  children  and  old  people  is  exceed- 
ingly grave. 

In  gastro-enteritis,  gastric  pains,  vomiting,  and  nausea  are  added  to 
the  preceding  symptoms.  In  entero-colitis  the  diarrhoea-like  stools  are  at 
times  blood-stained  and  slimy,  and  as  the  patient  suffers  from  tenesmus, 
the  enteritis  is  said  to  be  dysenteriform. 

Pathological  Anatomy. — The  mucous  membrane  of  the  intestines  is 
swollen,  red,  and  congested,  especially  around  the  solitary  follicles  and 
Peyer's  patches.  The  solitary  follicles  are  swollen  near  the  end  of  the 
ileum  (psoronteria),  and  at  times  small  ulcers  (follicular  ulcers)  develop. 

Treatment.— In  the  adult  we  must  prescribe  a  saline  purgative,  such  as 
sulphate  of  soda,  Pullna  water,  Birmenstorff  water,  etc.,  which  is  repeated 
if  necessary.  After  free  evacuation,  opiates  are  given,  either  by  the  mouth 
or  in  enemata.  The  diet  must  be  strict,  and  the  beverages  shoidd  consist 
of  rice-  or  albumin- water,  sweetened  with  syrup.     If  the  colic  is  very  severe, 


728  TEXT-BOOK  OF  MEDICINE 

subcutaneous  injections  of  morphia  should  be  given,  and  opium  fomenta- 
tions applied  to  the  abdomen.  Salicylate  of  bismuth  and  lime-water  in 
milk  may  also  be  employed. 


II.  INFANTILE  GASTRO-ENTERITIS  (INFANTILE  CHOLERA). 

In  young  children  digestive  disorders  acquire  additional  gravity  from 
the  special  importance  of  the  functions  of  nutrition  at  this  age.  Super- 
acute  gastro-enteritis  in  infants  deserves  mention,  because  of  its  frequency 
and  gravity  (H.  de  Rothschild).  We  shall  also  have  to  describe  chronic 
dyspepsia  of  infants,  which  often  paves  the  way  for  more  acute  complica- 
tions. Finally,  the  study  of  athrepsia  belongs  to  the  digestive  disorders 
of  early  infancy. 

Acute  Infantile  Gastro-Enteritis — Infantile  Cholera. — The  most  char- 
acteristic form  of  acute  gastro-enteritis  is  that  which  Trousseau  described 
under  the  name  of  "  infantile  cholera."  This  affection  is  most  common 
and  severe  during  the  summer.  It  attacks  bottle-fed  infants  of  four  or 
five  months  of  age,  or  older  children,  up  to  about  a  year  or  so,  who  have  been 
dyspeptic  since  weaning.  The  child  is  taken  ill  with  fever  and  restlessness, 
and  cries  constantly.  The  face  becomes  pale,  the  eyes  have  large  circles 
around  them,  and  prostration  succeeds  restlessness.  The  milk  is  vomited 
soon  after  ingestion,  but  this  act  is  a  regurgitation  without  effort  and  without 
nausea.  Diarrhoea  is  present,  and  the  stools  are  serous,  holding  in  suspen- 
sion fcjetid  greenish  particles,  and  mixed  with  gas,  so  as  to  form  a  green 
froth.  The  temperature  rises  to  103°  or  104°  F.  ;  in  some  cases  it  remains 
high.  The  skin  is  dry,  the  tongue  parched,  the  restlessness  constant,  and 
sleep  is  absent  (febrile  form).  But  in  other  cases  (algid  form)  the  initial 
rise  soon  gives  way  to  a  fall  of  temperature,  which  may  be  as  low  as  95°  F. 
The  little  patient  is  pale  or  cyanosed,  with  a  bistre  tint  under  the  eyes  and 
around  the  lips.  The  child  wastes  with  terrible  rapidity,  and  becomes 
dried  up,  while  the  abdomen,  at  first  ballooned  and  sensitive  to  pressure, 
becomes  scaphoid.  The  skin  of  the  abdomen  and  of  the  extremities  hangs 
in  folds,  the  eyes  sink  into  their  sockets,  the  scalp  falls  in  at  the  fontanelles, 
the  pulse  grows  weak,  and  the  respiration  becomes  slow  and  barely  per- 
ceptible. The  patient  looks  like  a  corpse,  and  passes  insensibly  from  life 
to  death.  In  some  cases  convulsions,  sclerema,  and  muscular  rigidity  are 
present  in  the  last  stage.  This  description  is  not  applicable  to  all  cases. 
Sometimes  diarrhoea  is  absent  (cholera  sicca,  Hutinel),  and  yet  the  toxi- 
infectious  condition  presents  the  same  characteristics.  In  the  less  acute 
forms  the  diarrhoea  is  not  so  liquid,  and  resembles  chopped  spinach.  The 
general  condition  fails  less  rapidly,  and  there  are  alternative  periods  of 


DISEASES  OF  THE  INTESTINE  729 

improvement  and  aggravation.  The  disease  may  be  prolonged  for  a  week 
or  a  fortnight.  With  proper  treatment,  the  child  may  regain  health,  and 
once  the  disease  is  checked  recovery  is  relatively  rapid.  In  the  very  slight 
forms  we  may  see  only  vomiting,  yellowish  or  greenish  foetid  diarrhoea, 
slight  fever,  and  restlessness,  and  in  a  few  days  the  danger  has  passed. 

Athrepsia. — The  onset  of  gastro- enteritis  is  not  always  so  sudden  as 
in  the  preceding  forms.  The  digestive  troubles  (vomiting  and  diarrhoea) 
insensibly  affect  the  general  condition.  The  nutrition  of  these  children 
has  been  defective  since  birth,  and  instead  of  developing  normally,  they 
waste  away.  The  skin  wrinkles,  the  cheeks  get  hollow,  the  face  becomes 
senile,  and  the  body  does  not  develop.  The  little  patient  may,  however, 
live  for  two  or  three  months,  although  he  weighs  less  than  at  birth. 
The  temperature  may  be  subnormal  or  raised.  The  child  flickers  out  like 
a  candle,  being  carried  ofE  by  latent  pulmonary  complications  or  by  con- 
vulsions. It  is  to  this  chronic  gastro-intestinal  cachexia  of  the  new-born 
that  Parrot  has  given  the  name  of  "  athrepsia." 

Chronic  Dyspepsia  of  Nurslings.— Chronic  digestive  troubles  are  less 
evident  in  older  nurslings,  because  they  only  affect  the  general  condition 
after  some  considerable  time.  This  chronic  dyspepsia  is  seen  especially  in 
children  overfed  wth  milk  that  is  too  rich  in  casein,  or  in  those  who  have 
been  prematurely  weaned,  or  fed  after  weaning  with  too  coarse  foods. 
These  children  are  too  fat ;  their  abdomens  are  too  prominent,  and  may  be 
soft  (large,  flabby  belly)  or  resistant.  The  stools  are  scanty,  hard,  whitish, 
dry,  and  chalky  (Marfan).  Such  infants  show  very  early  the  symptoms  of 
rickets.  At  the  time  of  weaning  they  are  especially  liable  to  acute  enteritis, 
and  later  their  flabby  belly  favours  hernia  and  visceral  ptoses.  If  these 
children  die,  the  lesions  of  gastro -enteritis,  with  lengthening  of  the  intestine, 
are  found  post  mortem. 

Pathogenesis. — Acute  or  chronic  digestive  troubles  in  infants  always 
come  from  improper  feeding.  The  digestive  canal  of  the  new-born  can  only 
digest  the  mother's  milk  in  a  perfect  manner.  The  breast  should  be  given 
at  most  every  two  hours  for  very  young  infants,  and  every  three  hours  from 
the  third  to  the  fourth  month,  so  that  the  next  meal  should  not  encroacli 
on  the  digestion  of  the  preceding  one.  Under  these  conditions  (the  child 
being  breast-fed),  digestive  troubles  are  exceptional.  They  mav  super- 
vene, however,  during  dentition,  upon  sudden  changes  of  temperature,  or 
from  illness  of  the  wet-nurse,  but  they  are  slight  and  transient.  It  is  in 
l)ottlc-fod  children  that  digestive  troubles,  and  especially  infantile  cholera, 
arise  in  the  great  majority  of  cases. 

The  weekly  returns  in  Paris  show  clearly  the  cause  of  this  disease.  We 
lind  that  the  infantile  mortality  from  gastro-enteritis,  which  is  very  low 
during  the  cold  months,  reaches  during  tiie  heat  of  summer  its  inaxinium. 


730  TEXT-BOOK  OF  MEDICINE 

which  is  then  ten  times  the  average.  Acute  gastro-enteritis  in  infants  is 
mostly  due  to  the  multiplication  of  the  microbes  of  fermentation  in  the 
milk  and  to  the  poisons  which  they  excrete. 

In  very  young  children,  even  in  perfect  health,  one  bottle  of  fermented 
milk  may  produce  an  attack  of  enteritis ;  but  older  children  can  offer  greater 
resistance,  and  the  disease  is  not  severe  unless  they  are  already  suffering 
from  chronic  dyspepsia.  In  dyspeptic  infants  the  least  alimentary  excess 
in  summer  may  be  fatal,  and  here,  as  in  the  new-born,  the  ferments  poured 
into  the  digestive  canal  are  the  cause  of  the  trouble. 

Bacteriology. — The  Bacillus  coli  is  found  in  the  stools  in  great  numbers, 
sometimes  in  a  state  of  pure  culture  and  of  exalted  virulence.  The  Bacillus 
coli  in  infantile  cholera  does  not  belong  to  a  special  kind,  and  though  the 
biochemical  characters  vary  in  each  case,  their  agglutination  by  the  serum 
does  not  allow  of  differentiation  from  other  coli  bacilli  (Widal,  Nobecourt). 
The  chromogenic  bacillus  of  Lesage  seems  to  be  a  variety  of  the  coli  bacillus, 
gifted  with  the  power  of  secreting  a  green  pigment.  It  is,  however,  not 
constant  in  green  diarrhoea  of  infants. 

Certain  microbes  are  often  found  associated  with  the  coli  bacillus,  and 
play  their  part.  The  chromophil  bacillus  of  Escherich,  the  streptococcus 
(Marfan  and  Marot),  the  pyocyaneus  (Nobecourt),  and  the  proteus  (Ardouin), 
are  amongst  the  number.  Nobecourt  has  insisted  on  the  gravity  of  this 
combined  infection. 

Pathological  Anatomy. — Histology  (Marfan  and  Bernard)  explains 
the  process  of  the  disease.  In  the  normal  condition  the  microbes  are  only 
found  on  the  surface  of  the  intestine  ;  in  acute  gastro-enteritis  they  penetrate 
into  the  lumen  of  the  glands,  and  invade  the  deep  layers,  whence  they  can 
enter  the  organism.  The  distant  lesions  are  explained  by  the  general 
infection  and  intoxication,  so  that  pulmonary  congestion  and  broncho- 
pneumonia due  to  the  coli  bacillus,  meningitis  due  to  the  same  microbe, 
phlebitis  of  the  abdominal  veins,  thrombosis  of  the  cranial  sinuses,  and 
degeneration  of  the  liver  and  kidneys,  may  be  found  on  post-mortem 
examination. 

Prophylaxis. — Careful  breast-feeding  insures  for  the  child  almost  certain 
immunity  from  gastro-enteritis.  It  is,  therefore,  the  duty  of  the  physician 
to  induce  every  mother  to  nurse  her  own  offspring.  Absence  or  insuffi- 
ciency of  milk  is  exceptional,  and  though  the  secretion  of  the  milk  must  be 
waited  for,  a  delay  of  forty-eight  hours  does  not  harm  the  infant.  If  the 
mother  is  unable  to  suckle,  a  wet-nurse  must  be  engaged.  It  is  only  as  a 
last  resort  that  the  bottle  should  be  made  use  of,  and  then  great  precautions 
must  be  taken  to  avoid  acute  gastro-enteritis.  In  order  to  diminish  the 
risk  of  gastro-enteritis  in  bottle-fed  infants,  rigorous  asepsis  must  be 
observed  in  the  administration  of  food.     The  greatest  cleanliness  must  be 


DISEASES  OF  THE  INTESTINE  731 

insisted  on  with  regard  to  the  bottle  and  to  the  nipple,  and  when  the  bottle 
is  finished,  no  milk  must  be  permitted  to  remain  in  it. 

Which  milk  should  be  used  ?  A  brand  of  milk,  sterilized  in  the  auto- 
clave at  120°  C,  and  preserved  in  sealed  bottles,  is  on  the  market.  If  care 
is  taken  to  open  the  bottle  only  at  the  time  of  pouring  out  the  milk  into  the 
feeder,  the  infant  is  certain  to  get  a  drink  free  from  microbes.  Unfortu- 
nately, sterilization  at  high  temperatures  increases  the  drawbacks  of  cow's 
milk,  which  is  naturally  thicker  than  human  milk.  It  is  richer  in  casein 
and  in  salts,  while  its  clot  is  firmer  and  more  resistant  to  the  digestive 
juices.  Moreover,  cow's  milk,  such  as  the  factories  produce,  sterilized  at 
high  temperatures,  is  only  suitable  for  strong  babies  of  several  months  old. 

To  remedy  these  drawbacks,  some  firms  prepare,  under  the  name  of 
"  maternal  "  or  "  humanized  "  milk,  a  milk  which,  by  centrifugalization, 
partial  coagulation,  sweetening,  and  skimming,  is  brought  down  to  a  com- 
position something  like  mother's  milk,  and  is  then  sterilized  at  120°  C.  The 
drawback  of  all  methods  of  sterilization  lies  in  the  partial  change  of  the 
lactose  into  caramel,  which  gives  a  brownish  colour  and  a  strange  taste  to 
the  milk. 

This  drawback  disappears  with  the  economical  method  of  sterilization 
invented  by  Soxhlet  and  popularized  by  Budin.  The  milk  is  divided  in 
as  many  bottles  as  may  be  required  during  the  day  or  half-day.  The 
bottles  are  then  plunged  for  twenty  minutes  into  a  water-bath  of  boiling 
water.  As  milk  only  boils  at  101°  C,  this  operation  does  not  cause  it  to 
boil,  and  its  composition  is  consequently  not  changed.  On  the  other  hand, 
all  the  pathological  germs  are  killed.  When  it  is  desired  to  use  a  bottle, 
all  that  is  necessary  is  to  substitute  a  nipple  for  the  rubber  disc,  and  a 
bottle  of  food  is  thus  obtained  without  decanting  the  milk. 

For  very  young  infants  indeed,  cow's  milk  may  be  diluted  with  a  third 
to  a  fourth  part  of  water  before  sterilizing  the  mixture,  and  this  precaution 
is  a  safeguard  against  chronic  dyspepsia  (dyspepsia  of  pure  cow's  milk, 
Marfan). 

The  Soxhlet-Budin  method  is  the  best  when  we  are  certain  of  receiving 
fresh  milk  from  a  good  dairy  several  times  a  day.  In  large  towns  these 
conditions  are  difficult  to  fulfil,  and  in  spite  of  Pasteurization,  which  to-day 
is  universally  adopted  in  the  milk  industry,  we  may  receive  milk  in  which 
microbes  have  commenced  to  grow.  The  passage  through  the  water- bath 
will  certainly  kill  the  microbes,  but  it  will  not  destroy  the  toxins  already 
poured  into  the  milk,  and  gastro-cntoritis  will  not  be  avoided.  In  large 
towns  milk  sterilized  in  the  laboratory  is  to  be  recommended  in  summer, 
but  humanized  milk  is  to  be  preferred  in  the  case  of  very  young  infants. 

The  use  of  milk  as  the  sole  food  of  the  child  may,  without  inconvenience, 
be  continued  until  the  age  of  one  year.     The  weaning  should  be  gradual, 


732  TEXT-BOOK  OF  MEDICINE 

and  soups,  milk,  panadas,  broths,  or  vegetable  purees,  are  tbe  first  kinds  of 
food  to  be  given  to  an  infant.  Infants  ought  not  to  be  weaned  during  very- 
hot  weather. 

Treatment. — Cases  of  chronic  dyspepsia  in  childhood  usually  recover 
on  a  return  to  rational  feeding,  but  in  acute  enteritis  treatment  is  more 
active.  It  is  first  of  all  necessary  to  cleanse  the  digestive  canal  of  its  toxic 
contents  by  a  small  dose  of  calomel,  and  next  to  withhold  fermentable  food. 
The  child  should  be  fed  with  boiled  w^ater,  given  as  required.  Mustard 
baths,  recommended  by  Trousseau,  injections  of  lukewarm  water,  and 
stimulation  by  rubbing,  may  be  employed  with  advantage.  Subcutaneous 
injections  of  artificial  serum  in  doses  of  50  to  100  grammes,  repeated  if 
need  be  several  times  a  day,  are  a  resource  which  sometimes  leads  to  recovery 
even  in  desperate  cases. 


III.  APPENDICITIS— APPENDICULAR  PERITONITIS— APPEN- 
DICULAR INTOXICATION— APPENDICiEMIA. 

During  the  last  few  years  I  have  devoted  ten  clinical  lectures  to  appen- 
dicitis, in  addition  to  my  numerous  contributions  to  theAcademie  de  Medecine. 
These  data  I  shall  use  in  the  present  section. 

Anatomy. — The  appendix  resembles  an  earthworm  suspended  from  the  caecum 
(appendix  vermiformis).  In  the  foetus  it  occupies  the  apex  of  the  ampulla  of  the 
caecum,  but  in  the  adult  its  situation  changes  ;  as  the  ampulla  is  much  dilated  below,  the 
appendix  is  attached  higher  up  to  the  postero -internal  part  of  the  caecum,  an  inch  above 
the  ileo-caecal  valve.  According  to  an  American  surgeon  (McBurney),  this  point  of 
attachment  corresponds  on  the  abdomen  with  the  centre  of  a  line  drawn  from  the 
antero -superior  iliac  spine  to  the  umbiHcus,  and  the  pain  in  appendicitis  is  generally 
situated  at  this  spot.  The  appendix  is  about  4  inches  in  length  and  J  inch  in  breadth. 
It  is  often  held  in  position,  in  the  middle  half  of  the  right  iliac  fossa,  by  a  fold  of  the 
peritoneum  (meso-appendix),  but  the  situation  and  direction  of  the  appendix  vary 
exceedingly.  In  the  descending  type  the  appendix  crosses  the  psoas,  and  dips  into 
the  pelvis,  a  situation  that  explains  the  topography  of  the  prerectal  abscess,  which 
tends  to  open  into  the  rectum,  vagina,  or  bladder.  In  the  ascending  and  posterior 
type,  which  is  frequent,  the  appendix  runs  upwards  along  the  posterior  face  of  the 
caecum  and  colon,  a  situation  which  explains  the  topography  of  the  retro-c^cal  abscess 
in  the  iUac  fossa  and  of  abscesses  situated  high  up  behind  the  colon.  This  means  that 
the  starting-point  of  the  appendicular  lesions  (with  or  -nithout  adhesions,  which  hmit 
these  lesions)  may  be  below,  above,  internal,  or  external  to  the  caecum. 

The  appendix  is  sometimes  provided  at  its  opening  into  the  caecum  with  a  valve, 
called  Gerlach's  valve,  which  prevents  the  entrance  of  faecal  matter  into  the  appendicular 
canal.  Though  Clado  and  Lafforgue  consider  this  valve  exceedingly  rare,  I  have  been 
able  to  find  it  frequently. 

The  appendix  has  the  same  structure  as  the  caecum,  and  is  composed  of  four  layers  : 
an  external  peritoneal  coat ;  a  muscular  coat,  with  longitudinal  and  circular  fibres  ;  a 
submucous  coat,  composed  of  connective  tissue  and  almost  lacking  in  elastic  fibres  ; 
and  a  mucous  tunica,  with  cylindrical  epithelium,  adenoid  stroma,  closed  follicles,  and 
tubular  glands.     It  must  be  noticed  that  the  appendix  grows  smaller  towards  its  tip. 


DISEASES  OF  THE  INTESTINE  733 

where  the  muscular  fibres  and  glands  gradually  disappear,  and  the  cellular  layer  becomes 
more  important. 

The  appendix  is  traversed  throughout  its  entire  length  by  a  central  canal,  the  lumen 
of  which  is  very  narrow  and  uneven,  and  does  not  measure  more  than  from  3  to  4 
millimetres  in  diameter. 

Discussion. — During  the  last  few  years  appendicitis  has  assumed  an  importance 
of  the  first  order  in  medicine  and  surgery.  Acute  general  or  local  peritonitis,  sub- 
phrenic empyema,  purulent  and  putrid  infection  of  the  pleura,  gangrene  of  the  lung, 
purulent  infection  of  the  fiver,  hsmorrhagic  ulcerative  gastritis,  nephritis,  perinephritic 
abscess,  endocarditis,  phlebitis,  icterus  and  icterus  gravis,  albuminuria,  anuria,  uraemia, 
etc.,  are  formidable  complications  due  to  toxi-infections  of  appendicular  origin,  so  that 
it  is  customary  to  class  them  under  appendicitis. 

But  from  the  outset  let  it  be  well  understood  that  the  appendix  is  the  starting-point 
of  these  complications,  which  were  formerly  put  down  as  typhUtis  and  perityphlitis. 

Our  knowledge  of  appendicitis  is  of  fairly  recent  date,  and  until  1888  typhlitis 
reigned  supreme.  This  stercoral  typhlitis,  as  it  was  called,  was  usually  ascribed  to 
obstruction  of  the  caecum  by  faecal  matter.  This  fsecal  obstruction  caused  an  inflam- 
mation of  the  walls  of  the  caecum,  called  typhlitis,  with  its  attendant  symptoms  of 
constipation,  pain,  sweUing,  induration  in  the  right  iUac  fossa,  and,  in  more  severe 
cases,  fever,  nausea,  and  vomiting.  This  so-called  typhlitis  generally  ended  in  resolu- 
tion, but  it  might  end  in  ulceration  and  perforation  of  the  caecum,  causing  perityphlitis, 
peritonitis,  or  iliac  phlegmon.  There  was  peritonitis  if  the  lesions  were  seated  on  the 
anterior  surface  of  the  caecum,  and  iliac  phlegmon  if  the  lesions  were  seated  on  the 
posterior  surface,  which  was  incorrectly  believed  to  be  lacking  in  peritoneum. 

These  ideas  were  held  for  a  long  time,  but  they  were  wrong,  for  stercoral  typhlitis, 
in  this  sense,  does  not  exist.  In  the  first  place,  the  posterior  surface  of  the  caecum  is 
not  lacking  in  peritoneum.  In  1887  Tuffier  showed  that  the  caecum  in  the  adult  and 
in  the  foetus  is  never  in  direct  communication  with  the  cellular  tissue  of  the  iliac  fossa. 
The  caecum  is  surrounded  by  peritoneum,  and  "  the  hand  can  be  passed  round  it  in  the 
same  manner  as  it  can  be  passed  round  the  apex  of  the  heart  in  the  pericardium." 

On  the  other  hand,  American  surgeons  had  begun  to  perform  early  laparotomy 
for  symptoms  formerly  attributed  to  typhhtis,and  they  saw  clearly  that  these  symptoms 
had  their  origin,  not  in  the  cescum,  but  in  the  appendix.  The  same  observation  was 
made  hundreds  of  times  by  surgeons  in  England,  Switzerland,  Germany,  and  France, 
so  that  the  precise  idea  of  appendicitis  was  gradually  substituted  for  the  mistaken 
description  of  the  old  typhlitis.  These  ideas,  which  some  authors  were  loath  to  admit, 
were  sanctioned  at  the  Surgical  Congress  of  1895,  and,  in  the  discussions  at  the  Societe 
de  Chirurgie,  Routier  took  care  to  state  that  in  a  large  number  of  personal  cases  the 
appendix  was  the  seat  of  the  mischief,  and  not  the  caecum.  I  have  witnessed  operations 
in  more  than  200  cases  of  appendicitis,  and  I  am  convinced  that  the  various  troubles 
formerly  put  down  to  typhlitis  must  always  be  put  doAvn  to  the  appendix,  and  never 
to  the  caecum. 

This  does  not  mean  tlxat  the  word  "  typhlitis  "  is  to  be  removed  from  our  nosology, 
but  a  clear  understanding  is  necessary.  The  ulcerations  of  typhoid  fever  and  of  tuber- 
cular disease  frequently  attack  the  ca-cum,  but  these  specific  lesions  are  beside  the 
question  wliich  at  present  occupies  our  attention.  Tuberculosis  may  be  locahzcd  in 
the  csccum  in  a  primary  or  chronic  form,  which  is  curable  by  operation,  but  this  tuber- 
cular typhlitis  which  simulates  cancer  so  closely  has  nothing  in  common  with  the 
typhlitis  now  under  discussion, 

A  perforation  of  an  unknown  nature  might  involve  the  caecum,  like  the  ileum,  but, 
once  again,  all  these  dissimilar  cases,  though  seated  in  the  ofocuni,  have  nothing  in 
common  with  the  question  before  us,  and  it  is  well  established  that  the  troubles  sot 
down  to  lyphUtis  must  now  bo  put  down  to  appendicitis. 


734  TEXT-BOOK  OF  MEDICINE 

Finally,  it  will  be  said  that  in  undeniable  cases  typhlitis  with  ulceration,  gangrene, 
or  suppuration  of  the  cajcum  has  been  found.  If,  however,  we  examine  them 
closely,  we  shall  see  that  these  lesions  are  consecutive  to  appendicitis,  and,  as  the 
appendix,  which  is  primarily  diseased,  runs  along  the  posterior  surface  of  the  caecum, 
the  csecal  and  retrocaecal  lesions  are  secondary  to  the  appendicitis.  Gambetta's  case 
was  of  this  nature.     Appendicitis  must,  therefore,  be  substituted  for  typhlitis. 

These  restrictions  being  established,  it  is  hardly  necessary  to  state  that  nobody  has 
ever  thought  of  denying  typhUtis  in  so  far  as  inflammation  of  the  mucous  membrane  of 
the  caecum  is  concerned.  The  caecum,  like  the  colon  or  the  ileum,  shares  in  the  infections 
of  the  intestinal  mucous  membrane.  Typhlitis  exists,  just  as  do  enteritis  and  colitis. 
Intestinal  infections,  classed  together  under  the  name  of  enteritis  or  of  folUcular,  muco- 
membranous,  or  sabulous  entero-colitis,  are  prone  to  affect  the  mucous  membrane  of 
the  caecum.  I  have  given  them  the  name  of  entero-typhlo-colitis,  and  yet  no  one  has 
ever  seen  typhlitis  or  typhlo-colitis  whether  it  is  accompanied  or  not  by  constipation, 
membranes,  or  sand,  produce  gangrene,  perforation  of  the  ca3.cum,  and  peritonitis. 

Pathological  Anatomy — Bacteriology.— According  to  the  particular 
case,  the  appendix  may  be  purple  in  colour,  lengthened,  doubled  in  size, 
indurated,  or  in  a  condition  of  erection.  We  may  find  suppuration,  fluctua- 
tion, gangrene,  perforation,  calculi,  twists,  or  kinks,  strangulation  by 
bands,  etc. 

Its  lumen  is  constricted  or  obliterated  at  its  origin,  or  at  some  point  of 
its  length.  The  canal  may  have  recovered  its  permeability  at  the  time  of 
operation.  The  obstructions  of  the  canal  favour  the  formation  of  closed 
cavities.  The  closed  cavity  may  be  small,  and  of  almost  the  normal  size 
and  shape  of  the  appendicular  canal.  In  other  cases  it  is  larger,  and  gives 
to  the  appendix  the  form  of  a  spindle,  club,  ch,erry,  pear,  etc.  The 
closed  cavity  contains  a  small  amount  of  muco-purulent,  faecal,  or  blood- 
stained fluid.  It  may  be  transformed  into  a  pseudo-cyst,  containing  in- 
offensive fluid.  The  pathogenic  microbes  of  appendicitis  are  the  microbes 
of  the  intestinal  flora,  and  the  coli  bacilli  are  most  in  evidence. 

Pathogenesis  of  Appendicitis. — The  pathogenesis  of  appendicitis  has 
been  influenced  by  the  views  held  as  to  the  causation  of  typhlitis.  Con- 
stipation and  diarrhoea  have  been  given  as  causes,  although  it  was  not 
known  w^hich  of  these  conditions  was  the  more  effective.  Foreign  bodies, 
such  as  fragments  of  bone,  fish-bones,  egg-shells,  pins,  needles,  prune-stones, 
fruit-pips,  etc.,  have  been  accused. 

I  may  say  at  once  that  fragments  of  bones,  prune-stones,  date-stones, 
cherry-stones,  etc.,  though  quite  capable  of  injuring  the  caecum,  are  abso- 
lutely incapable  of  entering  the  appendicular  canal.  At  most  only  very 
small  bodies  indeed,  such  as  grape-stones,  could  do  so,  and  even  then,  since 
appendicular  concretions  have  been  carefully  studied,  it  has  been  found 
that  these  concretions,  which  may  take  the  form  of  coffee-beans,  date-stones, 
grains  of  corn,  beans,  and  pips,  are  simply  calculi  formed  in  situ.  Thoir 
origin  and  structure  are  now  well  known. 


DISEASES  OF  THE  INTESTINE  735 

We  must  abandon,  then,  the  old  theory  of  a  foreign  body  entering  the 
appendix,  injuring  its  walls,  and  causing  peritonitis  by  perforation.  I 
have  tried,  by  collecting  the  anatomical,  bacteriological,  and  experimental 
proofs,  to  simplify  the  pathogenesis  of  appendicitis,  and  find  a  formula 
applicable  to  every  case.  In  my  opinion  the  theory  of  appendicitis  may 
be  summed  up  as  follows  :  Appendicitis  results  from  the  transformation 
of  a  part  of  the  appendicular  canal  into  a  closed  cavity,  which 
becomes  a  focus  of  infection  and  intoxication,  due  to  the  increased 
virulence  of  the  imprisoned  microbes.  Let  us  analyze  first  the  different 
ways  in  which  the  appendicular  canal  may  be  converted  into  a  closed 
cavity. 

Calculous  Appendicitis. — The  presence  of  a  calculus  in  the  appendicular 
canal  has  given  to  this  variety  the  name  of  calculous  appendicitis.  The 
calculus  is  found,  if  the  infectious  process  has  not  destroyed  it.  If  the 
appendix  has  become  gangrenous,  the  calculus  may  pass  into  the  peritoneum, 
where  it  is  found  at  the  time  of  operation  or  during  the  subsequent  dress- 
ings. These  calculi  have  been  described  by  Rochaz,  who  gives  a  description 
and  illustrations  of  sixty-five  appendicular  calculi.  They  are  usually 
elongated  and  fusiform  or  cylindrical.  As  a  rule,  one  calculus  is  found, 
but  as  many  as  three  or  four  may  be  present.  They  then  have  several 
facets.  The  colour  is  usually  brownish,  but  their  consistency  varies  in 
nature — friable  or  dense  and  of  stony  hardness,  while  every  intermediate 
degree  may  be  soen.  These  calculi  are  formed  of  different  elements. 
Berlioz  has  made  a  most  minute  analysis  of  several  calculi,  and  the  results 
of  his  researches  agree  absolutely  with  those  obtained  by  other  chemists 
(Vok,  Butler,  Pelet). 

In  these  calculi  we  find  brownish  faecal  matter,  soluble  in  ether  and 
mineral  salts,  principally  phosphates  and  carbonates  of  lime.  We  some- 
times find  salts  of  ammonia,  traces  of  chlorides,  sulphates,  and,  very  rarely, 
cholesterin  (Walt).  The  various  organic  and  mineral  elements  are  cemented 
by  mucus  from  the  glands  in  the  appendix. 

It  will  now  be  understood  why  the  appendicular  concretions  are  some- 
times soft  and  friable,  sometimes  hard  and,  as  it  were,  calcified.  If  the 
concretion  is  rich  in  organic  matter,  it  is  soft,  or  at  least  it  is  easily  softened 
at  the  time  of  infection  ;  if  the  concretion  is  rich  in  calcareous  salts,  it  may 
assume  a  stony  consistency,  like  a  true  calculus.  It  is  easy  to  find  these 
concretions  in  the  process  of  formation.  It  is  only  necessary  to  make  a 
section  of  them  to  see  that  they  are  usually  stratified.  Around  one  or 
several  nuclei  there  are  eccentric  layers,  the  stratification  of  which  proves 
that  the  calculi  grow  slowly  in  the  appendicular  canal  by  the  addition  of 
organic  and  mineral  layers. 

By  studying  this  process,  and  comparing  the  slow  formation  of  appen- 


736  TEXT-BOOK  OF  MEDICINE 

dicular  calculi  with  the  analogous  formation  of  biliary  calculi,  I  was  led  to 
propose  the  name  appendicular  lithiasis,  which  seems  to  me  to  be  very- 
similar  to  urinary  and  biliarj^  lithiasis. 

What  becomes,  then,  of  the  old  theory  (Talamon)  that  the  calculi 
reach  the  appendix  after  being  previously  formed  in  the  caecum  ?  Accord- 
ing to  Talamon,  it  is  in  the  caecum  that  the  scybala  are  rolled  and  mashed. 
— "  they  are  rounded  there  like  pellets  under  the  finger  " — and  after  this 
pill-making  process  they  pass  from  the  caecum  into  the  appendix.  This 
theory  has  been  upset  by  the  arguments  of  Rochaz  :  "  Talamon  supports 
his  theory  by  the  perfectly  spherical  form  of  the  calculi ;  but  we  only  met 
with  this  spherical  form  three  times  in  sixty-five  cases,  and  the  usual  shape 
of  the  calculi  is  cylindrical.  How  are  the  long  stercoral  sausages,  filling 
the  appendix  from  one  end  to  the  other,  to  be  explained  by  Talamon's 
pellets  ?  How  could  large  concretions  penetrate  by  an  opening  which  at 
most  has  a  diameter  of  only  5  millimetres,  and  which  is,  besides,  more  or 
less  completely  closed  by  a  valve  ?  On  the  contrary,  the  disposition  of  the 
calculi  in  concentric  layers  indicates  a  slow  formation,  which  could  only 
take  place  in  a  recess  separated  from  the  intestinal  canal,  and  not  in  the 
caecum,  where  the  calculi  would  be  carried  away,  after  a  short  time,  by  the 
flow  of  matter." 

I  have  nothing  to  add  to  the  excellent  reasoning  of  Rochaz.  It  is, 
indeed,  clear  that  the  so-called  calculous  appendicitis  is  associated  with 
a  process  of  lithiasis,  which  may  be  compared  in  some  measure  to  biliary 
and  urinary  lithiasis. 

Non-Calculous  Appendicitis. — Appendicitis  is  not  always  of  calculous 
orisin.  In  most  cases  it  runs  its  course  without  the  smallest  concretion 
being  found  in  the  canal.  It  is  here  a  question  of  an  infection  of  the  mucous 
membrane,  which  American  surgeons  have  called  catarrhal  appen- 
dicitis, for  want  of  a  better  name.  I  propose  to  call  it  obliterating 
appendicitis.  In  such  a  case,  perhaps  from  the  swelling  of  the  infected 
mucous  membrane,  the  appendicular  canal  is  obliterated  at  its  orifice, 
or  at  some  point  in  its  length,  exactly  as  the  biliary  canals  are  obliterated 
in  so-called  catarrhal  icterus,  or  as  the  Eustachian  tube  is  obliterated  in  a 
case  of  acute  otitis.  This  acute  process  terminates  in  the  formation  of  one 
or  several  subjacent  cavities  in  the  appendix,  and  causes  all  the  complica- 
tions. 

Several  causes  of  obliteration  are  sometimes  found  in  the  same  appen- 
dix, and  appendicitis  may  be  at  the  same  time  calculous  and  obliterating, 
The  calculi  may  be  free  in  the  closed  cavity. 

These  non -calculous  cases  of  appendicitis  are  just  as  serious  as  the 
calculous  forms,  and  the  symptoms  and  the  complications  are  similar.  They 
may  likewise  cause  appendicular  and  peritoneal  troubles,  and  give  rise  to 


DISEASES  OF  THE  INTESTINE  737 

gangrene,  or  to  perforation  of  the  appendix.  We  must  therefore  reject 
Talamon's  theory  that  a  calculus  (which  frequently  never  existed)  played 
an  important  role  in  the  compression  of  the  appendicular  vessels, 

I  have  just  spoken  of  the  acute  obliterative  process,  but  there  is  also  a 
chronic  form,  which  brings  about  fibroid  constriction  and  obliteration  of 
the  appendicular  canal  at  some  point  of  its  length  (a  stenosis  which  may 
be  compared  with  stricture  of  the  urethra).  This  process  may  be  chronic 
from  the  outset,  or  may  follow  attacks  of  acute  appendicitis,  just  as  endo- 
carditis is  sometimes  followed  by  mitral  constriction.  In  a  case  quoted 
by  Achard,  where  the  lesions  had  caused  perforation  of  the  appendix  and 
abscesses  of  the  liver,  the  infective  focus  in  the  appendix  was  due  to 
obliteration  of  the  orifice  of  the  canal  by  fibroid  tissue.  There  was  no  trace 
of  a  calculus.  Rendu  has  published  a  case  of  purulent  appendicitis 
caused,  not  by  calculi,  but  "  by  a  sort  of  fibrous  constriction,  which  separated 
the  diseased  appendix  from  the  healthy  caecum."  It  w^s  easy  to  see  that 
the  communication  between  the  caecum  and  the  appendix  was  completely 
obliterated. 

Appendicitis  caused  by  kinks  and  strangulation.— In  some  cases 
the  appendicitis  is  neither  calculous  nor  obliterating,  but  results  from 
kinking  of  the  appendix,  from  strangulation  by  bands  or  adhesions,  or  by 
twisting  of  the  appendix  around  its  mesentery.  In  such  cases  the  portion 
of  the  canal  below  the  kink  or  strangulation  is  converted  into  a  closed 
cavity. 

The  appendicitis  thus  caused  is  as  serious  as  that  due  to  calculus  or 
obliteration,  and  the  toxi-infection  in  the  appendicular  focus  causes  similar 
symptoms  and  results. 

The  Closed  Cavity. — From  the  various  processes  just  described,  it 
follows  that  the  canal  may  be  obstructed  either  at  its  csecal  orifice  or  in  its 
length  by  a  calculus,  by  inflammatory  swelling  of  the  walls,  by  twisting,  by 
kinking,  or  by  strangulation  of  the  appendix.  The  obliteration  may  be 
temporary  or  persistent.  It  matters  little  whether  the  obliteration  is  due 
to  a  calculus,  strangulation  of  the  appendix,  swelling  of  the  infected  walls, 
or  kinking  of  the  tube.  The  essential  fact  is  that  the  portion  of  the 
appendicular  canal  below  the  obliteration  is  converted  into  a  closed 
cavity.  The  microbes,  which  in  tlieir  normal  state  were  inoffensive  (as  are 
all  the  microbes  of  the  intestine  when  free),  are  now  imprisoned,  and 
therefore  able  to  increase  their  virulence,  as  shown  by  Klecki's  experi- 
ments, and  to  give  rise  to  acute  toxi-infection.  From  this  moment  appendi- 
citis is  present,  and  if  the  microbes  imprisoned  in  the  appendicular 
focus  are  endowed  with  suflicient  virulence,  abscess,  perforation,  or 
gangrene  of  the  appendix  may  result,  or  else  the  microbes  may  pass  through 
the  walls  of  the  appendix  and  reach  the  peritoneum,  without  these  walls 

i7 


738  TEXT-BOOK  OF  MEDICINE 

showing  the  slightest  perforation  ;  or,  again,  the  toxines  and  microbes 
may  reach  the  veins  and  infect  the  whole  system.  The  patient  is  now  liable 
to  multiple  complications,  which  are  only  too  often  dangerous. 

The  formation  of  a  closed  cavity  is  not  always  followed  by  complications, 
for  they  depend  on  the  virulence  of  the  imprisoned  microbes,  and  on  the 
toxicity  of  their  products.  This  virulence  may  be  insignificant,  or  may 
be  annihilated  by  the  phagocytes,  in  which  case  the  appendicular  lesions 
do  not  run  their  full  course.  A  chronic  process  may  obliterate  the  whole 
canal,  causing  a  spontaneous  and  radical  cure,  which  j)rotects  the  patient 
from  further  trouble. 

On  the  other  hand,  the  infection  of  the  walls  may  continue  its  course 
even  after  the  initial  obliteration  has  disappeared.  This  explains  why,  at 
the  time  of  operation,  we  may  find  a  canal  which  has  recovered  its  per- 
meability, the  closed  cavity  being  thus  destroyed,  after  having  been  the 
primum  movens  of  ,the  infection,  which  has  continued  its  course.  This 
view  of  appendicitis  due  to  a  closed  cavity  was  suggested  to  me  by  the 
beautiful  experiments  of  Klecki. 

Experimental  Research. — In  1889  Clado  presented  to  the  Surgical 
Congress  some  remarkable  clinical  and  experimental  work  on  hernial 
infection.  He  found  that  the  microbes  from  the  strangulated  intestine 
passed  into  the  sac,  without  any  perforation  of  the  gut,  as  early  as  the  day 
following  strangulation.  He  followed  the  migration  of  the  microbes  through 
the  unperforated  coats  of  the  bowel,  and  proved  that  the  peritoneal  cavity 
could,  in  its  turn,  be  invaded.  Finally,  he  noiJed  the-  possibility  of  general 
infection. 

Bennecken,  Oker-Blom,  and  many  others,  have  since  repeated  these 
experiments,  and  have  proved  that  the  coli  bacillus,  enclosed  in  a  strangu- 
lated or  invaginated  coil  of  gut,  may  pass  into  the  peritoneum  either  by 
penetration  through  the  coats  or  by  way  of  the  lymphatics,  and  thus  cause 
peritoneal  infection. 

The  most  important  work  on  this  subject,  however,  is  that  of  Klecki, 
who,  with  strict  aseptic  precautions,  occluded  an  intestinal  coil  in  dogs 
by  means  of  caoutchouc  rings.  After  twenty-four  to  forty-eight  hours 
the  dogs  were  killed.  The  strangulated  coil  was  not  perforated,  and  yet 
had  caused  peritonitis.  The  results  of  these  experiments  are  :  the  intestinal 
coil,  converted  experimentally  into  a  closed  cavity,  contains  swarms  of 
the  microbes  usually  found  in  the  bowel,  but  their  virulence  is  much 
increased.  The  microbes,  in  their  new  pathological  state,  can  traverse  the 
non-perforated  intestinal  wall,  and  cause  peritonitis.  The  virulence  of  the 
microbes  in  the  ligatured  coil  of  gut  is  greater  than  in  the  peritoneum. 
"It  is  therefore  not  in  the  peritoneum  that  the  solution  of  the  question 
must  be  sought.     The  coli  bacillus  and  the  other  microbes  which  give  rise 


DISEASES  OF  THE  INTESTINE  739 

to  polyinfection  reach  the  peritoneum  through  the  pathological  coil,  in  which 
they  have  already  undergone  biological  changes,  causing  an  increase  in  their 
own  virulence,  and  also  in  that  of  their  toxines." 

As  these  experimental  data  appeared  to  me  absolutely  applicable  to 
the  pathogenesis  of  appendicitis,  I  proposed  the  theory  of  the  closed  cavity. 
Roger  and  Josue  ligatured  the  appendix  in  a  rabbit,  taking  care  to  spare  the 
vessels.  They  killed  the  animal  some  time  afterwards,  and  found  that  the 
part  below  the  ligature  was  converted  into  a  purulent  cavity.  They  there- 
fore concluded  that  it  suffices  to  imprison  the  microbes  in  the  appendix, 
"  in  order  to  transform  the  inoffensive  microbes  of  the  intestine  into  patho- 
genic agents." 

De  Rouville  also  has  caused  appendicitis  experimentally  in  the  rabbit 
by  ligaturing  the  ileo-csecal  appendix  at  its  base.  He  was  thus  able  to 
reproduce  the  lesions  caused  by  the  closed  cavity.  His  conclusions  are  as 
follows  :  "  The  first  experiment  showed  the  only  too  frequent  course  of 
appendicitis  in  man,  ending  in  gangrene,  perforation  of  the  appendix,  peri- 
appendicular abscess,  and  general  peritonitis.  The  perforation  was  pro- 
duced apart  from  any  calculus  or  from  any  operative  injury  to  the  vessels. 
The  second  experiment  showed  that,  even  if  infective  lesions  may,  in  certain 
cases,  be  for  a  long  time  limited  to  the  appendix,  the  latter  is  none  the  less 
the  focus  of  an  extremely  violent  infection,  and  the  possible  starting-point 
of  formidable  complications,  which  nothing  but  early  surgical  intervention 
can  avoid." 

"  These  two  cases  testify  in  the  same  manner  as  the  one  recently  reported 
by  Roger  and  Josue,  and,  like  the  latter,  support  the  theory  of  the  closed 
cavity  maintained  by  Dieulafoy."* 

Another  experiment  :  De  Rouville  introduced  into  the  appendix  of  a 
rabbit  a  fine  stem  of  laminaria.  Appendicitis  did  not  appear  until  the 
swollen  laminaria  came  into  intimate  contact  with  the  walls  blocking  the 
opening,  and  converting  the  lower  portion  of  the  appendicular  canal  into  a 

*  The  new  theory  of  appendicitis,  as  maintained  by  myself,  differs  in  many  respects 
from  the  ideas  enunciated  by  Talamon.  According  to  Talamon,  the  calcuhis  "  enters 
the  appendix  suddenly  by  an  untimely  contraction  of  the  caecum,  penetrates  into  it  by 
rubbing,  and  encloses  itself  in  the  superior  portion  of  the  narrow  canal."  Kochaz,  as 
we  have  seen  above,  has  disproved  this  theory.  According  to  Talamon,  one  of  the 
consequences  of  the  calculus  thus  engaged  is  "  compression  of  the  walls  of  the  appendix 
and  stoppage  of  the  circulation  of  the  vessels  contained  in  the  walls  "  ;  then  "  the  in- 
offensive microbes,  which  are  powerless  against  the  healtliy  cells,  triumph  witliout 
difficulty  over  these  cells  when  they  are  deprived  of  their  blood-supply."  The  experi- 
ments of  Kouvillo  also  disprove  this  hypotliesis.  Accordingly,  the  various  experiments, 
and  tlio  numerous  cases  of  appendicitis  without  calculus,  condemn  Talamon's  theory, 
which,  however,  has  one  happy  expression — "  tlie  closed  vaso  "  ,  but  this  expression  was 
still-born,  lost  in  the  midst  of  inexact  theories  (see  Dclbet,  Arch.  Genir.  de  Medecine, 

1897,  p.  :m). 

47—2 


740  TEXT-BOOK  OF  MEDICINE 

closed  cavity.  Other  foreign  bodies,  such  as  small  grains  of  lead  or  pieces 
of  glass,  introduced  into  the  appendix  do  not  cause  appendicitis,  because 
they  do  not  gradually  swell  up,  causing  obliteration  of  the  canal,  and  con- 
verting it  into  a  closed  cavity.  These  experiments  prove  that  the  arrest 
of  foreign  bodies  or  of  appendicular  products  does  not  suffice  to  provoke 
appendicitis.  Appendicitis  is  only  produced  when  the  canal  is  completely 
obstructed  at  some  spot. 

Migration  of  Microbes. — If  it  is  in  the  closed  cavity  that  the  virulence 
of  the  microbes  is  increased,  we  must  prove  that  their  migration  takes  place 
through  the  walls  of  this  closed  cavity.  In  conjunction  with  Apert  and 
Caussade,  I  have  verified  this  point.  We  made  use  of  an  appendix  which 
had  been  removed.  The  histological  lesions  and  the  bacteriological  features 
are  noted  in  Plate  VI.  The  prominent  features  are  as  follows :  above  the 
obliteration,  the  wall  has  preserved  its  normal  structure ;  no  microbes  are 
found  in  it :  on  a  level  with  the  obliteration,  the  lumen  of  the  canal  has 
completely  disappeared,  and  the  wall  is  largely  replaced  by  fibrous  tissue. 
Microbes  are  few  in  number  :  below  the  obliteration,  in  the  closed  cavity, 
the  deep  part  of  the  mucous  membrane  still  exists,  but  its  superficial  part 
is  ulcerated.  The  baae  of  the  glands  only  is  seen.  The  subjacent  layer 
forms  two-thirds  of  the  thickness  of  the  wall.  It  has  a  lymphoid  structure, 
and  is  traversed  by  small  veins,  congested  with  blood,  and  by  a  few  thickened 
arterioles.  The  lymphoid  tissue  invades  the  muscular  layers,  and  separates 
the  bundles,  especially  those  of  the  circular  layer.  The  continuity  of  the 
longitudinal  layer  is  better  preserved.  The  peritoneum  is  very  much 
thickened,  and  the  subperitoneal  layer  is  traversed  by  numerous  blood- 
vessels. The  walls  of  the  closed  cavity  are  traversed  by  numerous  colonies 
of  microbes,  occupying  the  lymphoid  tissue  below  the  mucous  membrane, 
and  especially  the  spaces  of  the  reticulum.  These  microbic  masses  are  in 
part  engulfed  by  leucocytes,  and  are  formed  by  agglomeration  of  the 
microbes,  as  if  the  coli  bacillus  and  other  microbes  had  formed  colonies 
in  situ.  Similar  colonies  are  found  in  the  portions  of  lymphoid  tissue 
separating  the  layer  of  smooth  muscular  fibres.  They  can  be  followed  into 
the  subperitoneal  layer,  and  are  spreading  to  the  peritoneal  cavity.  The 
pathogenesis  of  certain  cases  of  appendicular  peritonitis  is  thus  explained, 
although  the  walls  of  the  appendix  are  neither  gangrenous  nor  per- 
forated. 

The  chief  fact,  which  by  itself  alone  would  suffice  to  prove  the  patho- 
genic role  of  the  closed  cavity,  is  that  the  colonies,  though  so  numerous 
in  the  walls  of  the  closed  cavity,  where  their  virulence  is  increased,  are 
absent  in  the  walls  of  the  appendix  above  the  closed  cavity.  The  infective 
process  is,  therefore,  much  the  same  in  a  closed  cavity  of  the  appendix  or  in 
a  strangulated  coil  of  bowel.     In  both  cases  the  increase  in  virulence  favours 


MIGRATION   OF  MICROBES  THROUGH  A  SEGMENT 

OF  THE  APPENDIX,  WHICH  HAS  BEEN 

TRANSFORMED    INTO    A    CLOSED    CAVITY. 

Plate  VI. 


m 


II 

a 


m 


D 
m 


Fig.  5o.  —  A  section  of  the  walls  of  the  appendix  on  a  level 
with  th.  closed  cavity. 

A.  —  The  Deep  Part  of  the  Ulcerated  Mucous  Membrane. 

B.  —  The  Submucous  Layer,  very  much  thickened,  forming 

Two-Thirds  of  the  Thickness  of  the  Wall. 
It  has  a  lymphoid  structure,  and  is  traversed  by  small  veins  (v) 
gorged  with  blood  (w),  and  by  arterioles  with  thickened  walls  [a). 

C.  —  Muscular  Layer,  separated  by  the  Lymphoid  Tissue. 

D.  —  Subperitoneal  Layer. 
m,  Numerous  colonies  of  microbes  {Bacillus  coli)  traversing 
the    appendicular    walls    from   the    mucous   towards   the    serous 
membrane.     To  facilitate  the  description,  the  microbic  elements 
have  been  diagrammatically  enlarged. 

To  face  p.  740 


DISEASES  OF  THE  INTESTINE  741 

the  migration  of  the  microbes  through  the  walls.  Mj  researches  as  to 
appendicitis  agree  absolutely  with  those  of  Klecki  as  to  the  intestinal  coil. 

It  is  now  easy  to  understand  how  the  infection  of  the  walls  of  the  appendix 
at  the  site  of  the  closed  cavity  takes  place.  We  see  the  pathogenesis  of 
certain  cases  of  appendicular  peritonitis,  the  peritoneum  being  infected, 
even  when  the  walls  of  the  appendix  are  neither  gangrenous  nor  per- 
forated. 

And  the  proof  that  this  is  the  crux  of  the  question  is  that,  while  the 
obliteration  may  be  due  to  kinking,  twisting  of  the  appendix,  strangulation 
by  a  band,  obliteration  by  calculi,  or  swelling  of  the  walls,  the  result  is 
always  the  same.  The  infection  starts  from  the  closed  cavity,  and  sets 
up  the  same  train  of  symptoms  and  complications. 

Increase  of  Virulence  in  the  Closed  Cavity. — The  following  experiment 
(Hartmann  and  Minot)  helps  us  to  comprehend  the  degree  of  virulence  which 
the  microbes  may  acquire  in  the  closed  cavity  : 

Hartmann  operated  upon  a  patient  for  acute  appendicitis,  and  found,  on  examining 
the  specimen,  that  the  canal  was  obliterated  in  its  middle  portion,  the  lower  portion 
being  converted  into  a  closed  cavity.  Two  sets  of  cultures  were  made  on  agar,  one  from 
the  mucus  taken  from  the  free  end  of  the  canal  and  the  other  from  the  mucus  of  the 
closed  cavity.  Twenty -four  hours  later  numerous  colonies  of  the  Bacillus  coli  had  grown 
on  both  cultures.  Two  tubes  of  broth  were  treated  separately  with  the  colon  bacilli 
taken  from  each  of  these  cultures.  On  April  19  fifteen  drops  of  these  two  broths  were 
injected  under  the  skin  of  the  Hank  of  two  guinea-pigs.  The  guinea-pig  inoculated 
Avith  the  broth  containing  the  bacillus  taken  from  the  free  ends  of  the  appendicular  canal 
remained  in  perfect  health,  whilst  the  fifteen  drops  of  the  broth  containing  the  bacillus 
from  the  closed  cavity  caused  considerable  oedema  and  loss  of  flesh  in  the  inoculated 
guinea-pig.  On  April  2-1:  the  experiments  were  repeated,  the  cultures  being  on  this 
occasion  four  days  old.  A  guinea-pig  inoculated  with  twenty  drops  of  the  first  broth 
suffered  no  ill-effects,  whereas  another  guinea-pig,  inoculated  with  twenty  drops  of  the 
second  broth,  died  in  thirty-six  hours,  with  an  enormous  phlegmon  of  the  wall,  and  pus 
in  the  pleura,  pericardium,  and  peritoneum. 

I  have  repeated  the  experiments  of  Hartmann  and  Minot  in  my  own 
laboratory  with  Caussade,  and  have  obtained  identical  results. 

For  our  experiments  we  took  an  acute  obhterating  appendicitis  in  which  the  closed 
cavity  was  absolutely  shut  off.  We  treated  two  broths,  the  one  (No.  1)  with  liquid 
taken  from  the  free  part  of  the  canal,  the  other  (No.  2)  with  liquid  taken  from  the 
closed  cavity.  These  broths  were  placed  in  the  oven.  They  contained  quantities  of 
colon  bacilli.  Wc  chose  twelve  guinea-pigs  of  about  the  same  weight,  and  divided  them 
into  two  series  of  six  each.  The  six  guinea-pigs  of  each  series  were  given,  by  injection 
under  the  skin  of  the  abdomen,  fifteen  drops  of  No.  1  broth,  in  the  one  case,  and  in  the 
other  five  drops  of  No.  2  broth.  The  twelve  guinea-pigs  were  not,  however,  inoculated 
at  the  same  time.  They  were  inoculated  two  at  a  time  on  succeeding  days,  the  last 
cultures  being  seven  days  old.  The  guinea-pigs  inoculated  with  No.  1  brotli  showed 
at  the  point  of  inoculation  a  small  indurat(!tl  nodule,  wliich  was  readily  absorbed.  They 
all  remained  in  lo.fect  health,  whilst  the  guinea-pigs  similarly  inoculated  with  No.  2 
brotii  sliowed  gangrenous  abscesses,  witli  pus  containing  tlio  liacillus  coli,  and  all  died 
from  the  infection.     These  experiments  are  therefore  couclusivo. 


742  TEXT-BOOK  OF  MEDICINE 

Manufacture  of  Toxines  in  the  Closed  Cavity.— The  preceding  experi- 
ments, though  conclusive  from  the  point  of  view  of  infection,  gave  no 
precise  information  as  to  the  toxicity  of  the  products  elaborated  in  the 
closed  cavity. 

As  I  was  anxious  to  make  some  experiments  concerning  the  toxicity,  Caussade  and 
I  filtered  the  culture  broths,  and  made  inoculations  with  the  filtered  hquid,  which 
contained  toxines,  but  not  bacilli.  Six  guinea-pigs  were  inoculated,  three  with  the 
filtrate  of  No.  1  broth  and  three  with  the  filtrate  of  No.  2  broth.  Each  guinea-pig 
received  an  injection  of  twenty  drops  of  filtered  broth  :  the  two  guinea-pigs  inoculated 
on  Monday  received  cultures  three  days  old,  those  inoculated  on  Tuesday  cultures  four 
days  old,  and  those  inoculated  on  Wednesday  cultures  five  days  old.  In  no  case  did  the 
inoculation  produce  either  abscess  or  induration. 

The  three  guinea-pigs  inoculated  with  the  filtrate  of  broth  No.  1  remained  alive  and 
well,  but  of  the  three  guinea-pigs  inoculated  with  the  filtrate  of  broth  No.  2  two  died 
on  the  fifth  and  sixth  days  of  the  inoculation.  They  did  not  die  of  infection,  but  of 
intoxication.  The  closed  cavity  is  a  focus  of  infection  and  of  intoxication,  and  the  con- 
clusion is  that  I  was  correct  in  calling  appendicitis  a  toxi-infectious  disease.  This 
explains  a  series  of  complications  which  will  be  studied  under  the  toxicity  of  appendi- 
citis. 

etiology. — As  we  have  discussed  fully  the  role  of  the  closed  cavity  in 
appendicitis,  we  can  pass  on  to  the  aetiology.  We  must  first  consider  the 
question  of  heredity.  Roux,  of  Lausanne,  rightly  maintained  that  appen- 
dicitis is  frequently  hereditary.  My  own  experience  has  shown  me  that 
appendicitis  is  often  seen  in  members  of  the  same  family,  both  in  collateral 
branches  and  in  descendants.  On  a  closer  study  of  the  question  it  has 
seemed  to  me  that  heredity  was  especially  noticeable  in  gouty  families,  and 
in  those  suffering  from  urinary  and  biliary  lithiasis,  so  that  I  would  include 
many  cases  of  appendicular  lithiasis  under  the  gouty  diathesis.  To  quote 
examples  : 

One  of  my  assistants  sometimes  has  renal  colic.  His  father  was  gouty  and  his 
brother  died  of  appendicitis.  A  few  years  ago  one  of  my  colleagues  died  of  diabetes 
and  his  daughter  of  appendicitis.  For  some  time  past  I  have  been  treating  a  family 
in  which  gout,  obesity,  and  diabetes  are  present.  In  this  family  I  know  of  three  cases 
of  appendicitis,  one  of  which,  in  a  child  of  ten  years  of  age,  was  fatal.  One  of  my  best 
friends  had  attacks  of  renal  colic.  His  son  was  attacked  by  appendicitis  ;  he  was 
operated  on  by  Bouilly  and  recovered.  I  know  a  lady  who,  for  the  past  fifteen  years, 
has  been  subject  to  hepatic  cohc,  and,  at  my  request,  her  son  was  operated  on  by 
Routier  for  calculous  appendicitis.  At  Trouville  I  saw,  with  Collet,  a  child  of  five 
years  of  age  taken  ill  with  appendicitis,  who  was  operated  on  by  Pozzi.  The  girl's 
mother  had  attacks  of  hepatic  colic.  In  1895  I  was  called  to  a  lady  of  seventy-two, 
who  was  suddenly  taken  ill  with  calculous  appendicitis.  Routier  operated  at  my 
request.  Two  months  later  it  was  the  fortune  of  her  granddaughter  to  be  operated 
upon,  and  she  also  had  calculous  appendicitis. 

Appendicular  lithiasis  is,  therefore,  a  family  and  hereditary  disease.  It 
is  sometimes  of  arthritic  origin,  and  it  must  therefore  rank  with  biliary  and 
urinary  lithiasis.     I  might  even  say  that  of  the  three  kinds  of  lithiasis,  the 


DISEASES  OF  THE  INTESTINE  743 

appendicular  form  generally  appears  first,  since  it  is  common  in  children. 
It  is  the  more  to  be  feared  because  the  complications  consequent  on  renal 
or  biliary  calculi  are  not  to  be  compared  either  in  gravity  or  frequency  with 
those  resulting  from  appendicular  lithiasis. 

In  other  cases  the  heredity  of  appendicitis  (calculous  or  non-calculous) 
is  manifest  apart  from  any  gouty  diathesis. 

Since  I  drew  attention  to  this  question  of  hereditary  and  family  appen- 
dicitis,* cases  have  multiplied.  Faisans  communicated  to  the  Societe 
Medicale  des  Hopitaux  six  cases  of  family  appendicitis,  in  which  two,  three, 
and  four  persons  of  the  same  family  were  taken  ill  with  appendicitis.  At 
the  same  meeting  Rendu  communicated  similar  cases.  La  Societe  de 
Chirurgie  has  also  found  identical  results  (Brun,  Berger,  Tufiier,  Jalaguier, 
Quenu). 

It  is  possible  that  the  malformations  of  the  appendix  may  also  be  heredi- 
tary (Talamon,  Pozzi),  and  ready  to  favour  the  formation  of  a  closed 
cavity. 

Determining  Causes. — Appendicitis  may  occur  during  pregnancy. 
Metchnikoff  has  blamed  intestinal  worms  and  the  trichocephalus.  Some 
authors  have  assigned  a  part  to  entero-colitis,  as  if  appendicitis  were  the 
result  of  entero-colitis,  but  this  opinion  seems  to  me  erroneous.  I  shall 
discuss  this  question  in  Section  IV.  Influenza  has  been  blamed  (Faisans), 
and  also  measles,  angina,  etc.  I  cannot  agree  with  this  opinion.  It  is 
more  correct  to  say  that  the  primary  cause  of  appendicitis  often  escapes  our 
notice. 

Onset  of  Appendicitis. — Every  intermediate  stage  is  seen  between  an 
insidious  onset,  whicli  is  almost  afebrile  and  painless,  and  a  sudden  onset, 
with  much  fever  and  pain.  As  a  general  rule,  prodromata  rarely  occur,  and 
the  disease  usually  starts  suddenly  in  the  midst  of  excellent  health,  so  that 
on  the  previous  day  there  is  no  suspicion  of  trouble. 

Mild  appendicitis  runs  the  following  course  :  The  patient  has  a  feeling  of 
pain  and  fullness  in  the  belly,  especially  in  the  right  iliac  fossa.  Nausea  or 
vomiting  is  generally  present,  but  the  fever  is  insignificant,  and  the  patient 
fancies  that  he  is  suffering  from  indigestion.  He  takes  a  purgative  and  an 
enema,  because  his  intestinal  functions  are  not  normal.  A  physician  is 
called  in.  The  patient  speaks  of  constipation  and  nausea,  and  calls  atten- 
tion to  the  pain  in  the  right  iliac  fossa.  "  Quite  so,"  says  tlie  doctor.  '"  I 
find  some  induration  and  tension."  And  if  the  physician  in  question  still 
believe  in  typhlitis,  he  will  diagnose  stercoral  typhlitis  or  CMJcal  obstruction, 
and  prescribe  "  a  purgative,"  or  even  leeches. 

In  other  cases  the  pain  rapidly  becomes  very  severe  in  the  right  iliac 

*  Diculafoy,  "  Cours  de  Pathologic  liitorno  dc  la  Faculty  <le  Paris  "  {Semestre. 
d'Hiver,  Novembre,  189")). 


744  TEXT-BOOK  OF  MEDICINE 

fossa,  though  it  may  radiate  in  various  directions.  The  fever  is  about  103°  F. 
or  more.  Vomiting,  especially  of  bile,  occurs.  A  doctor  is  called  in,  and  if 
he  is  imbued  with  the  old  and  false  ideas  which  I  have  tried  to  fight  against, 
he  declares,  after  having  examined  his  patient,  that  the  case  is  one  of  "  appen- 
dicular colic."  By  this  he  means  that  a  calculus  coming  from  the  caecum 
has  got  into  the  appendicular  canal,  and  provokes  pain,  accompanied  by 
nausea  and  vomiting. 

I  have  spoken  strongly  about  this  fatal  theory.  Rochaz  has  proved 
that  the  calculi  do  not  enter  the  narrow  lumen  of  the  appendix.  The  pain 
is  not  caused  by  the  passage  of  the  calculus,  and  "  appendicular  colic  "  in 
this  sense  does  not  exist.  As  this  term  perpetuates  an  error,  it  must  be 
abandoned.  It  is  as  incorrect  to  speak  of  appendicular  colic  as  it  is  erroneous 
to  admit  the  old  conception  of  typhlitis.  To  what,  then,  is  the  acute  pain 
at  the  onset  of  appendicitis  due  ?  There  can  as  yet  be  no  question  of 
perforation  or  of  peritonitis.  The  pain,  as  well  as  abdominal  distension, 
muscular  resistance,  nausea,  constipation,  and  vomiting,  result  from  the 
formation  of  the  closed  cavity,  and  from  the  toxi- infection  which  follows  it. 
The  course  of  events  in  the  appendix  is  similar  to  that  in  the  middle  ear, 
which  is  converted  into  a  closed  cavity  when  the  Eustachian  tube  is  blocked. 
As  soon  as  the  tube  is  obliterated,  the  microbes  which  have  entered  the  middle 
ear  increase  in  virulence,  and  acute  otitis  comes  on,  with  violent  pains,  which 
radiate  in  various  directions.  Otitis  often  terminates  without  perforation 
of  the  membrane  or  other  complications  if  the  Eustachian  tube  becomes 
permeable  once  more,  either  by  natural  or  artificial  means.  If  the  obstacle 
is  removed,  the  free  outflow  of  the  infective  matter  puts  an  end  to  the 
dangers  of  the  closed  cavity.  If  the  obstruction  persists,  the  microbes 
imprisoned  in  the  cavity  may  increase  in  virulence  to  such  a  degree  that 
complications  may  arise.  The  perforation  of  the  membrane  is  analogous 
to  that  of  the  appendix.  Phlebitis  of  the  lateral  sinus  and  jugular  vein  is 
analogous  to  appendicular  phlebitis.  Meningitis  is  analogous  to  appen- 
dicular peritonitis,  while  the  abscesses  in  the  cerebrum  and  cerebellum,  and 
even  remote  abscesses  in  the  opposite  cerebral  hemisphere  or  elsewhere,  are 
analogous  to  the  remote  abscesses  in  the  liver  or  spleen,  which  are  secondary 
to  appendicitis. 

The  complications  are  therefore  absolutely  analogous  in  acute  otitis  and 
in  appendicitis.  The  closed  cavity  and  the  appendicular  infection  cause 
acute  pains  in  the  abdomen,  which  were  formerly  mistaken  for  colic  caused 
by  the  passage  of  the  calculi.  They  also  cause  the  attacks  of  nausea  and 
vomiting,  as  in  strangulated  hernia.  It  is  the  closed  cavity  and  the 
appendicular  toxi-infection  which  cause  the  early  collapse,  and  add  to  the 
gravity  of  the  disease,  whilst  they  are  also  the  origin  of  diffuse  or  encysted 
peritonitis,  even  when  the  appendix  has  not  been  perforated.     Again,  the 


DISEASES  OF  THE  INTESTINE  745 

closed  cavity  and  the  appendicular  infection  are  the  points  from  which  the 
microbes  spread  to  the  liver,  spleen,  and  lungs,  and  these  same  two  factors 
cause  the  degeneration  of  the  cells  of  the  liver  (urobilinuria,  icterus,  icterus 
gravis)  and  kidney  (albuminuria,  anuria,  uraemia),  as  well  as  the  erosions 
in  the  stomach,  with  copious  hgematemesis,  etc.  Thus,  from  the  very  outset, 
and  prior  even  to  the  appearance  of  the  peritoneal  lesions,  the  appen- 
dicular toxi-infection  reveals  its  presence  by  some  of  the  troubles  just 
enumerated. 

It  is  the  pain  which  is  our  most  certain  guide,  for,  sharp  or  slight,  it 
always  has  certain  characteristics  in  appendicitis. 

The  pain  rarely  reaches  its  maximum  at  first,  and  thus  differs  from  the 
sudden  and  terrible  pain  (peritoneal  dagger-thrust)  due  to  perforation  of  a 
duodenal  or  gastric  ulcer.  The  pain  in  appendicitis  occupies  the  middle  of 
a  line  drawn  from  the  umbilicus  to  the  anterior  superior  iliac  spine  on  the 
right  side  (McBurney's  point).  This  region  must  be  examined  with  the 
greatest  care,  and  even  when  the  pains  are  slight,  or  preceded  by  pains  in 
the  epigastric  region  or  elsewhere,  or  even  when  they  radiate  to  other  points 
of  the  abdomen,  it  is  possible  by  means  of  careful  palpation  to  provoke  or 
increase  the  pain  in  the  appendicular  area  or  in  its  vicinity.  The  under- 
lying muscle  is  more  rigid  than  at  other  points.  This  muscular  resistance 
is  an  excellent  sign,  and  at  the  same  spot  we  may  find  another  sign  to  which 
I  attribute  great  value — viz.,  hyperaesthesia  of  the  skin  over  the  appendix. 
If  the  skin  is  stroked  gently  with  the  pulp  of  the  finger,  hyperaesthesia, 
which  exists  nowhere  else  over  the  abdomen,  will  be  found,  and  this  symp- 
tom is  at  times  accompanied  by  reflex  cramps  in  the  underlying  muscles. 

Summary.  —  Pain  at  McBurney's  point,  muscular  resistance,  hyper- 
aesthesia, nausea,  vomiting,  and  fever,  usually  mark  the  onset  of  appen- 
diciti.s. 

Course  of  Appendicitis. — Will  a  slight  or  violent  attack  of  appendicitis 
that  is  of  one  or  two  days'  duration,  remain  limited  to  the  appendix,  or 
will  it  be  followed  by  peritoneal  infection  and  toxic  complications  ?  Let 
us  examine  these  various  eventualities.  Sometimes  a  sharp  or  slight  attack 
of  appendicitis  ends  favourably,  and  after  a  few  days  of  pain,  with  moro  or 
less  frequent  attacks  of  vomiting,  the  fever  decreases,  constipation  ceases, 
and  the  right  iliac  fossa  is  less  sensitive  and  distended,  while  the  muscles 
become  relaxed,  and  the  patient  recovers.  What  has  happened  ?  Either 
tlie  microbes  causing  the  trouble  were  endowed  with  but  feeble  resistance, 
or  the  enemy  has  been  vanquished  ])y  phagocytosis ;  or  else  the  obstruction 
of  the  appendix  has  given  way  rapidly,  the  closed  cavity  no  longer  exists, 
free  circulation  is  re-established  in  the  canal,  and  the  appendicitis  is  cured, 
as  acute  otitis  is  cured  when  the  Eustachian  tube  recovers  its  permeability 
in  time. 


746  TEXT-BOOK  OF  MEDICINE 

In  other  cases  the  attack  is  more  severe,  and  the  pain  in  the  right  iliac 
fossa  is  more  intense  and  persistent.  The  distension  of  the  abdomen  is 
more  general,  and  the  vomiting  more  frequent;  but  yet  the  condition 
gradually  becomes  normal.  Convalescence,  however,  is  slow,  and  the 
patient  shows  traces  of  the  appendicitis  in  the  iliac  fossa  for  a  long  time. 
He  suffers  from  constipation,  and  is  afraid  to  shoot  or  ride,  and  if  he  decides 
later  upon  an  operation  during  the  quiescent  stage,  we  find  adhesions,  peri- 
appendicular peritonitis,  an  enlarged  appendix,  or  at  times  a  small  encysted 
abscess,  or  even  an  imminent  perforation  of  the  appendix.  All  surgeons 
have  seen  cases  of  this  kind.  I  have  noticed  them  myself  several  times.  I 
examined  the  appendix  of  a  boy  upon  whom  Koutier  operated  at  my  request 
in  the  Necker  Hospital.  He  went  to  work,  although  he  had  a  peri- appen- 
dicular abscess  resulting  from  acute  appendicitis. 

We  often  see  cases  in  which  appendicitis  ends  very  quickly  in  gangrene. 
The  illness  is  ushered  in  by  fever  and  pam.  Ice  is  placed  on  the  painful 
region,  and  injections  of  morphia  are  given,  while  hope  is  entertained  of 
being  able  to  limit  the  disease.  In  two  or  three  days  the  appendix  becomes 
gangrenous,  and  the  patient  dies  from  toxi-infection,  either  because  he  has 
not  undergone  an  operation,  or  because  the  operation  has  been  performed 
too  late.     I  could  cite  many  cases  of  this  kind. 

In  other  cases  appendicitis  seems  to  run  a  favourable  course,  and  is 
allowed  to  "  get  cold."  The  partisans  of  "  cooling  "  congratulate  them- 
selves, and  it  is  sometimes  whilst  they  are  quietly  contemplating  this 
"  cooling "  that  the  catastrophe  occurs.  The  recent  communication  of 
Legueu  to  the  Societe  de  Chirurgie  proves  this  point : 

Legueu  showed  the  perforated  appendix  of  a  child  of  five  years  of  age  who  succumbed 
suddenly  whilst  the  disease  was  "  coohng."  He  was  treated  medically  in  a  service 
where  early  surgical  intervention  has  been  systematically  banished.  This  "  coohng  " 
had  been  going  on  for  five  days,  and  his  general  condition  was  excellent  when  he  was 
taken  suddenly  ill  with  vomiting ;  the  pulse-rate  rose,  the  stomach  became  distended, 
and  the  extremities  grew  cold.  In  a  few  hours  he  was  dead,  before  there  was  time  to 
operate.  The  post-mortem  examination  showed  the  perforated  appendix  lying  in  a 
deep-seated  abscess,  which  was  separated  from  the  abdominal  wall  by  several  coils 
of  bowel.  The  abscess  had  burst  into  the  peritoneal  cavity,  causing  acute  peritonitis. 
It  is  probable,  adds  Legueu,  as  his  sole  commentary,  that  an  operation,  as  soon  as  the 
diagnosis  was  made,  would  have  saved  the  patient. 

Hartmann  has  described  an  analogous  case  : 

A  woman  suffering  from  acute  appendicitis  was  placed  under  my  care.  The  symp- 
toms were  improving,  and  it  was  thought  that  "  coohng  "  might  be  safely  awaited. 
After  some  days  passed,  the  situation  suddenly  became  so  bad  that  surgical  intervention 
was  impossible.  The  post-mortem  examination  showed  recent  general  peritonitis, 
and  a  large  retrocaecal  abscess  containing  the  gangrenous  and  perforated  appendix. 

I  must  now  mention  the  two  chief  forms  of  appendicitis — namely, 
appendicitis  accompanied  by  peritonitis  and  toxic  appendicitis. 


DISEASES  OF  THE  INTESTINE  747 

Appendicular  Peritonitis. — When  appendicitis  commences,  we  can  never 
be  sure  of  its  course.  The  disease  may  remain  limited  to  the  appendix. 
In  this  case  the  peritoneum  is  not  affected,  and  the  patient  recovers  from 
his  attack.  The  appendix,  however,  remains  normal,  but  may  become 
sooner  or  later  the  origin  of  fresh  mischief.  In  other  cases  the  process  is 
not  Hmited  to  the  appendix,  and  the  peritoneum  is  attacked,  but  only  to 
a  very  slight  extent.  The  peritonitis  is  then  strictly  limited.  Adhesions 
are  then  formed  between  the  appendix  and  the  neighbouring  parts,  and 
may  serve  to  limit  the  mischief  in  case  of  fresh  attacks.  Finally,  we  see 
many  cases  in  which  appendicitis  ends  in  diffuse  or  partial  peritonitis. 

Peritonitis  is  said  to  be  diffuse  when  it  spreads  without  showing  any 
tendency  to  become  encysted.  The  intestinal  coils  are  sometimes  sticky 
and  dull-looking  ;  the  exudate  is  scanty,  russet  in  colour,  and  thin.  It  is 
then  almost  always  a  question  of  acute  septic  peritonitis,  which  is  very 
rapid  in  its  course.  Sometimes  the  peritoneal  fluid  is  abundant,  and  more 
or  less  purulent,  while  false  membranes  float  in  the  effusion,  and  form  bands 
between  the  intestinal  coils.  This  purulent  variety  is  chiefly  seen  in  cases 
of  some  duration.  Peritonitis  may  occur  very  early,  and  appear  on  the 
second  day  of  appendicitis  ;  but  at  other  times  it  supervenes  later,  during 
the  first  or  second  week. 

Erroneous  ideas  have  been  long  prevalent  concerning  the  pathogenesis 
of  these  fornxs  of  peritonitis,  and  I  have  tried  to  rectify  these  errors.  They 
were  formerly  considered  to  be  due  to  perforation,  and  two  stages  were 
described — the  appendicular  stage,  with  symptoms  of  appendicitis  ;  and  the 
peritoneal  stage,  with  symptoms  of  peritonitis.  Talamon  says  :  "  In  appen- 
dicitis there  are  generally  two  distinct  periods — the  preparatory  period 
before  perforation,  which  I  propose  to  call  the  period  of  appendicular  colic  ; 
and  the  peritoneal  phase,  which  follows  the  rupture  of  the  appendix." 

The  question  was  simplified  when  thus  presented,  but  the  misfortune  is 
that  events  run  quite  a  different  course. 

In  the  first  place,  perforation  of  the  appendix  is  not  necessary  for  the 
production  of  peritonitis.  In  many  ca.ses,  no  doubt,  the  appendix  is  affected 
by  suppuration,  gangrene,  or  perforation,  and  the  residue  of  the  appendicular 
focus  discharges  itself  into  the  peritoneum.  Often,  however,  no  perforation 
is  found  in  the  appendix.  We  have  all  seen  such  cases,  and  the  peritonitis 
is  due  to  the  passage  of  microbes  through  the  walls. 

Furthermore,  while  there  are  cases  in  which  the  symptoms  of  peritonitis 
arise  with  the  suddenness  of  peritonitis  from  perforation,  there  are  others — 
and  in  my  opinion  they  are  the  more  numerous — in  which  it  is  difficult  to 
define  the  exact  onset  of  peritonitis. 

It  would  be  wrong,  therefore,  to  suppose  that  the  appendicular  and 
peritoneal  stages  are  always  distinct,  and  to  say  that  peritonitis  is  always 


748  TEXT-BOOK  OF  MEDICINE 

ushered  in  by  a  symptom-complex  which  allows  us  to  foresee  the  danger. 
It  is  often  impossible  to  recognize  at  what  moment  the  peritoneal  symptoms 
appear,  for  they  are  often  blended  with  the  appendicular  symptoms.  Pain, 
vomiting  of  food  and  bile,  changes  in  the  temperature  and  the  pulse,  con- 
stipation and  tympanites,  may  all  be  present,  whether  the  peritoneum  is 
affected  or  not.  We  watch  for  the  onset  of  peritonitis  when  it  is  already 
present ;  we  delay  when  we  ought  to  act ;  and  the  patient  succumbs  because 
we  have  not  operated. 

In  many  cases  the  peritonitis  is  encysted,  and  may  then  occupy  the 
most  diverse  situations  in  the  abdomen.  The  direction  of  the  normal 
appendix  prior  to  the  disease  (descendmg,  ascending,  or  retrocsecal  tj'^e), 
and  old  or  recent  adhesions  due  to  former  attacks,  explain  the  localization 
of  the  peritonitis  and  its  tendency  to  become  encysted,  and  to  give  rise  to 
ileo-inguinal,  retroceecal,  prerectal,  or  peri-umbilical  abscesses,  known  as 
iliac  phlegmon  and  perityphlitis  by  older  writers. 

The  ileo-inguinal  abscess  constitutes  the  most  common  variety.  The  pus 
is  found  in  the  right  iliac  fossa,  above  Poupart's  ligament.  It  is  bounded 
by  the  antero-internal  surface  of  the  caecum,  and  the  coUs  of  the  small 
intestine,  and  corresponds  on  the  belly  to  a  line  situated  a  little  above  the 
ligament,  and  internal  to  the  antero-superior  iliac  spine. 

The  prerectal  abscess  is  much  less  frequent  than  the  preceding  variety. 
In  some  cases  the  appendix  reaches  downwards  and  inwards  in  front  of  the 
rectum.  In  this  case  encysted  peritonitis  may  occur  between  the  rectum 
and  the  bladder  in  the  male,  and  between  the  rectum  and  the  vagina  in 
the  female.  Digital  examination  of  the  vagina  and  rectum  gives  informa- 
tion as  to  the  existence  and  situation  of  the  purulent  collection,  which  may 
open  spontaneously  into  the  rectum,  bladder,  or  vagina. 

A  few  cases  of  peri-umbilical  abscess  have  been  noted.  If  the  appendix 
is  displaced  inwards  in  front  of  the  caecum,  the  adhesions  favour  the 
limitation  of  the  collection  above  and  internal  to  the  iliac  fossa,  near  the 
umbilicus. 

It  is  of  the  utmost  importance  to  bear  in  mind  the  retrocsecal  abscess. 
In  many  cases  the  appendix  in  its  normal  state  ascends  behind  the  caecum 
as  far  as  the  colon.  It  may  even  be  fixed  in  this  region  by  adhesions  left 
by  former  attacks.  In  such  a  case,  pus  may  collect  behind  or  around  the 
caecum,  and  point  in  the  costo-iliac  space  or  in  the  lumbar  region  above  the 
iliac  crest.  If  the  appendix  has  a  mesentery,  the  abscess  may  develop  in 
the  subperitoneal  cellular  tissue,  above  the  iliac  fascia.  In  this  region  the 
peritoneal  abscess  readily  becomes  cellular,  and  the  varieties  may  be  con- 
founded.    Let  me  also  draw  attention  to  appendicular  psoitis. 

The  retrocsecal  abscess,  bounded  in  front  by  the  caecum  and  ascending 
colon,  may  sjjread  in  different  directions,  and  cause  the  following  varieties  : 


DISEASES  OF  THE  INTESTINE  749 

It  often  opens  into  the  caecum.  I  would  again  remark  that  many  cases 
formerly  considered  as  examples  of  typhlitis  ending  in  perforation  of  the 
caecum  and  in  perityphlitis  are  really  caecal  and  pericaecal  lesions  resulting 
from  a  primary  lesion  in  the  appendix.  This  variety  of  retrocaecal  abscess 
may  also  empty  itself  into  the  ascending  colon.  In  other  cases  the  retro- 
caecal abscess  is  directed  towards  the  inferior  surface  of  the  diaphragm  as 
a  subphrenic  abscess,  and  may  cause  perforation  of  the  diaphragm,  with 
empyema  and  vomica,  as  described  under  Appendicular  Pleurisy.  Finally, 
the  retrocaecal  abscess  may  spread  into  the  iliac  fossa,  and  open  into  the 
bladder,  rectum,  or  vagina,  or  pass  into  the  inguinal  canal  and  scrotum. 

I  may  note  also  perinephritic  abscess.  Brun  has  reported  a  case  of 
fatal  peritonitis  from  perforation  of  the  abscess  in  the  cavum  Retzii.  The 
abscess  was  secondary  to  perforating  appendicitis. 

These  are  the  principal  varieties  of  abdominal  abscess  due  to  appen- 
dicitis. Spontaneous  rupture  into  the  intestine  is  followed  by  recovery,  if 
the  diseased  appendix  has  been  destroyed ;  in  the  contrary  case,  a  fresh 
attack  of  appendicitis  may  supervene  (as  in  a  case  which  I  saw  with  Pozzi) 
a  few  months  after  the  spontaneous  opening  of  a  retrocaecal  abscess  into  the 
intestine.  Do  not  let  us  forget,  too,  that  an  encysted  abscess  may  subse- 
quently open  into  the  peritoneum,  and  cause  general  peritonitis. 

General  peritonitis  is  more  formidable  than  the  localized  form.  These 
varieties  of  peritonitis  are  due  to  the'toxi-infection  elaborated  in  the  appen- 
dix, although  it  is  impossible  at  present  to  assign  a  special  role  to  any  one 
microbe. 

Appendicular  peritonitis,  especially  in  encysted  cases,  is  often  of  a  very 
foitid  odour,  even  in  the  absence  of  gangrene  ;  and  yet  we  cannot  say  that 
it  is  putrid,  because  it  has  none  of  the  characteristics  of  putridity,  and  gas 
does  not  form.  It  is  by  an  abuse  of  language  that  these  cases  of  peritonitis 
are  labelled  putrid  when  they  are  only  foetid.  The  operator,  on  opening 
the  peritoneal  cavity,  is  struck  by  the  evil  odour  of  the  liquid,  and  speaks 
of  putrid  peritonitis. 

If  peritonitis  is  to  merit  the  term  "  putrid,"  the  symptoms  should  bo 
like  those  of  putrid  pleurisy.  We  ought,  on  opening  the  peritoneum,  at-  on 
opening  the  pleura,  to  find  a  mixture  of  liquid  and  gas.  Such  is  not  the 
case.  The  abdominal  wound,  like  the  thoracic  one,  should  be  liable  to 
invasion  by  gaseous  phlegmon.  This  is  not  so.  Cultures  of  the  peritoneal 
fluid,  like  those  of  the  pleural  effusion,  should  be  capable  of  producing  gas  ; 
and  inoculation  of  peritoneal  pus,  like  inoculation  of  pleural  pus  in  the 
guinea-pig,  should  cause  a  gaseous  phlegmon ;  but  this  result  is  not  seen. 

I  have  tried  in  vain  to  find  a  case  of  putrid  peritonitis,  whereas  cases 
of  putrid  pleurisy  are  counted  by  dozens.  And  when  putrid  pleurisy  follows 
a  pre-existing  peritonitis,  as  in  appendicitis,  we  find  that  the  pleurisy  is 


750  TEXT-BOOK  OF  MEDICINE 

frequently  putrid,  whereas  the  peritonitis  is  not.  And  yet  both  the  peri- 
tonitis and  the  pleurisy  have  the  same  origin,  and  appear  to  be  due  to  the 
same  microbes.     What,  then,  is  the  explanation  ? 

Although  this  fact  is  paradoxical,  it  exists,  nevertheless.  I  might  even 
say  that  it  is  the  rule.  In  the  chapter  on  Appendicular  Purulent  Pleurisy 
we  find  pneumothorax,  pyopneumothorax,  and  the  issue  of  gas  during  the 
operation,  whilst  similar  signs  of  putrefaction  in  the  case  of  peritoneum  are 
nowhere  described. 

I  am  not  speakmg  here  of  subphrenic  pyopneumothorax,  which  is  almost 
always  associated  with  the  perforation  of  a  neighbouring  organ.  I  am  not 
speakmg,  of  course,  of  the  case  where  gas  passes  into  the  peritoneum  through 
a  perforation  of  the  mtestitie.  This  is  peritoneal  pneumatosis  by  perfora- 
tion, comparable  to  pneumothorax  by  perforation.  In  both  cases  the 
presence  of  gas  is  caused  by  effraction,  and  this  has  nothing  to  do  with  the 
formation  of  gas  in  putrid  fluids.  This  fact  is  so  true  that  if  an  operator, 
on  opening  the  peritoneal  cavity  for  appendicitis,  notices  the  presence  of 
gas,  he  immediately  looks  for  a  perforation  in  the  caecum  or  elsewhere. 

I  am  not  sorry  to  make  a  parenthesis  on  this  topic,  and  I  have  shown 
by  the  clearest  proofs  that  the  toxi-infectious  focus  is  produced  in  the 
closed  cavity  of  the  appendix.  I  am  now  able  to  add  a  further  proof  in 
support  of  my  views.  The  frequency  of  gangrene  and  perforation  in  the 
course  of  appendicitis  is  well  known.  If  the  focus  were  not  produced  in 
the  closed  cavity,  or  if  it  communicated  freely  with  the  csecum,  as  has  been 
incorrectly  maintained,  the  mtestmal  gases  would  pass  into  the  peritoneum, 
and  would  cause  pyopneumoperitonitis,  which  is  not  the  case. 

I  have  still  a  few  words  to  add  on  peritoneal  infection  of  appendicular 
origm.  In  the  long  ascending  track  oi  infection  which  starts  from  the 
appendix,  climbs  into  the  peritoneal  cavity,  and  ends  in  the  pleura,  I  see 
three  stages  which  differ  according  to  the  nature  of  the  lesions.  The  chief 
lesion  in  the  appendix  is  mortification ;  fcetor  is  the  chief  symptom  in  the 
peritoneum,  and  putrefaction  is  the  chief  process  in  the  pleura.  And  yet 
we  find  the  same  microbes  m  all  three  stages,  thus  showing  how  premature 
are  conclusions  as  to  the  action  of  certain  microbes  in  appendicular  toxi- 
infection.  We  must  consider  not  only  the  quality  of  the  microbes,  but  also 
the  soil  in  which  they  live. 

It  is  to  be  remarked  that  the  process  of  putrefaction  does  not  take  place 
in  the  peritoneum,  but  in  the  pleura,  which  is  in  close  relation  with  the 
air-passages.  We  have,  therefore,  two  large  serous  membranes — the  peri- 
toneum and  the  pleura — inoculated  with  similar  micro-organisms  in  appen- 
dicitis. The  former  does  not  lend  itself  to  putrefaction,  though  it  is  pro- 
tected from  all  contact  with  the  air-passages ;  while  the  latter  lends  itself 
marvellously,  though  everywhere  it  is  m  most  intimate   contact  with  the 


DISEASES  OF  THE  INTESTINE  751 

air-passage.  I  am  content  to  draw  attention  to  this  fact,  which  does  not 
tally  with  our  knowledge  of  anaerobes,  which  become  more  active  in  the 
absence  of  air.     The  reason  has  still  to  be  discovered. 

In  order  to  finish  the  description  of  appendicular  peritonitis,  I  have 
still  to  speak  of  secondary  foci,  which  seem  sometimes  to  have  no  anatomical 
comiection  with  the  initial  focus.  These  remote  foci  (Tuffier)  resemble 
those  we  sometimes  meet  with  as  a  consequence  of  otitis  in  the  cerebral 
hemisphere  or  cerebellum  on  the  diseased,  or  even  on  the  opposite,  side. 
These  abscesses  are  due  to  microbes,  which  are  carried  to  a  distance  from 
the  place  of  origin.  Sometimes  the  secondary  abscess  is  already  present 
when  laparotomy  is  performed  for  peritoneal  symptoms,  but  at  other  times 
it  only  appears  one,  two,  or  three  weeks  after  the  cure  of  the  appendicitis. 
These  secondary  foci  are  usually  found  in  the  most  internal  and  inferior 
portion  of  the  caecal  region,  near  the  bladder.  In  a  patient  convalescent 
from  appendicitis  Tuffier  noticed  and  opened  a  remote  abscess  in  the  external 
oblique  muscle.  Routier  has  reported  four  cases  of  secondary  abscess, 
appearing  nine,  fourteen,  sixteen,  and  twenty-five  days  after  laparotomy. 
The  complications  usually  arise  in  the  following  way  :  the  patient  has 
undergone  the  operation,  and  everything  is  going  on  well.  Cure  appears 
certain,  when  new  and  alarming  symptoms  appear.  Sometimes  the  symp- 
toms clearly  indicate  the  formation  of  a  fresh  peritoneal  abscess,  which  is 
readily  diagnosed ;  at  other  times  the  symptoms  simulate  those  of  acute 
phthisis  or  typhoid  fever,  and  the  abscess  develops  behind  the  caecum, 
transverse  colon,  or  stomach,  or  in  the  left  iliac  fossa,  etc. 

Another  important  complication  is  secondary  perforation  of  the  intes- 
tine. In  addition  to  the  appendiculo-peritoneal  focus,  it  is  not  rare  to  find 
(especially  in  patients  who  have  been  operated  on  somewhat  late)  violet  or 
blackish  gangrenous  patches  on  the  caecum  and  colon.  These  lesions  often 
pass  unnoticed  at  the  operation,  and  all  danger  seems  passed,  when  gas  and 
matter  make  their  exit  through  the  wound.  Secondary  perforation  of  the 
gut  has  then  taken  place. 

Infection  of  the  Liver,  Pleura,  etc. — To  complete  the  description  of 
secondary  infections  due  to  appendicitis,  I  have  still  to  describe  purulent 
infection  of  the  liver  and  purulent  and  putrid  infection  of  the  pleura.  In 
view  of  the  great  importance  of  this  question,  I  have  devoted  three  special 
sections  to  it  under  Disease  of  the  Liver  and  of  the  Pleura. 

Toxic  Appendicitis— Appendicaemia. — I  have  so  far  described  the 
infective  lesions,  but  there  is  another  factor  with  which  wo  have  not 
reckoned — viz.,  the  toxines  found  in  the  appendicular  focus,  with  all  the 
complications.  This  focus  is  not  oidy  favourable  to  an  increased  virulence 
of  the  microbes,  but  serves  also  for  the  manufacture  of  toxines.  Clinical 
study  has  confirmed  the  experiments  of  the  laboratory,  and  has  furnished 


752  TEXT-BOOK  OF  MEDICINE 

me  with  irrefutable  proofs  as  regards  the  toxicity  of  appendicitis.  Thus 
are  now  explained  the  grave  and  fatal  complications,  the  cause  and  genesis 
of  which  were  formerly  unknown. 

If  I  am  not  mistaken,  it  was  from  the  rostrum  of  the  Academic  that 
the  idea  of  toxic  appendicitis  was  first  well  established.*  Since  then  I  have 
never  ceased  to  study  the  effects  of  the  poison  on  the  liver,  stomach,  kidneys, 
etc.  Thence  came  the  idea  of  toxic  appendicitis,  which  pours  its  poison  into 
the  blood,  and  leads  to  a  toxaemia  which  I  have  called  appendicsemia. 

We  shall  have  in  future  to  consider  albuminuria,  icterus,  and  hsema- 
temesis,  which  all  belong  to  appendicitis. 

Kidneys. — I  commenced  a  systematic  search  for  albummuria  in  acute 
appendicitis,  and  found  it  present  in  a  large  number  of  cases  even  early  in 
the  disease.  The  toxine  may  afiect  the  kidneys  by  the  second  day.  Some- 
times the  amount  of  albumin  is  small ;  at  other  times  it  amounts  to  10  or 
15  grains.  Generally  (and  I  am  speaking  of  successful  cases)  albuminuria 
which  has  been  marked  prior  to  the  operation  disappears  after  removal  of 
the  appendix. 

A  more  serious  point  is  that  from  the  onset  of  appendicular  nephritis 
granular  casts  may  be  noticed  in  the  urme.  The  lesions  in  these  varieties 
will  be  studied  under  Appendicular  Kidney, 

Liver. — In  some  patients  with  acute  appendicitis  of  moderate  intensity 
slight  jaundice  is  noticed  from  the  first.  It  must  be  carefully  looked  for, 
and  is  particularly  noticeable  in  the  conjunctivae.  The  skin  of  the  face  is 
earthy  and  of  a  salmon  tint.  Cases  of  this  appendicular  jaundice  will  be 
found  under  Lesions  of  Liver,  Stomach,  and  Kidney,  due  to  Appendicitis. 

This  early  toxic  jaundice  is  rarely  due  to  the  presence  of  true  bile 
pigments,  but  depends  chiefly  on  the  false  pigments  (urobilin)  which  are 
found  in  the  urine  on  chemical  and  spectroscopic  analysis.  In  appen- 
dicitis jaundice  may  appear  as  an  isolated  symptom  or  be  associated  with 
other  toxic  symptoms.  It  may  even  run  the  course  of  icterus  gravis.  I 
shall  describe  this  toxic  hepatitis  under  Diseases  of  the  Liver. 

Stomach. — The  vomiting  noticeable  in  appendicitis  may  be  caused 
not  only  by  the  appendicitis  or  the  concomitant  peritonitis,  but  may  also 
be  due  to  toxic  gastritis,  accompanied  in  some  cases  by  erosions  of  the 
stomach.  In  such  cases  blackish  streaks  will  be  seen  in  the  vomited  matter, 
indicating  slight  hsematemesis.  Only  too  often,  however,  repeated  attacks 
of  hsematemesis  occur,  and  are  of  exceedingly  grave  prognosis.  I  have 
called  them  appendicular  vomito  negro. 

Albuminuria,  icterus,  oliguria,  haemorrhage,  and  haematemesis  are  not 
always  present  together.     They  are  sometimes  isolated,  or  at  other  times 

*  Dieulafoy,  "  Toxicite  de  I'Appendicite  "  {Academie  de  Medecine,  1898,  et  Clinique 
Medicale  de  I'Hotel-Dieu,  1899,  l?"^^  Le^on). 


DISEASES  OF  THE  INTESTINE  753 

appear  i)i  succession  or  iii  combination.     The  prognosis  is  more  or  less  grave, 
according  to  the  particular  complication. 

Nervous  Troubles. — The  appendicular  intoxication  is  revealed  by 
nervous  troubles  simulating  meningitis  (epileptiform  convulsions,  coma), 
with  or  without  icterus  gravis,  and  with  or  without  uraemia. 

In  one  of  Renon's  cases  the  patient,  who  was  deeply  poisoned,  succumbed,  with 
bulbar  symptoms :  acute  dyspnoea,  cyanosis  of  the  face  and  extremities,  asphyxia, 
and  syncope.  In  consuUation  with  Legry  and  Hartmann  I  saw  a  woman  suffering 
from  gangrenous  appendicitis  and  peritonitis.  On  the  evening  after  operation  the 
patient  felt  relieved,  and  next  day  showed  an  improvement.  On  the  third  day  there 
was  sUght  jaundice,  and  on  the  fourth  Hartmann  found  that  the  patient  had  a  strange 
look.  She  was  not  clear  in  her  replies,  and  by  noon  was  miconscious,  rei^eating  the 
same  words  continually,  and  uttering  inarticulate  cries.  I  se,w  her  at  seven  in  the 
evening,  when  she  lay  motionless,  with  her  eyes  fixed,  uttering  a  short,  strident  cry 
at  intervals.  The  loss  of  consciousness  was  complete,  the  pupils  were  equal,  and  the 
respiration  was  shghtly  accelerated.  Ocular  paralysis,  facial  palsy,  hemiplegia,  and 
contractures  were  absent.  These  negative  symptoms  eliminated  any  idea  of  meningitis, 
and  the  patient  succumbed  the  next  day  from  cerebral  intoxication.  Marchant,  to 
whom  I  spoke  about  the  case,  told  me  of  a  similar  one  in  a  young  girl  operated  upon 
for  appendicular  peritonitis.  The  result  of  the  operation  was  excellent  when,  two 
days  later,  sUght  jaundice  of  the  conjunctivae  was  noticed.  The  restlessness  com- 
menced in  the  evening  with  involuntary  movements  of  the  head.  The  patient  uttered 
cries  at  intervals,  lost  consciousness,  and  succumbed  during  the  following  day,  \vithout 
fever  or  acceleration  of  the  pulse.     Death  in  this  case  was  due  to  intoxication. 

Such  are  the  toxic  nervous  complications.  They  must  not  be  con- 
founded with  cerebral  complications  of  an  infectious  origin  (ab.scess  of  the 
brain),  for  these  remote  infections  are  slower  than  the  toxic  coraphcations. 

Summary. — Clinical  study  and  laboratory  experiments  agree  in  demon- 
strating the  toxicity  of  appendicitis.  The  intoxication  may  be  slight  or 
intense  and  fatal.  The  poisonhig  is  slight  when  it  is  confined  to  transient 
changes  in  the  liver  and  kidneys,  and  when  it  does  not  show  itself  by  icterus 
and  albuminuria.  The  intoxication  is  then  not  very  formidable,  but  in 
appendicitis  we  never  know  what  may  happen.  The  first  sign  of  intoxica- 
tion must  sound  the  alarm,  and  we  may  fear  the  worst  if  icterus  gravis, 
uraemia,  copious  hajniatemesi,'-',  or  nervous  com])lications  supervene.  Val- 
mont's  patient  died  on  the  third  day  with  symptoms  of  icterus  gravis.  The 
patient  whom  I  saw  with  Hartmann  and  Legry  was  much  improved  by  the 
operation,  but  the  appearance  of  icterus  gravis  was  followed  by  symptoms 
of  cerebral  intoxication  and  death.  G.  Marchant's  patient  was  carried  off 
under  similar  conditions,  and  a  patient  of  Routier  with  epilejjtiform  symp- 
toms died  in  coma.  In  the  case  of  a  patient  whom  I  saw  with  Gros  and 
Cazin  the  toxic  phase  commenced  with  general  icterus,  oliguria,  and  anuria, 
and  ended  with  terrible  attacks  of  hajmatemesis. 

Appendicitis  is  essentially  a  toxi-infectious  disease,  and  therefore  not 
only  to  be  feared  because  of  the  peritoneal  or  remote  infections,  but  also 

48 


754  TEXT-BOOK  OF  MEDICINE 

because  it  poisons  its  victims,  in  addition  to  infecting  them.  Sometimes, 
indeed,  the  intoxication  is  worse  than  the  infection.  In  a  word,  one  of  the 
m.ost  redoubtable  results  of  appendicitis  is  appendicsemia.  I  cannot, 
therefore,  urge  too  strongly  that  the  only  rational  treatment  of  appendicitis 
is  early  surgical  intervention  and  removal  of  the  toxi-infectious  centre. 

The  Treacherous  Calm  in  Appendicitis. — I  desire  to  call  attention  to 
the  aj)parent  calm  which  occurs  when  the  condition  is  most  threatening. 
In  a  communication  to  the  Academie  de  Medecine  I  have  called  it  the 
treacherous  calm.     To  quote  a  characteristic  example  : 

On  Januaiy  14,  1899,  I  was  called  by  Pinard  and  Roques  to  see  a  young  woman 
■who  was  four  months  pregnant.  The  pregnancy  had  been  normal,  except  for  severe 
vomiting  in  the  second  and  third  months.  While  in  excellent  health  she  was  taken  ill 
with  pains  in  the  stomach,  vomiting,  and  severe  diarrhoea  during  the  night  of  January  9. 
She  had  six  stools  during  the  night,  and  two  more  next  daj''.  The  family  at  first  feared 
a  miscarriage,  and  sent  for  Pinard,  who  discovered  that  this  was  not  the  case.  The 
uterus  had  no  part  in  the  pains  on  the  right  side  of  the  abdomen.  On  January  10  the 
condition  was  unaltered.  Pinard  did  not  see  the  patient.  She  passed  a  bad  night 
on  January  11,  and  the  pains  in  the  right  iUac  region  were  intense.  Roques  was  called 
in.  On  the  12th  two  attacks  of  vomiting  and  pain  at  McBurney's  point.  On  the 
13th  vomiting,  meteorism,  and  muscular  resistance  in  the  appendicular  region.  Tem- 
perature in  the  morning  101°  F.  ;  in  the  evening  102°  F.,  preceded  by  a  slight  rigor. 

Such  was  the  situation  on  the  evening  of  the  13th.  It  was  a  severe  case  of  appendi- 
citis. The  danger  was  increasing,  and  the  time  was  ripe  for  operation.  Next  day,  at 
half -past  eight  in  the  morning,  I  was  called  in,  and  was  told  that  a  visible  change  had 
taken  place  since  the  previous  evening.  The  abdominal  pains  had  disappeared,  and 
the  vomiting  had  ceased.  The  patient  had  slept  well,  and  had  twice  passed  water  and 
gas.  The  temperature  had  fallen  to  99-5°  F.  The  patient  insisted  on  the  improve- 
ment during  the  night,  and  considered  herself  well.  At  first  sight  the  mischief 
seemed  to  have  stopped.  This  condition  was  in  some  degree  comparable  -nath  that  of 
a  patient  who  overnight  is  in  the  throes  of  pneumonia,  and  who  on  the  following  day 
experiences  the  rehef  of  the  crisis. 

The  chart  on  p.  755  gives  an  exact  idea  of  this  treacherous  cakn.  If  we  merely 
look  at  this  chart,  noting  the  maximum  and  the  fall  of  the  fever,  we  might  think  that 
the  disease  had  come  to  an  end.  We  shaU  see  that  nothing  of  the  kind  had  happened. 
I  first  examined  for  pain  at  McBurney's  point,  but  the  pain  which  had  been  so  well 
marked,  had  now  disappeared.  I  pressed  the  abdomen  in  all  directions,  especially 
over  the  right  ihac  fossa,  and  I  was  not  a  little  surprised  to  find  it  painless.  There  was 
no  question  of  a  change  brought  about  by  medical  treatment  (morphia,  antipyrin,  or 
the  appUcation  of  ice),  as  none  of  these  remedies  had  been  employed.  The  pain  had 
therefore  disappeared  spontaneously. 

One  abdominal  symptom  of  the  utmost  importance,  however,  persisted — namely, 
general  abdominal  tympanites. 

What  had  happened  since  the  previous  evening,  and  what  did  this  apparently 
complete  truce  mean  ?  We  all  agreed  that  the  patient  was  suffering  from  severe 
appendicitis. 

We  were  of  opinion  that  it  was  one  of  those  transient  calms  which  deserve  recog- 
nition. We  felt  that  the  i^aticnt  had  peritonitis,  basing  oiu*  diagnosis  on  the  general 
tympanites,  the  sHghtly  drawn  look,  and  the  acceleration  of  the  pulse,  which  stood  at 
104,  in  spite  of  the  fall  of  temperature. 

When  we  arrived  at  noon,  the  apparent  improvement  still  continued.     The  tem- 


DISEASES  OF  THE  INTESTINE 


755 


perature  had  fallen  still  lower,  to  98^  F.  Segond  found,  as  we  had  done,  absence  of 
pain,  but  general  distension  of  the  belly  and  acceleration  of  the  pulse,  while  the  eyes 
were  sUghtly  sunken.  He  advised  immediate  operation.  Hardly  was  the  peritoneum 
opened  when  a  flood  of  turbid  serous  fluid  of  most  foetid  odour  gushed  out.  Diffuse 
peritonitis  was  present,  and  the  appendix  was  gangrenous.  In  spite  of  these  com- 
plications, the  mother  recovered.  The  miscarriage  took  place  on  the  twelfth  day 
after  the  operation,  thd  foetus  having  succumbed  to  the  appendicular  toxinea. 

T  desire  particularly  to  point  out  in  thLs  case  the  treacherous  calm  of 
appendicitis.     In  the  very  midst  of  the  peritonitis  the  calm  came  on,  the 


103* 


Days 
III 

5 

6 

7 

8 

9 

10 

II 

12 

/5 

39' 

A 

J 

M 

J 

I 

r 

t 

} 

^           o 

rS 

\ 

' 

A 

a 

/ 

\i 

A 

A 

J7° 

/N 

^    i 

\\ 

i 

\    A 

[ 

Voor. 

/ 

r    ^ 

V 

\ 

Sw 

1 

V 

V 

A 

V 

V 

y 

\ 

Date: 

12 

15 

1 

/5 

16 

17 

16 

19 

20 

100°  ^ 


99° 


98' 


■97' 


JefPi/ctry 
Fig.  51.— Cuart  snowiKo  the  TKEAcnEROtrs  Calm  in  Appendicitis. 


fever  fell,  and  the  pains  disappeared,  and  yet  fatal  mischief  was  commencing. 
The  patient  would  have  been  dead  in  fcrty-eight  hours  but  for  the  opera- 
tion. 

This  treacherous  calm  is  not  uncommon.  Several  cases  will  be  found  in 
a  clinical  lecture  on  this  subject.*  This  apparent  arrest  or  period  of  calm 
is  frecjuent  in  appendicitis,  and  is  not  sufficiently  recognized,  because  it  has 
not  been  previously  described.  Whether  this  arrest  of  the  disease  is  caused 
by  treatment  (bags  of  ice  on  the  abdomen,  opium  pills,  injections  of  morphia) 
or  not,  it  Ls  none  the  less  true  that  the  acute  symptoms  that  signalize  the 
first  stage  of  appendicitis  are  sometimes  followed  by  a  well-being  which 
looks  like  a  real  improvement  in  the  condition.     In  such  a  case  we  pc»jtpone 

*  *•  Les  Accalmies  Traitresses  de  I'Appendicito  "  (CYuuV/wc  Medicale  dc  riI6tel-Ditu)t 
1899,  12'"*=  Lb9on). 

48—2 


756  TEXT-BOOK  OF  MEDICINE 

the  proi^osed  operation  in  the  false  hope  of  gaming  time.  Complications 
appear  quickly,  and  when  we  deem  it  desirable  to  intervene,  we  are  too 
late. 

Strange  though  the  fact  appears  to  be,  we  are  forced  to  admit  that  in 
a  fair  number  of  cases  the  most  severe  peritoneal  lesions  coincide  with  an 
apparent  arrest  m  the  appendicular  symptoms.  It  may  perhaps  be  possible 
to  find  an  explanation  of  such  discordant  facts.  The  remarkable  experi- 
ments of  Klecki  on  the  pathogenesis  of  peritonitis  of  intestinal  origin  have 
led  me  to  investigate  the  pathogenesis  of  the  closed  cavity  in  appendicitis. 
He  has  shown  that  the  virulence  of  the  coli  bacillus  reaches  its  maximum 
in  the  ligatured  coil,  which  is  thus  converted  into  a  closed  cavity.  The 
microbes  then  pass  through  the  walls  of  the  ligatured  coil,  reach  the  peri- 
toneum, and  cause  peritonitis  (a  process  identical  to  that  which  I  have 
found  in  the  closed  cavity).  The  unexpected  fact  which  results  from 
Klecki's  experiments  is  that  the  virulence  of  the  bacilli  taken  from  the 
peritoneal  fluid  is  in  most  cases  less  than  that  of  the  bacilli  in  the  loop  of 
gut.  In  other  words,  "  the  passage  of  virulent  microbes  into  the  peritoneal 
cavity  lessens  their  virulence." 

Without  wishing  completely  to  assimilate  clinical  and  experimental  facts, 
it  is  impossible,  nevertheless,  not  to  be  struck  by  their  analogy.  In  the 
experimental  case  (conversion  of  an  intestinal  loop  iato  a  closed  cavity), 
as  in  the  clinical  case  (conversion  of  the  appendix  into  a  closed  cavity),  an 
intense  exaltation  of  virulence  and  an  acute  focus  of  infection  are  produced. 
In  the  experimental,  as  m  the  clinical  case,  the  pathogenic  microbes  become 
more  virulent  in  the  closed  cavity,  traverse  the  waUs  of  the  appendix,  and 
cause  diffuse,  septic,  or  localized  peritonitis.  Why  not  admit,  then,  that 
the  onset  of  peritoneal  lesions  may  sometimes  coincide  with  the  temporary 
attenuation  in  virulence  of  the  microbes  which  have  come  from  the  appen- 
dicular focus,  thus  causmg  the  treacherous  calm  ? 

Theory  is,  however,  of  little  importance.  The  essential  clmical  fact  is 
that  it  is  not  possible,  in  the  great  majority  of  cases,  to  establish  two  distinct 
periods  in  the  course  of  the  appendicular  and  peritoneal  symptoms,  which 
are  similar  and  subintrant.  It  is  often  difficult  to  know  at  what  moment 
peritonitis  shows  itself.  Indeed,  the  treacherous  calm  appears  durmg  the 
onset  of  peritonitis. 

The  course  of  events  is  as  follows  :  A  patient  is  sufiering  from  appen- 
dicitis. Ice-bags  are  applied  to  the  abdomen ;  opium  or  aperients  are 
administered.  Next  day  the  disease  follows  its  course.  The  pain  at 
McBurney's  pomt  is  acute,  vomiting  occurs,  the  pulse  is  quick,  and  the 
temperature  rises  to  101°  F.  Medical  treatment  is  continued,  mjections  of 
morphia  are  administered,  and  the  patient  is  kept  absolutely  still  on  his 
back ;  and  yet,  m  spite  of  medical  treatment  (which  I  consider  is  useless). 


DISEASES  OF  THE  INTESTINE  757 

the  situation  becomes  alarming — the  pain  is  intense,  the  abdomen  ls  dis- 
tended, and  the  necessity  for  surgical  intervention  strikes  the  observer. 

Then,  in  the  midst  of  this  indecision,  an  improvement  takes  place — the 
pain  lulls,  the  temperature  falls,  the  vomiting  ceases,  and  the  disease  grants 
a  truce.  The  medical  treatment  is  given  credit.  But  the  truce  is  of  short 
duration.  Fresh  svmptoras  soon  appear,  and  the  danger  becomes  pressing. 
The  cloven  hoof  of  peritonitis  is  stamped  on  the  face  of  the  patient.  Surgical 
intervention  is  then  accepted  as  a  last  resort ;  but,  be  the  operation  per- 
formed or  not,  it  is  already  too  late,  and  the  patient  will  succumb.  Many 
cases  of  appendicitis  run  this  treacherous  course,  and  end  in  death  unless  we 
operate  in  time. 

In  appendicitis  we  must  distinguish  between  a  real  improvement  and  a 
treacherous  calm.  The  former  concerns  all  the  symptoms  at  the  same  time, 
and  there  is  no  marked  discord  between  them.  The  pulse-rate  and  the 
temperature  fall,  the  tympanites  decreases,  the  pains  disappear,  and  the 
abdominal  distension  becomes  less. 

The  treacherous  calm  is  very  difEerent.  The  temperature  falls,  but  the 
pulse  remains  small  and  quick  (100  to  120  beats).  The  abdominal  pains 
improve,  either  spontaneously  or  under  the  influence  of  ice  and  morphia, 
but  the  abdomen  remains  distended  and  tympanitic,  and  careful  observation 
shows  that  the  facies  is  peritoneal.  - 

Pregnancy  and  Appendicitis. — The  following  example  gives  an  idea  of 
the  relation  between  pregnancy  and  appendicitis  : 

On  January  6,  1896,  I  saw  a  young  woman,  recently  confined,  who,  within  the  last 
forty-eight  hours,  had  been  taken  ill  with  pains  in  the  abdomen  and  vomiting.  Budin, 
who  had  deUvered  the  mother,  gave  me  full  details.  The  pregnancy,  the  confinement, 
and  the  puerperium  had  all  been  normal.  Eighteen  days  after  the  confinement,  when 
everything  was  going  well,  the  young  woman  complained  of  abdominal  pains,  which 
were  slight  at  first,  but  soon  became  acute.  The  pains  had  been  followed  by  nausea 
and  vomiting.  Constipation  was  absolute.  The  pre^^ous  night  had  been  bad,  and  the 
situation  had  grown  worse.  I  found  the  features  drawn,  the  eyes  dark,  and  near  the 
bed  a  basin  containing  greenish  vomit.  The  fever  was  high  ;  the  puLse  was  small  and 
quick.  The  case  was  undoubtedly  one  of  peritonitis.  The  abdomen  was  uniformly 
distended  and  so  tender  that  the  patient  begged  me  not  to  touch  it.  I  wished,  however, 
to  be  certain  of  the  seat  and  origin  of  the  pain,  for  in  such  cases  diagnosis  is  impossible 
without  a  methodical  examination.  I  palpated  the  abdomen  with  the  greatest  care, 
and  when  I  came  to  the  right  ihac  fossa,  I  found  hyperaesthesia,  pain  on  pressure,  and 
muscular  resistance  so  marked  over  the  caecum,  that  I  felt  sure  of  appendicitis  during 
the  puerperium.     Budin  shared  my  opinion. 

Although  it  was  but  the  third  day  of  the  disease,  peritonitis  was  already  present. 
Immediate  operation  was  necessary,  for  the  symptoms  were  alarming,  and  the  prog- 
nosis was  growing  worse  every  hour.  I  asked  Routier  to  operate.  He  did  so  at  10  p.m., 
and  found  diffu.se  peritonitis.  The  appendix  was  enlarged,  of  a  purple  colour,  and  sur- 
roundetl  with  soft,  j)urulent  false  membranes.  It  was  removed,  and  I  found  that  a 
calculus  had  given  rise  to  a  closed  cavity,  which  was  filh'd  with  pus.  The  di.sease  did 
not  at  once  yield,  as  the  patient,  who  was  poisoned  by  toxines,  had  fever  for  several 


758  TEXT-BOOK  OF  MEDICINE 

days,  with  rapid  pulse,  nausea,  gastric  intolerance,  and  slight  jaundice  of  the  con- 
junctivae. The  situation  gradually  improved,  and  the  patient  was  cured  at  the  end  of 
three  weeks.  This  case  of  puerperal  appendicitis  is,  I  believe,  the  first  one  of  its  kind 
published  in  France.* 

Since  that  date  Pinard  has  published  several  cases,  and  has  addressed  a 
very  important  communication  to  the  Academic  de  Medecine.  His  statistics 
show  thirty-one  cases  of  puerperal  appendicitis  operated  on,  and  the  period 
of  pregnancy  when  the  appendicitis  occurred.  They  also  show  the  extent 
of  the  peritoneal  lesions,  the  nature  of  the  operation,  and  the  results  as 
regards  the  mother  and  the  foetus. 

We  have  now  to  discuss  the  pathogenesis  of  puerperal  appendicitis.  In 
a  general  manner  the  pathogenesis  of  appendicitis  is  invariable,  and  we 
must  always  return  to  the  frimum  movens — that  is  to  say,  to  the  con- 
version of  a  portion  of  the  canal  into  a  closed  cavity,  in  which  the  toxic 
products  causing  all  the  complications  are  manufactured.  We  have  to 
decide  whether  pregnancy  has  any  direct  influence  on  appendicitis.  I  can 
readily  believe  that  lithiasis,  which  is  one  of  the  causes  of  appendicitis,  may 
be  set  down  to  pregnancy,  as  may  other  forms  of  lithiasis,  and  especially 
biliary  lithiasis,  I  do  not  say,  of  course,  that  every  case  of  puerperal 
appendicitis  is  due  to  a  calculus.  We  possess  little  information  on  this 
subject,  for  the  examination  of  the  appendicular  lesion  is  generally  curtailed 
or  passed  over  in  silence.  Still,  the  two  cases  of  puerperal  appendicitis 
which  I  have  seen,  were  both  due  to  calculi. 

However  this  be,  as  Pinard  says,  "  the  fact,  which  is  well  established, 
and  which  must  henceforth  claim  attention,  is :  appendicitis  may  com- 
plicate child-bearing  in  all  its  stages — during  pregnancy,  during  labour, 
or  during  the  puerperium."  Thirty-one  operated  cases  prove  this  asser- 
tion. Observations  show  that  appendicitis  may  cause  trouble  during  any 
stage  of  pregnancy,  just  as  it  may  complicate  the  puerperium.  Appen- 
dicitis generally  interferes  with  the  pregnancy,  and  threatens  the  life  of 
the  foetus  as  well  as  that  of  the  mother.  Nearly  all  authors  have  remarked 
how  frequently  a  viable  foetus  has  been  expelled  dead,  or  has  died  from  some 
indeterminate  cause,  or  presented  signs  of  septicaemia  during  the  few  days 
of  life.  Our  case  may  furnish  an  example  of  the  fact.  The  culture  made 
by  Wallich  gave  pure  cultures  of  the  Bacillus  coli,  proving  the  infection 
in  utero,  the  blood  having  been  taken  from  the  vessels  of  the  umbilical 
cord. 

A  description  of  puerperal  appendicitis  is  unnecessary,  because  there  is 
no  difference  between  it  and  the  non-puerperal  form.  When  appendicitis 
supervenes  during  pregnancy  or  after  accouchement,  it  is  always  appen- 
dicitis with  its  many  varieties,  and  with  the  symptoms  which  I  have  de- 

*  Dieulafoy,  "  Manuel  de  Pathologie  Interne,"  1897,  t.  iii. 


DISEASES  OF  THE  INTESTINE  759 

scribed  in  detail.  It  begins  without  prodromata,  whilst  the  patient  is  in  a 
state  of  perfect  health,  with  pain,  localized  in  the  right  iliac  fossa.  This 
pain  does  not  attain  its  greatest  intensity  at  once,  and  no  matter  how  acute 
the  onset,  the  pain  gradually  increases.  Careful  interrogation  of  patients 
shows  that  the  pain  attains  its  maximum  only  after  one  or  several  hours. 

Furthermore,  the  localization  of  the  pain  is  of  much  help  in  diagnosis, 
and  even  if  it  spreads  in  various  directions,  the  seat  of  election  (pain,  mus- 
cular resistance,  and  hyperaesthesia)  occupies  the  middle  of  a  line  drawn 
from  the  umbilicus  to  the  right  antero-superior  iliac  spine.  The  prognosis 
in  appendicitis  is  certainly  aggravated  by  the  puerperal  condition.  Not 
only  the  infection,  but  also  the  toxicity,  is  to  be  feared,  and  it  must  not  be 
forgotten  that  in  the  pregnant  woman  the  liver  is  in  danger  of  becoming 
affected. 

Here,  as  in  every  case  of  appendicitis,  the  only  rational  and  efficacious 
treatment  is  surgical  intervention.  ,"I  cannot  but  agree  with  this  judg- 
ment," says  Pinard.  "  Perhaps  I  would  go  further,  and  say  that  appen- 
dicitis during  pregnancy  must  be  treated  surgically  more  rapidly  than  in 
any  other  case,  because  of  the  close  relation  of  the  infectious  focus  to  the 
genital  organs.  For  the  moment  I  am  not  concerned  with  the  question 
whether  the  infection  spreads  by  continuity  or  by  means  of  the  blood- 
vessels. Whatever  the  means,  infection  is  present,  and  two  lives  are  en- 
dangered. This  sums  up  the  whole  question.  These  conditions  may  not 
be  set  aside  when  the  practitioner  finds  himself  face  to  face  with  appen- 
dicitis in  a  young  woman.  Being  mindful  of  the  relation  of  appendicitis 
to  the  puerperal  condition,  it  will  be  found  wise  to  remove  the  infectious 
focus,  though  up  to  now  we  may  have  hesitated.  This  would  be,  in  my 
opinion,  good  prophylaxis." 

I  have  nothing  to  add  and  nothing  to  withdraw  from  the  views  I  have 
so  often  expressed.  Appendicitis,  whether  puerperal  or  not,  must  be 
operated  on  without  delay.  I  know  that  there  is  some  hesitation  in  opening 
the  abdomen  of  a  pregnant  woman  :  the  opposition  of  the  friends  is  not 
always  easy  to  overcome  ;  but  if  exact  examination  shows  us  that  the  patient 
is  suffering  from  appendicitis,  she  must  be  operated  on  at  once.  The  foetus 
will,  perhaps,  succumb,  but  the  mother  will  be  .saved.  Cases  will  be  quoted 
in  which  puerperal  appendicitis  was  not  operated  upon,  and  yet  neither  the 
foetus  nor  the  mother  died.  I  grant  this,  but  it  is  a  poor  argument  in  the 
face  of  our  knowledge  of  the  gravity  of  appendicitis,  and  especially  of  the 
puerperal  form. 

Diagnosis. — Appendicitis  is  the  most  important  of  all  abdominal 
maladies.  Its  frequency,  its  various  forms,  and  its  gravity,  uuist  always 
keep  us  on  the  alert,  so  that  we  may  diagno.se  it  and  act  at  once.  There  is 
a  toxi-infectious  focus,  which  must  be  removed  as  soon  as  it  appears.     To 


760  TEXT-BOOK  OF  MEDICINE 

temporize  is  to  court  disaster.  We  must  try,  therefore,  to  make  a  correct 
diagnosis. 

While  the  diagnosis  of  appendicitis  is  very  easy  in  some  cases,  there  are 
others  in  which  the  reasoning  cannot  be  too  close.  The  treatment  of  appen- 
dicitis demands  exact  diagnosis,  because  we  can  then  resort  to  opportune 
surgical  intervention.  Likewise,  it  is  by  a  correct  diagnosis  that  we  can 
eliminate  all  idea  of  an  operation  in  a  patient  whose  symptoms  merely 
simulate  appendicitis. 

In  this  discussion  I  shall  base  my  arguments  on  the  200  cases  of  appen- 
dicitis which  I  have  treated  during  the  past  eight  years.  As  they  were  all 
verified  by  operation,  the  correctness  of  the  diagnosis  cannot  be  called  in 
question. 

In  the  first  place,  it  will  be  well  to  establish  the  foundations  on  which 
the  diagnosis  must  rest  by  discussing  the  signs  and  symptoms  which  mark 
the  onset  and  the  course  of  the  disea^.  For  the  facility  of  description, 
the  different  varieties  of  appendicitis  may  be  placed  in  three  groups  : 

Group  I. — Appendicitis  of  benign  appearance.  The  onset  is  not  very 
painful ;  the  symptoms  are  classical,  but  not  very  severe ;  the  fever  is  not 
high  ;  vomiting  is  rare  or  absent ;  and  constipation  is  the  rule.  Methodical 
examination  of  the  abdomen  shows  that  the  pain,  muscular  resistance,  and 
cutaneous  hyperaesthesia  are  readily  appreciable  at  McBurne'y's  spot.  This 
type  of  appendicitis  formerly  swelled  the  list  of  cases  of  so-called  stercoral 
typhlitis,  but  we  know  to-day  that  the  disease  is  appendicitis,  not  typhlitis, 
and  the  diagnosis  has  become  easy ;  but  the  prognosis  is  impossible,  because, 
in  spite  of  its  benign  appearance  and  the  absence  of  urgent  symptoms,  the 
attack  may  on  the  third  or  fourth  day  pass  on  to  gangrene,  peritonitis,  or 
poisoning  of  the  patient,  who  dies  for  want  of  early  operation. 

Group  II. — The  disease  has  an  acute  onset  and  severe  course.  The 
patient,  who  was  in  good  health  the  night  before,  suddenly  feels  abdominal 
pain,  which  is  not  at  first  confined  to  the  right  iliac  fossa,  but  may  occupy 
the  epigastric  or  umbilical  regions,  though  it  soon  becomes  most  marked  in 
the  right  iliac  fossa,  and  rapidly  reaches  its  maximum.  "  The  pain  is  so 
severe  as  to  make  the  patient  cry  out  or  wi'ithe  in  agony."  Nausea  is  con- 
stant, and  vomiting  of  food  or  bile  is  sometimes  early  and  frequent.  Fever 
appears,  and  the  pulse  is  quickened.  On  the  first  day  the  facies  may  be 
anxious  and  drawn.  One  exainining  the  patient,  the  abdomen  may  be  found 
painless  in  different  regions,  and  especially  in  the  epigastric  region.  If, 
however,  the  examination  is  methodical,  we  find  the  painful  triad  localized  at 
McBurney's  point :  intense  pain  increased  by  pressure,  muscular  resistance, 
and  cutaneous  hyperaesthesia  form  the  triad.  If  we  watch  the  face  of  the 
patient,  we  see  that  the  features  contract,  and  that  a  look  of  agony  is  present 
when  but  slight  pressure  is  made  over  the  appendix.     On  the  first  or  second 


DISEASES  OF  THE  INTESTINE  761 

day  the  temperature  may  rise  to  103°  F.  The  urine  is  sometimes  albu- 
minous. This  form  of  appendicitis  certainly  presents  the  least  difficulties 
in  diagnosis,  because  the  severity  and  the  clearness  of  the  symptoms  leave 
no  room  for  doubt. 

It  must  be  admitted  that  this  symptom-complex  much  resembles  that 
of  peritonitis.  The  peritoneum,  however,  may  be  absolutely  intact,  and 
appendicitis  alone  is  capable  of  causing  all  these  symptoms.  The  appen- 
dicular and  peritoneal  symptoms  may  be  similar.  It  is  often  impossible  to 
say  when  peritonitis  complicates  appendicitis,  as  I  have  previously  pointed 
out. 

Group  III. — The  disease  may  be  called  larval,  as  it  assumes  the  mask 
of  some  other  disease.  The  triad  of  appendicitis  is  not  wanting  if  carefully 
sought  for,  but  it  is  partially  masked  by  other  symptoms  which  alter  the 
nature  of  the  morbid  picture.  In  one  patient,  for  instance,  the  vomiting 
of  food  and  of  bile  is  so  marked  that  it  simulates  ordinary  indigestion.  The 
physician  is  often  called  to  a  child  some  twenty-four  hours  after  the  so-called 
indigestion,  when  the  fits  of  vomiting  associated  with  the  painful  triad 
(which  is  to  be  found,  if  carefully  looked  for)  were  but  the  prelude  of  an 
appendicular  infection.  When  the  parents  know  the  truth,  they  say  : 
"  We  thought  that  it  was  a  case  of  simple  indigestion  !" 

If  we  are  forewarned,  we  shall  not  be  deceived  by  these  appearances. 
In  the  case  of  a  child  or  an  adult  who  has  been  taken  ill  some  hours  before 
with  so-called  indigestion,  let  us  always  remember  that  the  vomiting  may 
be  of  appendicular  origin.  Let  us  think  of  appendicitis,  and  carefully 
explore  McBurney's  region,  looking  for  pain,  muscular  resistance,  and 
hyperajsthesia.  Careful  examination,  which  may  be  repeated  twice  or 
three  times  during  the  day,  will  give  the  true  diagnosis,  and  show  that 
the  vomiting  put  down  to  indigestion  is  really  due  to  appendicitis. 

In  some  cases  the  disease  is  masked  at  its  onset  by  the  profuse  diarrhoea 
which  I  have  called  "  defensive."  The  intestine,  by  copious  secretory 
action,  apparently  tries  to  get  rid  of  the  poison.  This  diarrhoea,  wrongly 
taken  for  enteritis  or  for  entero-colitis,  has  falsified  the  pathogenesis  of 
appendicitis.  The  case  may  be  thus  stated  :  A  person  is  taken  ill  with 
intestinal  pain  and  diarrhoea.  His  first  idea  is  that  "  his  stomach  is  upset," 
and  he  treats  himself  with  cataplasms  and  laudanum.  He  then  sends  for 
a  doctor,  who  sometimes  accepts  the  diagnosis  of  enteritis,  relying  on  the 
information  furnished  by  the  patient.  The  cause  of  the  enteritis  is  then 
sought  for,  and  the  mischief  Is  attributed  to  indigestible  food,  iced  drinks, 
or  a  chill.  The  supposed  enteritis  m  treated  with  opium,  bismuth,  and 
cataplasms.  In  spite  of  the  treatment,  the  situation  does  not  improve  :  the 
abdominal  pains  become  sharper,  and  constipation  follows  the  diarrhoea, 
while  the  abdomen  becomes  distended,  vomiting  appears,  and  the  patient 


762  TEXT-BOOK  OF  MEDICINE 

on  tlie  third  or  fourtli  day  of  his  supposed  enteritis  is  really  suffering  from 
well-developed  appendicitis.  We  then  recognise  that  the  diagnosis  of 
enteritis  was  incorrect,  but  we  try  to  explain  matters  by  saying  that  the 
appendicitis  has  been  the  outcome  of  entero- colitis.     This  is  a  mistake. 

I  have  often  seen  appendicitis  commence  with  diarrhoea,  and  I  know  of 
no  better  example  of  this  masked  form  of  appendicitis  than  one  of  the  cases 
of  which  I  have  spoken  in  connection  with  the  treacherous  calm.  We  have 
become  so  accustomed  to  see  constipation  accompany  appendicitis  that  we 
may  not  recognize  appendicitis  accompanied  by  diarrhoea.  An  error  in 
diagnosis  may  then  readily  occur.  If  a  patient  is  taken  ill  with  abdominal 
pain  and  diarrhoea,  we  must  investigate  the  cause  and  the  seat  of  the  pain. 
Methodical  exploration  of  the  appendicular  region  allows  us  to  make  our 
diagnosis. 

Another  form  of  masked  appendicitis  simulates  renal  colic.  I  had  under 
my  care  the  following  remarkable  case  : 

A  man  of  twenty-eight  had  had  attacks  of  pains  for  the  past  two  years.  The  first 
attack  occurred  on  March  30,  1896.  His  previous  health  was  good,  but  he  was  seized 
with  "  cramp  "  in  the  right  side  of  the  belly.  The  pain  was  accompanied  by  vomiting 
and  fever,  and  he  was  obHged  to  keep  his  bed  for  several  days.  His  doctor  diagnosed 
hepatic  coUc,  and  prescribed  purgatives  and  milk  diet.  In  December,  1896,  he  had 
a  second  attack  of  pain,  which  radiated  to  the  right  groin  and  testicle.  The  third 
attack  took  place  in  July,  1897,  and  was  characterized  by  acute  pain  in  the  right  side 
of  the  belly,  fever,  fits  of  vomiting,  and  radiation  of  the  pain  into  the  thigh  and  the 
right  testicle.  The  diagnosis  pointed  to  renal  colic,  and  the  patient  was  kept  in  bed  for 
a  week.  Finally,  the  fourth  and  last  attack  occurred  on  April  20,  1898,  and  was  in  every 
respect  like  the  preceding  ones.  The  pain  radiated  to  the' umbihcus,  the  right  thigh, 
and  the  right  testicle.  At  times  it  caused  retraction  of  the  testicle,  just  as  in  renal 
cohc.  The  patient  had  to  keep  his  bed  for  eighteen  days,  and  avoid  all  movement. 
The  convalescence  was  unsatisfactory,  and  the  abdominal  pains  did  not  completely 
disappear. 

I  examined  liim,  and  found  pain  localized  over  the  caecum.  Hypersesthesia  and 
muscular  contraction  were  also  noticed,  together  with  indefinite,  deep-seated,  indura- 
tion. The  triad  in  question  (pain,  muscular  resistance,  and  hypersesthesia  over  the 
appendix)  was  in  favour  of  appendicitis.  It  was,  however,  difficult  to  explain  the 
symptoms  of  renal  colic  in  the  two  last  attacks. 

In  spite  of  these  symptoms,  I  discarded  the  diagnosis  of  renal  coKc  and  substituted 
that  of  appencUcitis.  ]My  reasons  for  doing  so  were  as  follows.  In  renal  coUc  the 
lumbar  region  on  the  affected  side  is  always  painful ;  it  was  not  so  in  this  case.  Further- 
more, the  pains  of  renal  colic  appear  and  cease  suddenly.  The  pains,  though  atrocious 
for  a  few  hours,  disappear  as  if  by  magic  as  soon  as  the  stone  has  passed  into  the  bladder. 
In  this  patient  the  abdominal  pain  lasted  eighteen  days  ;  indeed,  pain  in  the  right  iliac 
fossa  was  present  when  I  examined  him.  And,  again,  the  disease  had  left  signs  at 
McBurney's  point  which  are  characteristic  of  appendicitis,  and  not  of  renal  coUc. 
I  therefore  asked  Marion  to  operate  on  the  appendix. 

The  diagnosis  was  found  to  be  correct,  and  the  operation  cleared  up  the  symptoms 
which  had  been  set  down  to  renal  cohc.  The  appendix  reached  up  behind  the  caecum, 
and  was  surrounded  by  a  mass  of  false  membranes,  which  united  the  posterior  surface 
of  the  cascum  to  the  iho -psoas  muscle.  The  adhesions  were  due  to  the  attacks  of 
appendicitis,  which  had  been  mistaken  for  renal  coUc. 


DISEASES  OF  THE  INTESTINE  763 

The  large  adherent  appendix  was  difficult  to  remove.  It  was  obliterated  at  its 
base,  and  we  found  below  the  stricture  a  small,  deep  ulceration,  which  would  soon  have 
perforated.  The  tumour,  adherent  to  the  anterior  surface  of  the  psoas,  was  in  intimate 
coimection  with  the  genito-orural  nerve,  which  passes  over  this  muscle.  The  stimula- 
tion of  the  branch  of  this  nerve,  which  is  distributed  to  the  skin  of  the  scrotum  and  the 
cremaster,  explains  the  pain  and  the  retraction  of  the  testicle.  The  stimulation  of 
the  crural  branch,  which  sends  out  cutaneous  twigs  to  the  superior  and  anterior  part 
of  the  thigh,  explains  the  pains  in  that  region.  The  pathogenesis  of  the  symptoms 
which  in  my  patient  hadcaused  appendicitis  to  simulate  renal  coUc  was  thus  verified. 

This  is  by  no  means  an  isolated  case,  and  I  have  collected  several  in  one  of  my 
clinical  lectures.* 

Tuffier  has  published  some  examples  of  pseudo -nephritic  symptoms  in  appendicitis. 
He  mentions  the  case  of  a  patient  taken  ill  with  vomiting,  ballooning  of  the  abdomen, 
and  acute  pain  in  the  right  side,  radiating  into  the  groin.  The  diagnosis  of  renal  colic 
was  made.  As  the  situation  grew  worse,  laparotomy  was  performed,  and  revealed 
appendicitis.  Tuffier  asks  whether  the  association  of  pseudo -nephritic  pains  v,iih. 
appendicitis  may  not  be  attributed  to  the  ureter  being  enveloped  by  adhesions.  Vesical 
symptoms  sometimes  attract  special  attention  in  appendicitis.  A  few  years  ago  I 
saw  with  Pinard  a  man  of  about  fifty  years  of  age  who  had  an  attack  of  appendicitis 
with  anuria,  and  was  sounded  because  he  was  convinced  that  he  had  a  stone  in  the 
bladder. 

Let  us  next  consider  appendicitis  which  simulates  hepatic  colic.  In 
some  cases  of  appendicitis  the  appendix  ascends  so  high  behind  the  caecum 
and  the  ascending  colon  that  the  pain  radiates  up  to  the  hypochondria. 
The  patient  complains  of  abdominal  pains,  and  at  the  same  time  indicates 
the  subhepatic  region,  so  that  we  may  hold  the  bile-ducts  at  fault. 

Furthermore,  some  patients  have  jaundice,  and  if  a  patient  has  jaundice, 
vomiting,  and  pains  in  the  h}^ochondriac  region,  the  idea  of  hepatic  colic 
naturally  presents  itself.  On  closer  inspection,  however,  we  find  that  in 
appendicitis,  although  the  pain  is  felt  as  high  as  the  hepatic  region,  there 
is  always  local  pain  at  McBurney's  point,  which  is  never  the  case  in  hepatic 
colic.  Again,  the  pains  of  hepatic  colic  frequently  radiate  into  the  shoulder. 
This  never  happens  in  appendicitis.  The  jaundice  of  hepatic  colic  is  ob- 
structive, and  is  generally  characterized  by  clay-coloured  stools,  and  tmie  bile- 
pigments  in  the  urine  ;  whilst  the  toxic  jaundice  of  appendicitis  does  not 
cause  decoloration  of  the  faeces,  and  Is  generally  characterized  by  the  presence 
of  urobilin  and  brown  pigment  in  the  urine.  Furthermore,  in  toxic  appen- 
dicitis with  jaundice  the  urine  nearly  always  contains  albumin.  These 
different  points  should,  therefore,  prevent  our  mistaking  appendicitis  for 
h-ipatic  colic. 

We  may  now  discuss  the  diagnosis  of  diseases  which  simulate  appen- 
dicitis. I  must  insist  particularly  on  entero-typhlo-colitis,  which  is  often 
mistaken  for  appendicitis.  Mucous,  membranous,  or  calculous  entero- 
typhlo-colitis  always  presents  a  symptom-complex,  in  which  diffuse  pain  is 
the  chief  feature.  The  intestinal  colic,  which  may  or  may  not  be  acconi- 
*  "  Diagnostic  de  rAppendicit©  "  (Clinique  Medicate  deV Hotel- Dieu,  1899,  IS"*  lefon). 


764  TEXT-BOOK  OF  MEDICINE 

panied  by  fever  and  vomiting,  i,s  most  marked  over  the  ascending,  trans- 
verse, and  descending  colons.  When  the  csecum  is  especially  affected 
(typhlitis,  or  typhlo-colitis),  the  pain  is  very  near  the  region  of  the  pain 
due  to  appendicitis.  While,  however,  the  pain  is  most  severe  in  the  right 
iliac  fossa,  we  have  in  favour  of  the  diagnosis  of  entero-typhlo-colitis  the 
diffusion  of  pain  along  the  colon.  The  patient  by  a  gesture  may  give  a 
diagnostic  hint.  He  speaks  of  a  "  painful  bar,"  and  indicates  the  trans- 
verse colon  with  his  hand.  In  other  cases  he  will  complain  of  a  "  painful 
circle  "  in  the  abdomen,  and  at  the  same  time  trace  by  a  significant  gesture 
the  diffusion  of  the  pain  along  the  three  colons. 

On  examination,  the  right  iliac  fossa  is  often  painful,  but  still  you  do 
not  find  the  triad  as  clearly  defined  as  in  appendicitis.  Besides,  other 
painful  points  exist  over  the  ascending  colon,  the  hepatic  flexure  (in  front 
and  behind),  or  the  transverse  and  the  descending  colons.  Appendicitis 
does  not  show  this  feature. 

In  appendicitis  the  patient  is  almost  always  taken  ill  while  in  good 
health.  Prodromata  are  rare,  judging  by  the  200  cases  which  I 
have  verified  by  operation.  On  the  other  hand,  a  patient  with  entero- 
colitis will  say  that  some  weeks  or  months  previously  he  had  pain  in  the 
left  iliac  fossa  (descending  colon),  or  in  the  subumbilical  region  (transverse 
colon).  He  will  say  that  for  months  or  years  he  has  been  subject  to  intes- 
tinal derangements,  and  that  a  chill,  indigestible  food,  and  fatigue  give  him 
colic  and  diarrhoea.  He  often  suffers  from  constipation.  He  watches  his 
stools  carefully,  and  has  noticed  mucus,  slimy  matter,  or  "  skins."  Analysis 
of  the  fseces  after  an  attack  reveals  the  presence  of  sand.  Nothing  of  this 
kind  occurs  in  appendicitis,  and  there  is  only  "  an  intestinal  history  "  when 
the  patient  has  already  had  several  attacks  of  appendicitis. 

It  will,  however,  be  urged  that  entero-colitis,  or  typhlo-colitis,  may  lead 
to  appendicitis.  I  do  not  share  this  view.  Appendicitis  is  neither  the 
consequence  nor  the  outcome  of  entero-colitis.  This  question  will  be 
discussed  m  detail  under  Entero-colitis.  I  may  state  here  that  if  in  an 
intestinal  attack  we  find  symptoms  and  signs  of  mucous,  membranous,  or 
calculous  entero-colitis,  there  is  practically  no  fear  of  appendicitis. 

I  cannot  lay  too  great  stress  on  the  differential  diagnosis  between  appen- 
dicitis and  entero-typhlo-colitis.  As  appendicitis  inspires  widespread  alarm, 
care  must  be  taken  not  to  see  appendicitis  everywhere,  and  to  advise  opera- 
tion for  appendicitis  which  does  not  exist.  If  I  insist  on  this  point  with 
some  complacency,  it  is  because  I  have  advised  patients  against  an  opera- 
tion which  had  been  advised.  They  were  suffering  from  mucous,  mem- 
branous, or  calculous  typhlo-colitis,  and  had  not  appendicitis. 

Cholecystitis  might  simulate  appendicitis,  were  it  not  that  the  pain 
occupies  a  different  region.     There  are  cases,  however,  in  which  appendicitis 


DISEASES  OF  THE  INTESTINE  765 

is  associated  with  cholecystitis.  I  have  made  a  special  communication  on 
this  point  to  the  Academic  de  Medecine,*  and  when  I  speak  of  the  diseases 
of  the  gall-bladder,  I  shall  discuss  this  association  of  cholecystitis  and  appen- 
dicitis. 

The  diagnosis  between  appendicitis  and  lead  colic  is  not  always  easy. 
The  pain  in  lead  colic  is  sometimes  very  marked  in  the  right  Hiac  fossa — 
that  is,  in  the  region  of  the  caecum — and  may  be  called  saturnine  typhlalgia. 
Do  not  let  us  forget  that  there  may  be  typhlalgia,  just  as  there  may  be 
enteralgia  or  colalgia.  In  the  case  of  typhlalgia,  spontaneous  pain  and 
pain  due  to  pressure  exist  in  much  the  same  region  as  in  appendicitis.  The 
history,  the  blue  line,  the  previous  attacks  of  lead  colic,  and  the  absence  of 
fever  are,  however,  opposed  to  the  idea  of  appendicitis.  Furthermore,  the 
pain  in  lead  colic  is  diffused  over  the  whole  abdomen,  which  is  tense  and 
painful  at  other  spots  than  the  right  iliac  fossa,  and  pressure  often  relieves 
the  pain. 

I  have  previously-  quoted  several  cases  of  gastric  or  duodenal  perforation 
mistaken  for  appendicitis.  We  may  succeed  in  making  a  correct  diagnosis 
by  the  following  points  :  The  suddenness,  severity,  and  localization  of  the 
pain  are  in  no  wise  comparable  in  the  two  cases.  The  pain  following  per- 
foration of  an  ulcer  is  sudden  and  agonizing,  and  I  have  called  it  "  the 
peritoneal  dagger-thrust."  The  pain  of  appendicitis  is  neither  so  sudden 
nor  so  acute,  and  may  take  several  hours  to  reach  its  maximum.  The 
localization  of  the  painful  triad  is  likewise  different,  being  most  marked  in 
the  right  iliac  fossa  in  the  case  of  appendicitis.  In  the  case  of  perforation 
of  the  stomach  it  is  most  severe  in  the  epigastric  region. 

It  is  sometimes  difficult  to  distinguish  between  appendicitis  and  primary 
pneumococcal  peritonitis.     I  shall  here  mention  the  chief  diagnostic  points. 

Primary  pneumococcal  peritonitis  attacks  young  children  at  the  very 
age  when  appendicitis  is  frequent.  In  both  cases  there  is  sudden  and  acute 
abdominal  pain,  with  vomiting  of  food  and  bile.  In  both  cases  the  fever 
may  be  severe  or  slight.  Pneumococcal  peritonitis,  however,  causes  even 
at  its  onset  severe  foetid  diarrhoea,  whilst  diarrhoea  is  exceptional  at  the 
commencement  of  appendicitis.  Finally,  though  the  pain  of  pneumococcal 
peritonitis  often  commences  in  the  iliac  fossa,  the  "  painful  triad  "  is  in 
favour  of  appendicitis. 

Inflammation  of  the  right  adnexa  is  sometimes  difficult  to  diagnose 
from  appendicitis.  While  the  former  disease  k  essentially  pelvic,  and  the 
latter  abdominal,  the  diagnosis  is  very  complicated  where  previous  inflam- 
mation of  the  tube  and  ovary  has  formed  permanent  adhesions  with  the 
appendix.     A  history  of  gonorrhoea  or  puerperal  mischief,  the  onset  and 

*  Dieulafoy,  "  Association  do  rApiJcndicito  et  do  h\  Choleoystite,  avcc  ou  sans 
Peiitonite  "  {Academie  de  Medecine,  Seance  du  IG  Juin,  I9<)3). 


766  TEXT-BOOK  OF  MEDICINE 

the  course  of  the  symptoms,  and  the  exact  localization  of  the  pain  must 
then  be  taken  into  consideration. 

Some  women  at  the  approach  of  the  menstrual  periods  suffer  from  con- 
gestion, ovarian  pain,  vomiting,  and  tympanites,  with  radiating  pains  and 
hypersesthesia  of  the  abdomen.  The  least  touch  causes  sharp  pain  over 
the  appendix.  We  find  on  closer  inspection  that  pain  is  most  marked,  not 
at  McBurney's  point,  but  lower  in  the  ovarian  region.  I  once  saw  this 
happen  in  a  young  girl  who  was  said  to  be  suffering  from  appendicitis. 
Next  day  all  the  symptoms  disappeared  with  the  onset  of  the  menses. 

Tubal  pregnancy  shows  some  analogy  with  appendicitis  when  the  lesion 
is  on  the  right  side,     I  saw  the  following  case  with  Moizard  and  Nelaton  : 

A  young  -woman  had  been  taken  suddenly  ill  -with  pain  in  the  right  iliac  fossa, 
vomiting,  and  syncope.  A  few  hours  later  the  facies  was  drawn,  the  pulse  was  small  and 
quickened,  and  the  face  extremely  pale.  These  are  not  the  symptoms  of  appendicitis. 
Excessive  pallor,  acceleration  of  the  pulse,  and  a  tendency  to  syncope  are  rather  the 
result  of  haemorrhage.  Besides,  in  this  case  the  subumbihcal  region  of  the  abdomen 
was  absolutely  dull,  which  already  indicated  a  large  effusion.  -The  diagnosis  of  intra- 
peritoneal haemorrhage  from  rupture  of  the  tube  was  made.  She  was  two  months 
pregnant.  The  operation  verified  the  diagnosis  and  brought  about  recovery.  About 
3  pints  of  blood  were  sponged  out. 

A  floating  right  kidney  causes  sometimes  very  severe  pain  in  the 
right  iliac  fossa,  with  or  without  vomiting,  and  must  not  be  mistaken  for 
appendicitis.  Careful  exploration  of  the  region  will  allow  of  a  diagnosis 
being  made. 

I  would  remind  the  reader  that  hysterical  patients  may  present  the 
foUowmg  symptom-complex  :  ballooning  of  the  abdomen,  pains  in  the  iliac 
fossa,  and  vomiting.  The  condition  somewhat  resembles  the  picture  of 
appendicitis,  but  in  such  cases  we  find  stigmata  of  hysteria,  with  hystero- 
genic zones,  and  pain  localized  in  the  ovarian  region,  and  not  in  that  of  the 
appendix. 

Chronic  Appendicitis. — I  do  not  allude  to  tuberculosis,  cancer,  actino- 
mycosis, etc.,  which  may  attack  the  walls  of  the  appendix.  They  do  not 
show  the  infective  type,  which  alone  deserves  the  name  of  appendicitis. 
I  would  divide  chronic  appendicitis  into  two  groups — the  one  in  which  the 
mischief  becomes  chronic  after  one  or  more  acute  attacks,  the  other  in 
which  it  is  chronic  from  the  first.  The  first  group  is  the  more  common. 
Appendicitis  which  has  thus  become  chronic,  is  sometimes  the  fault  of  the 
patient,  who  has  refused  a  timely  operation,  and  is  therefore  the  victim  of 
chronic  mischief  in  the  appendix. 

This  form  is  often  the  fault  of  physicians  or  surgeons,  who  put  aside 
"  the  early  operation,"  thus  exposing  the  sufferer  to  very  grave  risks,  and 
who  prolong  "  medical  treatment,"  which  allows  appendicitis  ample  time 
to  become  chronic. 


DISEASES  OF  THE  INTESTINE  767 

In  chronic  appendicitis  we  always  find  lesions  around  the  appendix — 
viz.,  false  membranes  and  caseous  or  purulent  material.  As  the  chronic 
infection  spreads  beyond  the  appendix,  it  ends  in  the  production  of  "  irregular 
fibrous  adhesions,  which  fix  the  appendix  to  the  caecum,  ileum,  mesentery, 
or  peritoneum."  Patients  complain  of  dragging  pain  in  the  right  iliac  fossa 
or  at  other  spots.  The  pain  is  aroused  by  walking  or  other  exercise,  and 
may  occur  in  acute  attacks. 

Chronic  appendicitis  at  times  affects  the  digestive  organs.  The  patient 
complains  of  gastric  or  intestinal  trouble,  and  becomes  dyspeptic.  We 
usually  see  constipation,  with  the  passage  of  mucus  or  membranes  in  stools, 
but  diarrhoea  is  also  seen.  We  are  then  prone,  through  inaccurate  observa- 
tion, to  suppose  that  chronic  appendicitis  is  consecutive  to  mucous  colitis. 
If,  however,  we  arrange  the  history  of  events  in  chronological  order,  we 
find  that  the  chronic  appendicitis  has  caused  these  intestinal  troubles, 
which  roughly  resemble  muco-membranous  colitis. 

Appendicitis  is  more  rarely  chronic  from  the  first.  In  this  event  we 
find  calculi,  ulcers  in  the  mucosa,  small  abscesses  in  the  wall  of  the  appendix, 
and  purulent  fluid.  These  lesions  run  a  slow  course.  Fever  is  absent,  but 
dragging  pain  is  present  in  the  right  iliac  fossa  or  other  regions.  Marked 
exacerbations  may  occur,  and  closely  simulate  an  acute  attack  of  appen- 
dicitis. There  is,  however,  no  reason  to  suppose  that  these  cases  of  chronic 
appendicitLs  are  consecutive  to  colitis. 

Treatment  of  Appendicitis. — At  the  Academic  in  1896  I  stated  (and 
my  statement  still  holds) :  "  There  is  no  medical  treatment  for  appendicitis. 
Medical  treatment  simply  causes  loss  of  valuable  time.  It  is  obvious  that 
the  patient  can  be  relieved  by  injections  of  morphia,  application  of  ice-bags 
to  the  affected  region,  and  other  soothing  measures  ;  but  do  not  let  us  be 
mistaken  as  to  the  efficacy  of  these  means.  Too  often  they  lead  us  to 
believe  in  cure,  when  they  only  mask  the  symptoms.  In  view  of  this  ficti- 
tious improvement,  we  speak  of  typhlitis,  or  appendicular  colic,  and  prophesy 
recovery  ;  but  yet  the  patient  dies  for  want  of  proper  surgical  intervention." 

The  various  descriptions  of  this  medical  treatment  are  a  mass  of  con- 
tradictions. Some  writers  say  :  "  Avoid  enemata  and  purgatives,  which 
excite  peristalsis,  and  favour  the  spread  of  the  disease.  Give,  rather,  opium, 
which  checks  peristalsis  and  induces  constipation."  Other  writers  say  : 
"  Give  purgatives  in  appendicitis,  because  they  favour  intestinal  antisepsis 
and  lessen  the  infection  in  the  intestine." 

These  theories  regarding  purgatives,  balladonna,  or  opium  prove  that 
the  old  views  of  the  pathogenesis  of  ajjpendicitis  have  still  some  weight. 
This  arises  from  the  fact  that  we  are  still  fettered  by  wrong  theories,  which 
confound  apjiendicitis,  typhlitis,  and  enteritis,  and  deny  to  appendicitis  its 
proper  independence.     1  would  ask  of  what  use  is  it  in  appendicitLs  to 


768  TEXT-BOOK  OF  MEDICINE 

administer  .some  castor-oil  or  magnesia  ?  There  exists  in  tlie  appendix  a 
focus  absolutely  isolated  from  the  rest  of  the  intestine,  in  which  the  toxi- 
infection  is  being  elaborated.  What  benefit,  then,  can  result  from  purga- 
tives, belladonna,  or  opium  ?  Physicians  hold  that  they  can  cure  appen- 
dicitis with  purgatives  or  other  medical  measures.  They  exaggerate  the 
importance  of  these  measures,  and  they  wrongly  suppose  that,  in  order  to 
act  on  the  appendix,  they  must  act  through  the  intestine  !  To  reach  the 
appendix  we  must  open  the  abdomen. 

The  so-called  medical  treatment  is  both  inefficient  and  inopportune, 
because,  as  soon  as  pain  heralds  the  onset  of  appendicitis,  the  mischief  is 
already  done — the  canal  is  obstructed,  the  focus  is  formed,  the  toxi-infection 
elaborated  in  the  appendix  is  beginning  its  work,  and  no  one  can  tell  where 
this  work  will  end.  Colonies  of  virulent  microbes  traverse  the  walls  of  the 
closed  cavity,  the  appendicular  vessels  become  thrombosed,  gangrene  is 
imminent,  the  toxines  are  absorbed,  and  the  poison  is  spread  through  the 
system,  while  the  relative  merits  of  belladonna  and  opium  are  being  dis- 
cussed !  Moreover,  we  know  the  result  of  this  medical  treatment,  Chauvet 
says  that  the  death-rate  has  been  30  per  cent.,  without  counting  the  patients 
who  did  not  succumb  to  the  first  attack  of  appendicitis,  but  recovered  with 
a  damaged  appendix,  and  were  therefore  predisposed  to  fatal  recurrence  at 
an  earlier  or  later  date  (Reclus).  A  death-rate  of  30  per  cent,  is  not  equalled 
in  the  annals  of  the  most  deadly  of  our  diseases,  even  though  we  go  back 
to  former  epidemics  of  typhoid  fever,  scarlatina,  or,  diphtheria. 

As  regards  the  cause  of  death  in  these  cases,  Chauvet  writes  :  "  The 
patients  usually  succumb  from  general  suppurative  peritonitis,  sometimes 
from  peritoneal  septicaemia,  or  at  other  times  from  an  infection  of  the  entire 
system,  starting  from  purulent  or  gangrenous  sinuses  that  originate  in  the 
appendicular  focus."  Since  this  focus  is  the  cause  of  the  disease  and  of 
death,  would  not  early  surgical  intervention  be  better  than  ice,  purgatives, 
or  opium  ? 

Early  surgical  intervention  is  the  only  rational  treatment  of  appendicitis, 
because  it  alone  affords  protection  from  immediate  and  remote  complica- 
tions, and  because  it  alone  forestalls  relapses  and  the  results  seen  in  appen- 
dicitis which  has  not  been  operated  on.  We  sometimes  operate  too  late. 
We  all  know  of  such  cases,  and  if  we  count  them  up  we  shall  gain  a  more 
accurate  idea  of  the  value  of  medical  treatment.  I  cannot  see  the  advantage 
of  temporizing.  A  patient  has  acute  appendicitis,  and  the  ajDpendix  is, 
perhaps,  on  the  point  of  perforating  or  becoming  gangrenous,  and  you 
temporize.  A  patient  has  peritonitis  which  is  becoming  diffuse,  and  you 
are  satisfied  to  use  purgatives,  opium,  or  the  ice-bag.  My  opponents  will 
say  :  "  We  only  advise  operation  in  cases  of  appendicitis  with  peritoneal 
complications,  in  which  it  has  been  proved  to  us  that  medical  treatment  is 


DISEASES  OF  THE  INTESTINE  769 

insufficient.  I  would,  however,  ask  them  :  "  By  what  signs  and  symptoms 
can  you  prophesy  as  to  the  course  of  appendicitis  ?  Can  you  say  that  the 
Case  is  not  one  of  toxic  appendicitis,  which  is  more  to  be  feared  than  the 
infective  form  ?"  When  appendicitis  has  commenced,  no  one  can  say 
what  terrible  surprises  may  happen.  I  have  repeatedly  said  that  the 
violence  of  the  fever  and  the  rise  in  temperature  have  absolutely  no  precise 
signification.  In  many  cases  the  temperature  is  but  slightly  raised,  in  spite 
of  peritonitis.  The  intensity  of  the  pain  and  the  general  symptoms  are 
deceptive  when  we  have  to  distinguish  between  appendicular  and  peri- 
toneal lesions,  because  peritonitis  is  often  insidious,  and  appears  without 
hiccough,  vomiting,  or  rise  of  temperature. 

In  my  clinical  lectures  I  have  described  apparently  benign  cases  of 
appendicitis  in  which  gangrene,  perforation  of  the  appendix,  and  peritonitis 
had  set  in  within  forty-eight  hours. 

In  my  first  case  the  fever  was  insignificant,  and  the  appendicitis  appeared  to  be 
most  benign  ;  but  yet  in  forty  hours  the  appendix  had  perforated,  and  the  peritonitis 
was  fully  developed.  In  my  second  case  the  appendicitis  seemed  so  trifling  at  first 
that  the  patient  thought  it  was  indigestion,  and  yet  in  twenty-eight  hours  the  appendix 
had  jjerforated  and  the  peritonitis  was  diffuse.  In  my  fourth  case  the  fever  was  slight 
and  the  symptoms  were  very  trifling,  but  yet  the  operation,  though  performed  twenty- 
eight  hours  after  the  onset  of  symptoms,  proved  the  existence  of  diffuse  peritonitis. 
The  indication,  or  the  contra-indication,  for  an  operation  cannot,  therefore,  be  based 
on  the  severity  or  on  the  apparent  benignity  of  the  disease. 

If  the  reader  will  refer  to  the  sections  on  toxic  infection  of  the  liver, 
kidneys,  and  stomach  in  appendicitis,  he  \vill  find  numerous  cases  of  patients 
who  were  either  not  operated  upon  or  were  operated  upon  too  late.  They 
succumbed,  not  to  the  infection,  but  to  the  intoxication,  because  the  latter 
invades  the  system  more  quickly  than  the  former. 

In  most  cases  of  appendicitis  it  is  impossible  to  foretell  the  course  of 
events,  and,  a  fortiori,  it  is  impossible  to  push  the  finesse  of  diagnosis  so  far 
as  to  say  that  appendicitis  is  plastic,  parietal,  or  otherwise.  These  classifi- 
cations, which  are  faulty  in  pathological  anatomy,  are  absolutely  illusionary 
in  clinical  medicine.  As  regards  treatment,  appendicitis  is  indi\'isible.  We 
can  never  say  whether  appendicitis  may  not  be  complicated  with  severe 
infection  or  toxaemia.  On  the  second,  third,  or  fourth  day  the  appendix 
may  perforate,  and  death  may  threaten.  Medical  treatment  masks  the 
symptoms,  dulls  the  pain,  and  quickly  leads  the  patient  to  his  death. 

As  regards  the  surgical  treatment  of  appendicitis,  two  camps  have  been 
formed.  To  the  one  camp  belong  those  who  advise  the  "  cold  "  operation — 
that  is,  they  do  not  operate  until  the  appendicitis  has  "  cooled  ";  the  other 
camj)  comprises  the  partisans  of  the  "  hot  "  operation  — that  is,  those  who 
operate  during  the  acute  stages  in  order  to  suppress  quickly  the  cause  of 
the  mischief. 

49 


770  TEXT-BOOK  OF  MEDICINE 

It  is  evident  that  someone  is  at  fault  in  proclaiming  that  the  operation 
should  be  performed  when  "  cold,"  or  that  it  should  be  carried  out  when 
"  hot." 

The  adherents  of  the  "  cold  "  operation  publish  statistics  which  have 
the  appearance  (and  nothing  but  the  appearance)  of  success.  It  is  said 
that  the  "  cold  "  operation  gives  remarkable  successes,  whilst  the  "  hot " 
operation  shows  many  failures. 

Let  me  explain.  The  wonderful  results  of  the  "  cold  "  operation  are 
stated,  and  when  these  figures  are  compared  with  those  of  the  "  hot " 
operation,  at  first  sight  they  appeal  to  our  imagination.  This  is  only  an 
optical  delusion,  for  these  figures  do  not  really  state  the  case  fairly.  Let 
us  place  the  matter  in  its  real  light,  and  consider  the  question  of  postponing 
operation  in  acute  appendicitis  until  the  disease  has  "  cooled."  In  the  first 
place,  the  success  of  the  "  cold  "  operation  need  cause  no  surprise.  The 
"  cold  "  operation  is  performed  on  a  patient  who  is  practically  weU.  The 
acute  phase  has  passed,  the  more  or  less  poisoned  system  has  issued  vic- 
toriously from  the  strife,  and  when  the  peril  is  passed  the  "  cold  "  operation 
collects  the  remains  lying  on  the  field  of  battle.  Let  us  beware  of  ascribing 
to  such  belated  surgical  intervention  the  honours  of  the  cure.  The  "  cold  " 
operator  extinguishes  a  focus  which  is  no  longer  on  fire.  Nevertheless,  he 
performs  a  useful  piece  of  work  in  safeguarding  the  future,  but  do  not  let 
us  give  to  these  statistics  an  importance  which  they  do  not  possess. 

These  statistics  ought  to  be  all  the  more  modest,  because  they  should 
give  the  number  of  victims  who  have  succumbed  to  acute  appendicitis 
during  the  so-called  "  hot "  stage.  Many  patients  while  awaiting  the 
"  cold  "  stage  succumb  in  the  very  midst  of  the  "  hot "  stage."  My 
grievance  against  these  statistics  is  that  they  only  refer  to  the  actual  opera- 
tion, and  take  no  count  of  the  deaths  due  to  putting  off  the  operation.  In 
forty  cases  of  acute  appendicitis,  ten,  on  an  average,  die  of  infection  and 
intoxication  whilst  awaiting  the  "  obligatory  cooling."  The  statistics  which 
have  only  the  "  cold  "  operation  in  view  take  care  not  to  mention  these 
deaths,  which,  however,  may  clearly  be  laid  to  the  teaching  deduced  from 
these  figures  ;  and  hence  the  said  statistics  falsify  our  conclusions  and  our 
judgment,  as  well  as  that  of  the  public.  For  several  years  past  I  have  care- 
fully considered  appendicitis  from  the  medical  and  the  surgical  point  of 
view.  I  have  kept  in  touch  with  these  questions,  and  the  catastrophes  I 
have  seen  have  led  me  to  protest  against  the  unsound  idea  of  "  cooled- 
down  "  appendicitis. 

The  partisans  of  "  cold  "  operations  do  not  fail  to  point  out  the  inferiority 
of  the  statistics  concerning  "  hot "  operations.  Here  again  the  statistics, 
as  they  are  presented  to  us,  are  merely  an  optical  delusion.  Faulty  com- 
pilation and  wrong  interpretation  lead  to  error.     As  a  matter  of  fact,  in 


DISEASES  OF  THE  INTESTINE  771 

these  statistics  of  "  hot "  operations,  writers  have  classed  together  opera- 
tions performed  at  every  period  of  the  so-called  "  hot  "  stage,  and  do  not 
take  the  trouble  to  tell  us  whether  the  operation  was  performed  on  the  first 
day  of  the  disease  or  at  some  later  date.  Exact  details  which  would  be  of 
the  greatest  value  are  generally  passed  over  in  silence.  We  are  informed 
of  one  thing  only — viz.,  that  the  patient  was  operated  on  in  the  "  hot " 
stage,  and  statistics  drawni  up  en  hloc  are  naturally  erroneous,  because  they 
omit  the  most  important  thing — viz.,  the  day  on  which  the  operation  was 
performed.  This  point  sums  up  the  whole  question.  A  case  of  appen- 
dicitis which  would  have  been  cured  by  timely  operation  may  end  in  death 
if  the  operation  is  postponed  to  the  third  day  or  later.  If  the  operation  is 
done  too  late  in  the  "  hot  "  phase,  when  the  patient  is  already  hopelessly 
poisoiied,  failure  will  result.  The  failure  is  then  wrongly  attributed  to  the 
"  hot  "  operation.  These  statistics  ew  bloc  concerning  the  failure  of  "  hot  " 
operations  are  therefore  worthless,  and  we  must  be  the  more  on  our  guard 
because  by  their  apparent  simplicity  they  falsify  our  judgment  and  they 
deceive  the  pubUc. 

On  the  other  hand,  if  we  analyze  carefully  cases  of  appendicitis  operated 
upon  at  various  periods  of  the  so-called  "  hot "  stage,  we  shall  see  that  the 
ideal  plan  is  to  operate  as  soon  as  possible  after  the  onset — not  later  than 
forty  hours — because  in  almost  every  case  the  danger  is  at  that  time 
limited  to  the  appendicular  focus.  By  removing  this  focus  we  cut  away 
the  root  of  the  disease. 

I  know  that  it  is  not  always  easy  to  intervene  so  c^uickly,  but  we  as 
physicians  and  surgeons  are  responsible  for  postponing  the  operation  until 
tlie  appendicitis  has  "  cooled,"  because  we  expose  the  patient  to  the  risk  of 
death  by  so  doing. 

I  can,  moreover,  give  exact  details  of  more  than  200  cases  of  appen- 
dicitis which  have  been  operated  upon  by  well-kno^vn  surgeons.  Cases  of 
grave  appendicitis  operated  on  in  the  first  forty-eight  hours  have  almost  all 
recovered.  The  few  failures  were  cases  of  toxic  appendicitis,  with  gangrene, 
high  fever,  great  pain,  and  profuse  vomiting.  In  such  cases  the  operation 
at  the  end  of  the  second  day  is  almost  too  late. 

Until  lately  neither  the  appendicular  intoxication  nor  the  rapidity  of  its 
course  has  been  studied.  The  disease  makes  irremediable  progress  in  a  few 
hours.  A  patient  who  would  have  been  saved  by  an  operation  before  the 
end  of  the  second  day  may  succumb  if  he  has  been  operated  on  a  few  hours 
later,  because  his  organs  have  become  poisoned  by  the  toxines. 

In  severe  cases  of  acute  appendicitis  operation  on  the  third  day  may 
be  succes.sful,  but  such  a  result  is  not  constant.  The  toxi-infection  has 
already  made  headway,  and  is  more  to  be  feared  than  on  the  second  day. 
Amongat  those  who  recover,  some  arc  in  great  danger  for  a  time. 

4'J— 2 


772  TEXT-BOOK  OF  MEDICINE 

As  for  cases  of  severe  appendicitis  operated  upon  on  the  fourth  day,  and, 
a  fortiori,  later,  I  can  give  no  definite  answer.  There  have  been  numerous 
successes,  but  the  failures  depend  on  the  degree  of  the  infection  and  poison- 
ing which  have  had  time  to  act  before  the  operation.  Too  often  the  opera- 
tion is  performed  too  late. 

These  facts  prove  that  we  must  strive  to  make  a  correct  diagnosis. 
The  patients  or  their  friends  sometimes  tell  us  that  the  disease  began  twenty- 
four  or  forty-eight  hours  previously,  because  they  make  the  onset  of  the 
disease  coincide  with  the  greatest  pain.  Methodical  examination  may 
rectify  the  error,  showing  us  that  a  case  of  appendicitis  said  to  be  two  is 
really  three  or  four  days  old.  These  details  are  of  extreme  importance,  for 
everything  is  of  importance  in  a  disease  where  even  twelve  hours  or  less 
can  change  the  course  of  events. 

These  ideas  must  be  universally  taught.  At  different  times  men  of  the 
highest  authority  have  proclaimed  similar  views,  and  have  done  much  for 
their  adoption.  My  colleague  Lucas-Championniere  recently  made  an 
interesting  communication  to  the  Academic  de  Medecine,*  and  even  more 
recently  Legueu,  Chaput,  G.  Marchant,  Segond,  Routier,  Hartmann,  Poirier, 
and  Villard,  have  collected  cases  and  communicated  their  views  to  the 
Societe  de  Chirurgie.  I  trust  their  teaching  will  banish  into  oblivion  the 
practice  which  exposed  patients  to  the  danger  of  death,  because  the  opera- 
tion was  delayed  until  the  appendicitis  had  "  cooled  down." 

Our  duty  as  physicians  is  to  come  to  a  decision,  and  to  imbue  the  laity 
with  our  convictions.  The  surgeon  is  too  often  called  in  after  we  have 
temporized  with  futile  medical  treatment.  It  is  not  sufficient  to  operate  : 
the  operation  must  also  be  timely. 

In  my  opinion,  thirty-six  hours  should  be  the  maximum  delay  in  grave 
cases  of  acute  appendicitis,  and  a  delay  of  forty-eight  hours  should  be  the 
maximum  in  less  severe  cases.  This  formula,  I  believe,  gives  absolute 
security.  By  it  the  toxic  focus  will  be  removed  before  irreparable  infection 
and  poisoning  have  had  time  to  occur. 

A  final  word  as  to  an  attack  of  appendicitis  which  has  not  been  operated  on. 

I  cannot  share  the  mental  calm  of  those  who  abandon  all  fear  when  the 
patient  has  recovered  from  the  attack  of  appendicitis.  The  fire  often 
smoulders  under  the  ashes,  and  the  appendix  is  ready  to  cause  relapse, 
perforation,  or  secondary  infection. 

Hceret  lateri  lethalis  arundo. 

There  is  one  formula  which  I  should  like  to  engrave  on  the  mind  of  those 

who  may  still  be  inclined  to  hesitate  :  You  will  never  repent  having  operated 

*  Academie  de  Medecine,  seance  du  15  Juillet,  1902,  et  Journal  de  Medecine  et  de 
Chirurgie  Pratiques,  10  Aout,  1902. 


DISEASES  OF  THE  INTESTINE  773 

on  a  case  of  appendicitis,  but  you  may  often  repent  that  you  did  not  do 
so  or  that  you  operated  too  late.  Given  a  correct  diagnosis  and  a  timely 
operation  performed  with  proper  skill,  patients  ought  not  to  die  of  appen- 
dicitis. 

Summary. — The  evolution  of  the  operative  indications  in  appendicitis 
is  the  natural  consequence  of  recent  research  which  has  elucidated  the 
question. 

If  we  look  backwards,  we  see  that  at  no  very  distant  date  the  danger 
of  appendicitis  was  supposed  to  consist  in  perforation  and  peritonitis. 
Peritonitis  was  looked  upon  as  the  only  complication  to  be  feared,  and 
it  sufficed,  so  it  was  thought,  to  watch  its  onset,  in  order  to  intervene 
successfully. 

The  question  of  appendicitis  was  soon  found  to  be  far  more  complicated. 
In  the  first  place,  the  symptoms  of  appendicitis  and  of  peritonitis  often 
blend,  so  that  it  is  almost  impossible  to  say  when  the  latter  commences. 
It  is,  therefore,  impossible  to  watch  for  its  appearance.  Furthermore, 
histological  and  bacteriological  researches  have  shown  that  the  patho- 
genic agents,  after  becoming  more  virulent  in  the  closed  cavity,  pass 
through  the  walls  of  the  unperforated  appendix,  and  at  times  cause 
acute  peritonitis.  As  this  form  has  not  the  sudden  onset  of  perfora- 
tive peritonitis,  its  appearance  mp.y  escape  the  notice  of  the  cleverest 
physician.  The  idea,  then,  commenced  to  gain  ground  that  in  operative 
interference  we  must  not  consider  the  peritonitis,  which  is  a  secondary 
complication,  but  only  the  appendicular  focus,  which  is  the  primary 
trouble. 

More  attention  was  paid  to  the  suppurative  infections  of  the  liver, 
pleurae,  pericardium,  lungs,  etc.  The  pathogenesis  of  these  remote 
infections  was  traced  out,  showing  that  they  arose,  not  from  the  peritonitis, 
but  from  the  appendicular  focus  whilst  it  was  cooHng  down.  It  became 
obvious  from  the  point  of  view  of  surgical  success  that  we  must  early  remove 
the  appendicular  focus. 

Finally,  the  toxicity  of  appendicitis  was  proved,  and  it  was  shown  that 
the  intestinal  microbes  in  the  closed  cavity  may  kill  by  the  toxines  which 
they  produce.  These  toxines  cause  the  early  lesions  in  the  kidneys,  liver, 
stomach,  etc.,  and  are  in  a  large  degree  responsible  for  the  rapidly  fatal 
complications  of  appendicitis.  To  this  toxaemia  of  appendicular  origin  I 
have  given  the  name  of  appendicaemia.  Peritonitis  has  nothing  to  do 
with  it. 

Peritonitis  has,  therefore,  lost  its  former  importance.  It  is  no  longer 
the  solo  object  considered  by  the  operator,  though  it  remains  one  of  the  most 
formidable  complications  in  appendicitis.  The  predominant  importance  of 
the  appendicular  focus  as  being  the  origin  of  the  infection  and  of  the  poison 


774  TEXT-BOOK  OF  MEDICINE 

is  now  recognized.  The  danger  is  not  limited  to  the  peritoneum.  The  focus 
in  the  appendix  can  produce  appendicaemia,  and  peritonitis  is  of  minor 
importance.  Surgical  intervention  must  systematically  and  promptly 
attack  the  frimum  movens  of  the  trouble  in  the  appendix. 

We  must  never  think  solely  of  the  peritonitis,  thereby  overlooking  the 
rapidly  fatal  complications  due  to  the  appendicular  toxines.  Delay  in 
operation  till  the  appendicitis  has  "  cooled  down "  may  condemn  the 
patient  to  death  by  giving  the  terrible  toxi-infection  time  to  spread ;  an  evil 
that  is  too  often  irremediable. 


IV.  MUCOUS,  MEMBRANOUS,  AND  SABULOUS  ENTERO-TYPHLO- 
COLITIS— INTESTINAL  LITHIASIS. 

This  section  deals  with  mucous,  membranous,  and  sabulous  entero- 
t5^hlo-colitis,  because  all  these  forms  may  show  similar  symptoms,  and 
may  coexist  or  follow  one  another  in  the  same  individual.  A  description 
limited  to  muco- membranous  entero-coHtis  and  omitting  the  sabulous  variety 
would  be  quite  incomplete.  "  Entero-colitis  "  has  always  appeared  to  me 
an  imperfect  name,  because  it  only  includes  the  small  intestine  and  the 
colon,  and  apparently  disregards  the  caecum,  which  plays  a  very  important 
part.  I  have,  therefore,  substituted  the  name  "  entero-tyjjhlo-colitis,"  in 
order  to  comprise  the  small  intestine,  the  caecum,  and  the  large  intestine, 
which  all  take  their  share  in  this  disease.  The  colon,  however,  takes  the 
chief  share,  whilst  the  small  intestine  plays  but  a  minor  part.  Before 
describing  entero-typhlo-cohtis,  I  think  that  it  will  be  useful  to  quote  cases 
from  my  clinical  lectures.* 

A  young  woman  was  suffering  from  severe  attacks  of  abdominal  pain,  which  was 
most  marked  in  the  right  iliac  region,  and  thus  simulated  appendicitis.  This  condition 
had  begun  a  few  months  previously,  and  was  characterized  by  attacks  of  colic,  with  the 
passage  of  mucus  and  skin-like  membranes  in  the  stools.  The  attack  of  cohtis  was 
followed  by  acute  enteritis,  and,  later,  by  habitual  constipation.  Intestinal  crises 
occurred  from  time  to  time,  the  pain  being  present  both  night  and  day.  The  pains 
were  accompanied  by  tympanites  ;  they  lasted  for  several  hours  and  spread  over  the 
whole  abdomen,  though  they  were  sometimes  more  marked  in  the  right  iliac  fossa. 
After  examination,  and  for  reasons  which  I  shall  detail  later,  I  dismissed  the  idea  of 
appendicitis,  as  I  thought  the  case  might  be  one  of  sabulous  typhlo-colitis.  I  had  the 
faeces  examined.  My  opinion  was  confirmed,  for  abundant  sand,  as  well  as  membranes, 
was  present. 

A  little  boy  had  for  a  year  suffered  from  sharp  attacks  of  pain  along  the  descending 
colon.  The  parents  had  noticed  that  the  attacks  were  followed  by  the  appearance  of 
shme  and  membranes  in  the  stools.  As  I  thought  that  sand  might  also  be  present,  I 
had  the  faeces  examined.  They  contained  an  enormous  amount  of  sand.  I  saw  several 
of  the  attacks.     The  pains  were  not  general,  but  were  confined  chiefly  to  the  left  ihac 

*  Clinique  Medicale  de  V Hotd-Dieu,  1897,  14""*  le9on. 


DISEASES  OF  THE  INTESTINE  775 

fossa,  in  the  region  of  tlie  descending  colon.  The  crises  lasted  from  a  few  hours  to  a 
whole  day,  or  even  longer,  the  pain  being  as  severe  as  in  renal  coUc,  and  causing  the 
patient  to  cry  out. 

In  1892  I  saw  a  lady,  aged  about  fifty,  with  abdominal  pains,  which  came  on  without 
appreciable  cause  at  indeterminate  periods.  The  pains  were  accompanied  by  ballooning 
of  the  abdomen,  nausea,  and  constipation.  In  1895  the  crises  became  more  frequent 
and  severe,  lasting  for  days  and  simulating  the  intense  suffering  of  hepatic  coUe.  The 
pain  was  sometimes  accompanied  by  a  feehng  of  faintness.  I  thought  of  hepatic  cohc, 
appendicitis,  and  ulcer  of  the  stomach  or  of  the  duodenum ;  but  I  soon  rejected  these 
ideas,  because  the  locahzation  of  the  pains  and  the  other  symptoms  did  not  justify 
them.  The  pain  was  certainly  not  confined  to  any  precise  spot,  and  though  it  seemed 
to  commence  in  the  epigastric  region,  it  soon  invaded  the  hypochondria,  the  flanks, 
and  the  hypogastrium,  extending  up  as  high  as  the  thorax.  One  day,  after  a  violent 
crisis,  the  patient  showed  me  some  pieces  of  stone  ^nd  a  quantity  of  coarse  sand  which 
she  had  passed  per  rectum.  It  was,  therefore,  a  clear  case  of  intestinal  Uthiasis.  I 
may  add  that  this  patient  had  for  some  years  been  subject  to  attacks  of  muco-mem- 
branous  colitis,  the  stools  often  containing  slime  and  membranes.  The  sand  was 
composed  of  organic  matter  and  a  small  quantity  of  hme  salts  ;  the  larger  fragments 
were  made  up  of  phosphate  of  lime  and  of  organic  matter  in  smaller  proportion. 

Description. — We  find  a  chronic  form  of  colitis,  in  which  constipation  is 
the  chief  symptom.  The  pains  are  at  times  very  sharp,  and  appear  a  few 
hours  after  meals,  either  daily  or  at  longer  intervals.  They  are  limited,  for 
the  most  part,  to  the  region  of  the  transverse  colon,  giving  rise  to  the  sensation 
of  a  painful  bar  across  the  upper  part  of  the  belly.  The  constipation  is  so 
obstinate  that  it  may  continue  for  a  fortnight  or  even  longer.  The  patient 
complains  of  heaviness  in  the  head.  In  order  to  overcome  the  constipation, 
he  makes  immoderate  use  of  enemata  and  purgatives.  At  meals  he  selects 
"  the  most  nourishing  foods."  He  has  a  constant  desire  to  stool,  and 
becomes  h}^ochondriac  and  neurasthenic.  During  this  obstinate  constipa- 
tion hard  and  dark-coloured  matter,  blood-stained  mucus,  and  membranes 
are  passed. 

In  another  variety  we  find  entero-colitis,  accompanied  by  frequent  and 
at  times  continuous  diarrhoea.  This  form  is  rarely  chronic  at  first.  It  is 
almost  always  preceded  by  acute  or  subacute  attacks.  Colic  may  not  exist, 
and  diarrhoea  is  the  chief  symptom.  This  diarrhoea,  which  may  be  accom- 
panied by  borborygmi,  usually  comes  on  after  meals,  and  several  stools  are 
passed  in  the  twenty-four  hours.  The  character  of  the  dejecta  varies.  They 
are  often  yellowish  or  greenish,  and  horribly  foetid.  In  some  cases  bloody 
mucus  and  membranous  ribbons  are  noticed.  When  the  stools  contain 
food  which  is  incompletely  digested,  we  speak  of  lienteria  (laxitas  intes- 
tinarum)  (Xeto?,  gliding ;  evrepov,  intestine).  There  are  periods  of  remission 
and  of  exacerbation,  and  even  if  the  disease  is  only  of  short  duration,  it 
induces  a  loss  of  flesh  which  attracts  attention,  and  causes  us  to  think  of 
intestinal  tuberculosis. 

Muco-mombranous  and  sabulous  entero-typhlo-colitis  are  common  in 
children.     With  Hutinel  and  Valmont  I  saw  a  little  girl  of  four  and  a  half 


776  TEXT-BOOK  OF  MEDICINE 

years  of  age  who  had  been  suffering  for  a  long  time  from  muco-membranous 
colitis,  the  stools  at  times  containing  much  intestinal  sand.  Analysis  by 
Berlioz  showed  that  it  was  composed  of  organic  matter,  with  salts  of  lime 
and  magnesia. 

Subacute  follicular  enteritis  is  the  most  typical  form  of  entero-colitis  in 
children.  It  is  fairly  frequent  between  one  year  and  five  years  of  age,  and 
may  last  for  months  or  years.  We  often  see  acute  attacks  of  intestinal 
infection,  accompanied  by  alarming  symptoms — infectious  erythema,  fever, 
vomiting  of  food,  mucus,  or  bile,  slimy  or  blood-stained  stools,  and  sharp 
pains  in  the  descending  colon  or  caecum. 

The  above  symptom-complex  is  characteristic  of  entero-colitis.  If  the 
symptoms  chiefly  afiect  the  region  of  the  ceecum,  a  correct  diagnosis  may 
be  difficult,  and  an  operation  may  be  advised  for  appendicitis,  which  does 
not  exist. 

The  course  of  entcro-typhlo-colitis  varies.  The  disease  may  take  the 
form  of  acute  crises,  which  recur  year  after  year,  or  may  install  itself  slowly 
with  diarrhoea  or  constipation,  fever,  and  the  passage  of  membranes  and 
sand.  Typhlo-colitis  may  be  simply  sabulous,  though  it  is  more  frequently 
muco-membranous.  Nevertheless,  a  patient  who  has  passed  mucus  and 
membranes  for  a  long  time,  may  also  have  passed  intestinal  sand  which  has 
not  been  noticed.  As  a  matter  of  fact,  slime  and  membranes  are  more 
easily  distinguished  by  their  form  and  colour  than  sand,  which  is  intimately 
mixed  with  the  fseces. 

The  pains  of  typhlo-colitis  have  no  definite  seat.  They  may  be  most 
marked  in  the  transverse  colon  as  a  painful  bar,  in  the  caecum,  at  the  hepatic 
flexure,  or  along  the  course  of  the  descending  colon.  It  is  rare,  however, 
for  the  pains  to  remain  localized  to  one  of  these  regions.  They  usually 
become  general  over  a  part  of  the  abdomen.  I  have,  too,  seen  patients 
who  had  lumbar  pains  somewhat  like  those  of  renal  colic,  and  thoracic 
and  precordial  pains  somewhat  Hke  those  of  angina  pectoris.  These 
facts  had  already  been  noticed  by  Potain  in  his  masterly  description  of 
colitis. 

The  attack  of  entero-typhlo-colitis  does  not  always  begin  suddenly.  It 
is  often  preceded  by  malaise  and  ballooning  of  the  abdomen.  I  may  even 
say  that  tympanites  (with  or  without  eructations)  is  one  of  the  most  fre- 
quent and  pronounced  symptoms.  The  crisis  which  is  preceded  by  these 
prodromata  may  last  as  long  as  thirty-six  hours.  These  attacks  of  intes- 
tinal colic  are  frequently  followed  by  the  passage  of  firm  motions,  which 
contain  slime,  membranes,  and  sand. 

The  crises  may  be  repeated  for  several  days  following  at  a  fixed  hour 
shortly  after  meals.  They  may  recur  several  times  a  month  or  several 
times  a  year.     One  patient  may  have  a  series  of  crises  lasting  for  some  days 


DISEASES  OF  THE  INTESTINE  777 

or  weeks,  and  may  then  remain  well  for  a  long  time.  Another  patient,  on 
the  contrary,  may  from  time  to  time  have  a  crisis  lasting  some  hours,  and 
recurring  every  month  for  many  years. 

Entero-typhlo-colitis  is  often  associated  with  dilatation  of  the  stomach, 
flatulence,  and  loss  of  appetite.  In  some  instances  the  gastric  symptoms 
precede  the  intestinal  troubles.  The  patient  is  disposed  to  nervous  symp- 
toms (hypochondria,  neurasthenia,  melancholia),  and  to  reflex  troubles, 
which  comprise  dyspnoea,  transient  tricuspid  insufficiency,  precordial  pain 
resembling  angina  pectoris,  vertigo,  and  tremors,  supervening  during  intes- 
tinal digestion. 

Some  patients  stand  entero-colitis  without  ill-efPect  and  finally  recover, 
but  others  are  more  seriously  affected,  losing  flesh  and  appearing  to  have 
tuberculosis. 

Many  explanations  are  given  of  the  intestinal  infection  just  described. 
It  is  hereditary,  and  I  have  seen  several  cases  of  entero-colitis  in  the  same 
family.  It  has  been  asserted  that  entero-cohtis  is  more  frequent  in  people 
who  lead  a  sedentary  life  or  give  themselves  up  to  overstudy.  Muco-mem- 
branous  colitis  is  often  associated  with  uterine  lesions,  and  is  said  to  be 
due  to  an  infection  of  the  intestine  from  the  genital  organs.  We  shall  see 
later  the  effect  of  arthritism. 

The  membranes  and  the  sand  deserve  notice.  The  false  membranes 
may  be  passed  in  fragments  or  rolled  up  in  balls.  They  are  whitish,  firm, 
thick,  and  ribbon-like,  so  that  the  patient  takes  them  for  pieces  of  a  tape- 
worm. The  ribbons  may  be  ^  inch  broad,  and  4  or  5  inches  long.  They 
are  formed  of  mucus,  degenerated  epithelial  cells,  salts,  and  in  exceptional 
cases  cholesterin. 

The  sand  appears  in  various  forms.  Most  frequently  it  is  a  yellowish 
or  brownish  sand,  mixed  with  matter,  from  which  it  must  be  separated  by 
washing  and  sifting.  Sometimes  we  find  sand  and  pieces  of  gravel  as  large 
as  a  grape-pip  or  a  haael-nut.  The  chemical  composition  is  always  the 
same,  and  we  find  two  elements  present  in  variable  proportions — stercoral 
matter  and  salts  of  lime  and  magnesia,  with  traces  of  silica  and  chlorides. 
Cholesterin,  which  is  present  in  gall-stones,  is  not  found.  On  the  other 
hand,  gall-stones  never  contain  organic  matter  of  stercoral  origin. 

It  may,  therefore,  be  said  that  sand,  gravel,  or  calculi  composed  of 
stercoral  matter  and  of  lime  and  magnesia  salts  are  of  intestinal  origin. 
Mixed  calcuU  may,  however,  be  found  containing  cholesterin,  salts  of  lime, 
and  stercoral  matter.  In  this  case  the  sand  or  the  calculi  have  originated 
in  the  gall-bladder,  and  have  taken  up  the  stercoral  matter  in  their  ])assage 
through  the  intestine.  I  would,  however,  add  that  cases  of  mixed  hthiasis 
(sand  or  gravel)  must  be  exceedingly  rare.  I  shall  shortly  speak  of  a  patient 
ill  whom  attacks  of  biliary  and  intestinal  litliiasis  appeared,  together  or  in 


778  TEXT-BOOK  OF  MEDICINE 

succession,  and  yet  the  gall-stones  and  the  intestinal  gravel  (analyzed  by 
Berlioz)  retained  their  own  characters,  never  showing  a  mixed  composition. 

Intestinal  Lithiasis. — Intestinal  sand  is  of  minor  importance  in  entero- 
typhlo-colitis.  I  have  always  seen  it  associated  with  muco-membranous 
coKtis.  We  might  admit  in  such  a  case  an  infectious  catarrh  dependent  on 
microbic  agents,  and  giving  rise  to  the  intestinal  sand  or  gravel  (lithogenous 
catarrh).  In  the  pathological  history  of  these  patients  we  may  find  typhoid 
fever,  dysenteric  catarrh,  profuse  diarrhoea,  or  obstinate  constipation.  The 
production  of  intestinal  sand,  therefore,  would  be  simply  an  epiphenomenon, 
associated  with  the  infectious  lesions  in  the  intestine.  This  view  of  the 
question  is  perfectly  reasonable,  and  I  believe  that  the  presence  of  intestinal 
sand  is  part  and  parcel  of  chronic  colitis  or  muco-membranous  entero- colitis, 
without  any  other  designation. 

In  other  cases  the  facts  may,  I  believe,  be  interpreted  differently,  intes- 
tinal lithiasis  being  looked  upon  as  one  of  the  most  interesting  manifesta- 
tions of  the  gouty  diathesis  (Mongour,  Fontet).  The  question  has  been 
asked,  and  I  should  like  to  add  certain  proofs  that  intestinal  lithiasis  is 
sometimes  of  gouty  origin,  just  as  much  as  renal  gravel  or  tophi  are. 

Laboulbene  reports  the  case  of  a  man  having  haemorrhoids,  asthma,  and  renal  colic 
as  evidences  of  the  gouty  diathesis.  He  had  been  sent,  when  forty  years  of  age,  to 
Vichy  for  phosphatic  gravel.  When  the  gravel  disappeared  from  the  in-ine,  he  suffered 
from  enteralgia,  and  passed  intestinal  sand,  composed  of  organic  matter  and  phosphates 
of  hme  and  magnesia. 

I  saw  with  Charrier  a  lady  of  gouty  stock  who  passed  gall-stones  and  coarse  intestinal 
sand.  The  calculi  and  sand  were  analyzed  by  Berhoz,  and  the  interesting  feature 
was  that  each  preserved  its  own  proper  composition — cholesterin  in  the  gall-stones, 
stercoral  matter  and  salts  of  hme  in  the  intestinal  gravel.  Her  brother  has  several 
times  passed  renal  calculi,  and  has  been  operated  upon  for  vesical  calculus.  Their 
parents  are  gouty  and  suffer  from  haemorrhoids. 

I  saw  the  following  case  with  Renon  :  A  man  of  thirty-three,  whose  family  was 
eminently  arthritic  (the  father  and  mother  having  suffered  from  sick  headache,  eczema, 
and  gall-stones,  while  the  grandparents  were  rheumatic,  stout,  diabetic,  and  gouty), 
had  been  subject  to  sick  headache  since  the  age  of  five.'  A  few  years  before,  eczema 
appeared  on  the  hands  and  face,  and  resisted  all  treatment.  Three  years  ago  haemor- 
rhoids appeared  and  the  sick  headaches  disappeared.  Some  months  ago  he  noticed 
slimy  mucus  in  his  stools.  They  were  carefully  examined,  and  about  forty  stones  of 
the  size  of  a  grape-stone  were  found.  This  voiding  of  gravel  was  neither  preceded  nor 
accompanied  by  abdominal  pains,  which  are  so  common  in  sabulous  colitis.  It  is 
worthy  of  note  that  the  patient  was  in  excellent  health  at  this  time.  On  the  other  hand, 
the  sick  headaches  and  the  eczema  of  the  hands  and  of  the  labial  commissures  returned 
six  weeks  after  the  disappearance  of  the  gravel. 

These  examples  prove  the  close  connection  between  entero-colitis,  intes- 
tinal hthiasis,  and  the  gouty  diathesis.  They  show  that  gout,  renal  calculi, 
gall-stones,  and  intestinal  gravel  may  appear  in  the  same  individual  at 
different  periods  of  hfe,  or  exist  in  the  same  family  as  hereditary  manifesta- 
tions.   The  passage  of  intestinal  gravel  coincides  or  alternates  with  the  other 


DISEASES  OF  THE  INTESTINE  779 

manifestations  of  arthritism.  It  may  replace  them,  and,  as  I  said  in  my 
communication  to  the  Academic  de  Medecine,*  I  propose  to  include  intes- 
tinal hthiasis  under  the  gouty  diathesis.  I  do  not  say,  of  course,  that 
every  case  of  intestinal  gravel  is  of  gouty  origin,  for  here,  as  elsewhere,  it 
may  be  independent  of  the  gouty  diathesis.  We  see  patients  who  are 
suffering  from  renal  colic,  though  we  are  not  able  to  find  gout  in  their  personal 
or  hereditary  antecedents.  The  same  fact  appHes  in  intestinal  Hthiasis.  It 
is,  then,  a  purely  local  complication,  almost  always  associated  with  muco- 
membranous  cohtis.  At  other  times  the  intestinal  gravel,  with  or  without 
muco-membranous  catarrh,  has  an  essentially  gouty  origin. 

From  this  point  of  view  the  phosphatic  composition  of  intestinal  gravel 
occasioned  some  doubt  in  the  mind  of  Mathieu,  who  asked  whether  con- 
cretions, principally  formed  of  salts  of  lime  and  magnesia,  could  be  con- 
sidered diathetic,  like  renal  calculi,  rich  in  urates,  or,  Hke  gall-stones,  rich  in 
cholesterin.  It  seems  to  me  that  the  composition  of  the  gravel  is  only  of 
secondary  importance  in  the  present  discussion,  because,  firstly,  clinical 
facts  point  to  the  diathetic  and  gouty  nature  of  this  gravel  in  certain  patients  ; 
and,  secondly,  because  gouty  patients  have  often  been  attacked  with  renal 
colic,  and  have  passed  gravel  composed  both  of  urates  and  phosphates.  I 
think  it  is  quite  clear  that  certain  cases  of  entero-typhlo-colitis  and  of 
intestinal  gravel  are  of  diathetic  origin. 

Diagnosis  of  Entero-Typhlo-Colitis.— I  shall  not  delay  in  diagnosing 
entero-typhlo-colitis  and  its  painful  crises  from  all  the  abdominal  pains 
which  may  simulate  it.  We  must,  however,  consider  how  to  distinguish  it 
from  hepatic  cohc  and  from  appendicitis.  Many  cases  of  so-called  hepatic 
colic  without  icterus  are  nothing  but  entero-coUtis.  The  study  of  these 
cases  shows  the  source  of  the  mistakes  made.  In  both  cases  the  pain  may 
reach  its  maximum  near  the  hepatic  flexure  of  the  transverse  colon.  In 
both  cases  food  and  bile  may  be  vomited.  The  radiation  of  the  pain,  how- 
ever, is  not  similar,  being  rather  thoracic  and  scapular  in  hepatic  colic,  and 
abdominal  in  entero-typhlo-colitis.  Tympanites  is  much  more  pronounced 
in  entero-cohtis  than  in  hepatic  colic.  The  only  true  way  of  making  an 
exact  diagnosis  is  to  examine  the  stools  for  membranes,  sand,  or  gravel. 
Chemical  analysis  will  reveal  their  origin. 

The  diagnosis  from  appendicitis  is  given  fully  in  the  last  section.  We 
must  now  consider  the  relations  said  to  have  been  noticed  between  entero- 
colitis and  ap|x;ndicitis. 

Appendicitis  is  not  the  Outcome  of  Entero-Colitis. — We  must  here 
discuss  a  most  important  question  in  pathogenesis  :  Have  enteritis  and 
typhlo-colitis  a  direct  influence  in  the  causation  of  appendicitis  ?     In  short, 

*  "  La  Lithiase  Intestinalo  ot  la  Clravcllo  do  I'lntcstin  "  {Acadeniie  de  Medecine, 
Boanco  du  9  Mars,  1897). 


780  TEXT-BOOK  OF  MEDICINE 

is  appendicitis  secondary  or  not  to  inflammations  or  infections  of  the  rest 
of  the  intestine  ? 

In  a  communication  to  the  Academic  de  Medecine  on  March  9,  1897, 
and  in  the  discussion  which  followed,  as  also  in  my  clinical  lectures  at  the 
Hotel-Dieu,  there  is  one  fact  which  I  have  tried  to  emphasize — viz.,  that 
patients  who  are  suffering  from  membranous  or  calculous  entero -typhlo- 
colitis rarely  suffer  from  appendicitis,  and  that  this  proves  that  appen- 
dicitis is  neither  the  consequence  nor  the  outcome  of  entero-colitis.  This 
rule,  of  course,  is  not  absolute.  Reclus  and  other  authors  have  collected 
cases  which  prove  that  the  same  subject  may  at  different  times  suffer  from 
muco- membranous  enteritis  and  appendicitis.  The  question,  however,  is 
not  whether  entero-colitis  and  appendicitis  may  sooner  or  later  succeed 
one  another  in  the  same  individual.  We  wish  to  know  to  what  extent  they 
can  coexist  or  follow  after  one  another.  If  people  with  entero-colitis  were 
really  threatened  with  appendicitis,  entero-colitis,  which  hitherto  has  been 
considered  as  a  benign  disease,  would  then  become  a  far  more  serious  malady. 

Comby  has  devoted  a  chapter  to  muco-membranous  entero-colitis  in  the 
*'  Traite  des  Maladies  de  I'Enfance,"  but  he  evidently  lays  no  stress  on  the 
relations  of  appendicitis  and  enteritis,  because  the  word  "  appendicitis  "  is 
not  mentioned.  Letcheff,  in  his  thesis,  reports  twenty-four  cases  of  muco- 
membranous  entero-colitis  collected  in  France  and  abroad,  but  he  makes 
no  mention  of  appendicitis.  Potain,  in  a  lecture  on  chronic  muco-mem- 
branous colitis,  makes  no  allusion  to  appendicitis, ,  and  yet  he  bases  his 
description  on  103  cases  of  colitis.  He  also  said  during  the  discussion  at 
the  Academic  :  "I  agree  entirely  with  Dieulafoy  in  considering  appen- 
dicitis during  the  course  of  entero-colitis,  not  as  the  rule,  but  as  a  most  rare 
exception." 

Bottentuit,  publishing  the  results  of  his  observations  for  some  twenty 
years,  saw  at  Plombieres  460  patients  suffering  from  muco-membranous 
entero-coUtis.  These  cases  are  subdivided  in  the  following  manner  :  250 
cases  in  women,  150  in  men,  and  60  in  children  ;  and  yet,  amongst  these 
460  patients,  not  one,  to  his  knowledge,  was  taken  ill  with  appendicitis, 
though  they  were  seen  several  years  following. 

Glenard  had  made  the  following  statement  :  "In  my  last  100  cases  of 
mucous  or  membranous  colitis  I  have  not  seen  a  single  example  of  appen- 
dicitis, and  I  have  no  recollection  of  having  ever  seen  one  previously." 
Tanche,  of  Lille,  has  told  me  of  three  persons  who  suffered  for  ten  years 
from  attacks  of  muco-membranous  entero-colitis,  but  yet  "  not  one  of  the 
three  had  any  sign  of  appendicitis."  Chabert,  of  Bagneres-de-Bigorre,  has 
communicated  to  me  his  observations  in  thirty-six  cases  of  patients  suffering 
from  muco-membranous  colitis,  and  "  not  one  of  them  showed  the  least 
symptom  denoting  infection  of  the  appendix," 


DISEASES  OF  THE  INTESTINE  781 

Langenhagen,  in  his  article  on  muco-membranous  colitis,  arrives  at  the 
following  conclusions  :  "  To  sum  up  the  debate,  I  cannot  do  better  than 
give  the  conclusions  of  Dieulafoy,  whose  ideas  have  been  confirmed  by 
Potain,  Duguet,  Hutinel,  Glenard,  Berger,  Hirtz,  Hudelo,  etc.  Appen- 
dicitis— I  do  not  mean  pseudo-appendicitis  (attacks  of  pain  in  the  ileo- 
csecal  region),  but  true  appendicitis,  verified  by  operation — is  quite  excep- 
tional in  the  course  of  entero- colitis.  We  must  not,  therefore,  consider 
appendicitis  as  the  consequence  or  the  cause  of  entero-colitis  until  we  are 
possessed  of  further  information." 

Ewald,  of  Berlin,  is  of  the  same  opinion,  and  holds  that  there  is  no 
relation  between  appendicitis  and  muco-membranous  colitis. 

I  quote  here  Pinard's  opinion  :  "  For  more  than  twenty  years  I  have 
observed  many  cases  of  membranous  entero -coKtis  in  women,  and  I 
find  that  appendicitis  is  exceedingly  rare.  I  can,  therefore,  confirm  my 
friend  Dieulafoy's  opinion." 

For  several  years  I  have  seen  repeatedly,  and  followed  most  closely,  150 
patients  with  divers  forms  of  entero-typhlo-colitis.  Only  two  were  attacked 
with  appendicitis  after  several  years. 

A  summary  of  the  above  cases  is  of  value,  since  it  is  based  on  some 
800  to  900  cases.  Many  of  the  patients  were  seen  several  times  and  at 
several  years'  interval,  and  yet  it  is,  most  difficult  to  find  a  case  of  appen- 
dicitis. Such  is  the  clinical  fact,  and  no  matter  how  strange  and  para- 
doxical it  may  appear,  it  must  be  admitted.  If  appendicitis  were  really 
the  consequence  or  the  cause  of  entero-colitis,  it  would  be  very  strange  if 
it  had  not  been  observed  several  times  in  this  large  number  of  cases.  As 
a  matter  of  fact,  if  there  is  a  disease  favourable  to  enteritis  and  intestinal 
ulcerations,  it  is  typhoid  fever,  where  the  lesions  show  a  remarkable  pre- 
dilection for  the  ileo-cajcal  region,  which  includes  the  appendix. 

If  appendicitis  were  often  the  consequence  of  entero-typhlitis,  as  has 
been  maintained,  it  would  surely  occur  under  these  conditions,  and  yet 
nothing  is  rarer  than  appendicitis  in  typhoid  fever.  The  same  remark 
applies  to  tubercular  entero-typhlitis,  as  will  be  seen  later. 

As  we  have  shown  that  entero-typhlo-colitis  does  not  cause  appendicitis, 
it  will  be  interesting  to  ascertain  in  what  proportion  appendicitis  properly 
confirmed  by  operation  is  preceded  by  entero-colitis.  On  consulting  my 
personal  statistics,  based  on  200  cases  of  appendicitis  with  operation,  I  can 
find  only  four  patients  who  had  previously  had  symptoms  of  entero-colitis. 

Why,  then,  have  some  authors  so  readily  admitted  that  entero-colitis 
may  lead  to  apjxMulicitis  ?  This  fact  is  due,  in  the  first  place,  to  the  mis- 
taken ideas  on  the  pathogenesis  of  a])pendicitis  ;  and,  secondly,  to  inaccurate 
diagnosis,  in  which  pseudo-appendicitis  is  wrongly  taken  for  true  appen- 
dicitis. 


782  TEXT-BOOK  OF  MEDICINE 

The  discussion  just  undertaken  yields  a  practical  interest  of  tlie  first 
order,  and  after  so  many  accumulated  proofs  I  may  be  permitted  to  restate 
my  dictum  :  "  Appendicitis  (not  pseudo-appendicitis)  is  very  exceptional 
in  the  course  of  entero-cohtis."  The  conclusion  is  that  people  with  muco- 
membranous  or  calculous  entero-typhlo-coUtis  need  not  unduly  fear  appen- 
dicitis. The  attacks  of  pain,  due  either  to  membranes  or  to  gravel,  may 
commence  in  the  ileo-csecal  region  (caecum  and  ascending  colon),  the  left 
iUac  fossa  (descending  colon),  or  the  epigastric  region  (transverse  colon) ; 
but  the  physician  will  know  that  the  case  is  entero-typhlo-colitis,  which  is 
a  benign  disease,  and  not  appendicitis,  which  is  a  most  formidable  malady. 

Treatment. — Much  has  been  written  on  the  treatment  of  entero-cohtis, 
and  I  may  state  here  the  most  salient  points. 

Diet. — Milk,  milk  foods,  farinaceous  foods,  eggs,  soups,  vegetables  en 
puree,  green  vegetables  in  small  quantities,  a  little  bread  or  meat ;  no  wine, 
no  pork,  no  game,  no  acid  foods,  no  fatty  foods. 

Treatment  when  Diarrhoea  occurs. — If  milk  disagrees,  we  may  add 
lime-water,  8  ounces  ;  hydrochlorate  of  cocaine,  |  grain ;  hydrochlorate  of 
morphia,  ^  grain.  Five  tablespoonfuls  to  be  taken  daily  (one  in  each  cup  of 
milk).  In  some  cases  raw  meat  may  be  added  to  the  milk  diet  or  may 
replace  it.  Sahne  purgatives  in  very  small  doses — for  example,  1  drachm 
of  sulphate  of  soda  every  morning — give  good  results.  Bismuth,  prepared 
chalk,  pure  talc  (Debove),  opiates,  astringents,  and  nitrate  of  silver,  either 
in  pills  or  enemata,  have  been  prescribed.  I  have  proved  the  efficacy  of 
ipecacuanha  in  small  doses,  and  prescribe  four  or  five  pills,  each  containing 
J  grain  of  ipecacuanha  and  -jV  grain  of  opium  daily. 

Treatment  in  Obstinate  Constipation. — Castor-oil,  2  drachms,  several 
times  a  week,  7  or  8  grains  of  rhubarb  before  each  meal ;  cascarine  or  Vichy 
laxative  powder  before  going  to  bed  ;  cream  of  tartar ;  sulphur  and  magnesia, 
small  enemata  of  glycerine,  oil,  or  soap. 

Treatment  of  Pain. — Antipyrin,  opium  pills  of  }  grain  each,  a  tea- 
spoonful  of  syrup  of  codeine,  small  injections  of  morphia,  hot  compresses 
to  the  abdomen. 

Local  Treatment. — Large  enemata  (2  or  3  pints)  of  water  at  104°  F. 
(Mathieu).  Enemata  of  infusion  of  marsh-mallows ;  avoid  medicated 
enemata  ;  wear  a  belt  to  prevent  enteroptosis  (Glenard). 

Hydrotherapy. — Cures  at  Pougues,  Chatel-Guyon,  and  especially  at 
Plombieres. 

V.  FALSE  APPENDICITIS. 

This  section  is  the  complement  of  the  two  preceding  sections,  and  deals     1 
with  a  most  important  question  in  medicine  and  surgery,  because  an  error 
in  diagnosis  may  lead  either  to  useless  operation  or  to  fatal  inaction. 


DISEASES  OF  THE  INTESTINE  783 

For  some  years  past  I  have  been  at  paiiis  to  prove  the  falsity  of  the 
teaching  which  holds  that  appendicitis  is  commonly  the  result  of  entero- 
coHtis.  I  do  not  know  how  far  this  teaching  is  responsible  for  past  mis- 
takes, but  I  am  struck  by  the  fact  that  many  persons  sufiering  from  muco- 
membranous  or  sabulous  t}'phlo-colitis  are  operated  upon  for  appendicitis. 

I  am  a  very  warm  partisan  of  surgical  treatment  in  appendicitis.  Every- 
day experience  confirms  the  common-sense  rule,  which  says  :  "  Remove  the 
toxic  focus  early,  before  it  can  cause  fatal  mischief.'" 

When  I  found  that  many  persons  with  typhlo -colitis  were  operated 
upon  for  appendicitis,  and  when  I  saw  diagnostic  and  operative  errors 
condoned  on  the  plea  of  the  histological  examination,  I  raised  the  point  for 
discussion  at  the  Academic  de  Medecine. 

I  wall  first  quote  certain  cases  which  are  conclusive  evidence : 

1.  I  saw  in  consultation  a  j'oung  girl  who  had  suffered  for  two  years  from  muco- 
membranous  typhlo-colitis.  At  times  attacks  of  pain  came  on  without  any  appreciable 
cause.  The  motions  were  loose,  and  contained  mucus  and  membranes.  During  the 
later  attacks  the  pain  was  most  marked  in  the  right  iliac  fossa,  and  appendicitis  had 
therefore  been  diagnosed. 

In  consequence,  an  operation  had  been  proposed,  and  been  accepted  by  the  patient, 
who  hoped  that  surgery  would  accompUsh  what  medicine  had  failed  to  do.  I  examined 
the  patient,  who  had  just  had  a  sharp  attack.  The  belly  was  supple,  and  the  walls 
were  flabby.  Pressure  caused  sharp  pains  over  the  transverse  colon  and  the  hepatic 
flexure,  but  the  pain  was  most  marked  in  the  right  iliac  fossa.  This  feature,  however, 
did  not  convince  me  that  the  case  was  one  of  appendicitis,  for  past  experience  has 
shown  me  that  marked  pain  in  the  right  iliac  fossa  during  an  attack  of  muco-membranous 
typhlo-colitis  is  nearly  always  the  result  of  typhlitis,  and  not  appendicitis.  My 
diagnosis,  therefore,  was  muco-membranous  typhlo-colitis,  and  I  advised  against  an 
operation. 

My  colleagues  took  the  opposite  view,  and  decided  upon  an  operation  for  appen- 
dicitis. The  appendix  was  sent  to  me,  and  I  examined  it  with  Jolly.  It  was  absolutely 
healthy  ;  the  canal  and  the  walls  were  normal,  and  no  lesion  was  discoverable  on  micro- 
scopic examination.  For  the  last  two  years  the  patient  has  had  attacks  of  muco- 
mcrabranous  typhlo-colitis.     She  was  operated  upon  for  non-existent  appendicitis. 

2.  Some  years  ago  I  was  called  in  to  see  a  young  man  who  had  had  muco-ineiu- 
branous  typhlo-colitis  for  some  time.  The  symptoms  were  :  Acute  attacks  of  pain  and 
passage  of  mucus  and  membranes.  When  I  examined  the  abdomen,  I  found  a  typical 
scar  in  the  right  iliac  fossa.  I  said  at  once  :  "  You  have  been  operated  upon  for  appen- 
dicitis ?"  "  Yes,"  he  rejjlied,  "  for  appendicitis  which  I  never  had.  My  abdomen 
was  opened  by  mistake,  and  the  attacks  of  entero-colitis  still  continue." 

3.  Some  two  years  ago  I  saw  a  woman,  who  described  her  case  to  me.  For  some 
years  past  she  had  had  symptoms  of  muco-membranous  typhlo-cohtis.  The  last  attack 
had  not  ended  when  I  saw  her.  I  found  in  the  right  iliac  fossa  a  scar  of  unmistakable 
signiHcance.  "  But,"  said  I,  "  you  have  been  operated  upon  for  aj)pendicitis."  "  Yes," 
she  answered,  "  for  appendicitis  which  I  did  not  have,  and  I  am  just  as  great  a  sufferer 
as  I  was  before  tlie  operation.  I  have  the  same  abdominal  pain,  and  still  [)ass  mucus 
and  skins."  It  was  an  excellent  opportunity  to  examine  a  painful  civciini,  when  llic 
appendix  had  been  removed  ten  months  before.  I  recognized  pain  in  tlie  right  iliac 
fossa,  due  to  tyj^hiitis,  and  comparable  to  the  pam  in  many  cases  of  appendicitis.  I 
also  saw  clearly  the  error  of  those  who,  sotting  aside  the  other  elements  in  tiio  diagnosis, 
mistake  typhlitis  for  appendicitis,  and  perform  an  urmeccssary  operation. 


784  TEXT-BOOK  OF  MEDICINE 

Discussion.  —  In  certain  cases  of  muco  -  membranous  or  sabulous 
typhlo-colitis,  typhlitis  is  the  chief  factor,  and  the  pain  is  most  marked  in 
the  right  iliac  fossa  ;  and  then,  because  it  is  said  that  appendicitis  often 
results  from  entero-colitis,  our  diagnosis  may  be  led  astray,  and  we  operate 
for  appendicitis  which  is  not  present.  These  diagnostic  and  operative  errors 
have  increased  of  late  years  to  a  surprising  extent,  especially  since  it  has 
become  customary  to  base  the  diagnosis  of  certain  so-called  cases  of  appen- 
dicitis upon  a  histological  examination  of  the  appendix  (after  its  removal). 
Let  me  explain. 

You  are  called  to  see  a  patient  in  a  severe  attack  of  muco-membranous 
entero-coKtis.  He  knows  the  illness  is  not  dangerous,  although  he  suffers 
considerably.  On  palpation,  you  find  the  abdomen  is  very  tender,  especially 
over  the  course  of  the  colon  ;  when  you  press  in  the  right  iliac  fossa,  the 
patient  cries  out  that  the  pain  is  more  severe  there  than  at  other  places. 
If  you  are  a  believer  in  the  doctrine  that  appendicitis  follows  entero-colitis, 
you  make  a  wrong  diagnosis  of  appendicitis,  and  advise  an  operation.  A 
surgeon  is  called  in,  and  when  he  opens  the  abdomen,  the  operation  gives 
the  lie  to  your  diagnosis.  The  appendix  is  absolutely  healthy ;  typhlitis 
has  been  mistaken  for  appendicitis,  and  an  unnecessary  operation  has  been 
performed. 

The  microscope  now  comes  in,  and  we  hear  of  a  new  variety  of 
appendicitis  (non-existent,  it  is  true),  which  I  have  called  "  microscopic 
appendicitis."  If  anyone  wishes  for  information  about  this  microscopic 
appendicitis,  he  need  only  consult  the  theses  of  our  faculty,  in  which  are  pub- 
lished observations  where  the  histological  examination  of  the  appendix  has 
the  unjustifiable  pretension  of  substituting  itself  for  any  other  diagnosis. 
This  means  that  'jlinical  methods,  being  powerless,  yield  to  histology  the 
right  of  deciding,  after  operation,  whether  appendicitis  was  present  or  not. 
When  we  read  these  observations,  we  find  that  the  appendix  was  healthy 
— too  healthy,  indeed,  for  those  who  made  the  diagnosis.  It  is,  then,  neces- 
sary to  bring  in  the  histological  examination  to  clear  up  matters  which 
demand  an  explanation.  Bands  of  fibrous  tissue,  hypertrophy  of  the 
closed  follicles,  and  hgemorrhagic  folliculitis,  are  the  chief  findings  in  many 
cases  of  "  appendicitis,"  when  the  post-operative  diagnosis  is  left  to  the 
microscope.  These  histological  findings  only  have  the  signiiicance  that  the 
observer  desires  to  give  to  them.  Conviction  will  follow  the  reading  of 
LetuUe's  important  work  on  this  subject.  If  we  take  at  random  the 
appendices  from  several  adults,  it  is  quite  a  common  thing  to  find  fibrous 
tissue  in  process  of  formation  or  thickening  of  the  lymphatic  follicles, 
especially  in  the  lower  segment  of  the  organ.  These  changes  are  quite 
commonplace  in  the  tissue  of  the  appendix,  and  we  must  banish  the  idea 
that  these  changes  are  appendicitis  secondary  to  entero-colitis.    Under  the 


DISEASES  OF  THE  INTESTINE  785 

term  "  folliculitis "  ordinary  hypertrophy  of  the  closed  follicles  of  the 
appendix  has  acquired  too  lasting  an  importance.  I  have  often  heard 
the  following  phrase  :  "  Did  the  patient  have  appendicitis  ?"  "  Not 
exactly ;  but  he  had  folliculitis."  We  know  the  meaning  of  such  a  state- 
ment, and  we  must  banish  this  variety  of  follicular  appendicitis  into 
oblivion. 

Orth,  in  a  recent  communication  to  the  Berlin  Medical  Society,  speaks 
thus  of  folliculitis  :  "  It  is  always  difficult  to  say  in  the  case  of  a  section  of 
an  appendix  whether  the  lymphatic  follicles  have  undergone  pathological 
increase  or  whether  the  appendix  in  question  is  normal,  but  especially  rich 
in  lymphatic  follicles";  and  he  has  shown  that  in  9  or  10  out  of  every  100 
appendices  examined  after  removal  for  appendicitis  the  macroscopic  and 
microscopic  findings  were  absolutely  normal.  I  hope  in  future  that  we 
shall  not  take  refuge  under  a  commonplace  hypertrophy  of  the  follicles 
when  we  have  removed  in  error  a  healthy  appendix. 

There  is  another  lesion  which  histological  examination  has  given  us  as 
an  integral  part  of  the  so-called  appendicitis  consecutive  to  entero- colitis.  I 
mean  hsemorrhagic  folliculitis. 

This  interpretation  is  wrong  :  the  follicular  haemorrhages  looked  upon 
as  a  lesion  of  appendicitis  are  really  due  to  operative  trauma.  On  this 
point  LetuUe  says  :  "  I  have  never-  found  hsemorrhagic  folliculitis,  save  in 
appendices  removed  by  operation.  The  forcible  Ugation  of  the  appendix, 
before  its  removal,  explains,  in  my  opinion,  the  circumscribed  or  diffuse 
effusions  of  blood  in  the  reticulated  or  follicular  tissue." 

It  is,  of  course,  understood  that  I  am  not  speaking  of  the  haemorrhages 
which  sometimes  accompany  the  gross  inflammatory  lesions  of  true  appendi- 
citis. Mention  is  here  made  simply  of  the  follicular  haemorrhages  which 
are  found  in  the  healthy  appendix  after  removal,  and  which  are  wrongly 
supposed  to  be  caused  by  appendicitis. 

Fig.  52  leaves  no  doubt.  It  represents  the  traumatic  haemorrhage  in 
the  walls  of  a  healthy  appendix  removed  by  operation. 

Fig.  53  represents  a  longitudinal  section  of  the  meso-appendix  above 
the  ligature.  The  tissues  are  healthy  ;  there  is  no  trace  of  appendicitis ; 
the  hgature  has  produced  the  hccmorrhagic  foci. 

We  know,  therefore,  that  the  follicular  and  extrafollicular  haemorrhages 
which  are  found  (as  Letulle  has  so  clearly  shown)  in  the  healthy  appendix 
after  removal  are  the  result,  not  of  appendicitis,  but  of  an  operative  pro- 
cedure. Heubner,  from  an  experimental  study  of  this  question,  arrives  at 
the  same  conclusions. 

This  so-called  appendicitis,  which  has  found  shelter  under  the  microscopic 
examination,  is  non-existent  either  anatomically  or  clinically.  It  cannot 
even  find  a  place  under  the  heading  of  "  chronic  appendicitis,"     It  was  this 

50 


786  TEXT-BOOK  OF  MEDICINE 

form  which  gave  the  chief  support  to  the  theory  that  appendicitis  is  com- 
monly the  outcome  of  entero-coHtis. 

And  if  this  variety  is  non-existent,  I  would  ask  those  who  beUeve  in  it  to 
tell  me  on  what  symptoms  they  base  their  diagnosis.  A  patient  is  suffering 
from  muco-membranous  typhlo-colitis  :  what  are  the  clinical  indications 
for  operation  ?  I  do  not  lay  stress  on  the  point.  I  have  mentioned  the 
numerous   operative   mistakes  that  have   been   made.     Richelot,   at  the 


y- 


ii 


m 


/ 


.■'••hi 


ili:;'  '■    -'"■  "'''•';'--•% ■■::M 

Fig.  52.— Section  through  a  Submucous  Follicle  (Letulle). 

sm.,  Submucosa,  quite  free  from  any  lesion  ;  gl,  tubular  gland  in  the  normal  mucous 
membrane  ;  ch,  chorion  of  the  mucous  membrane  (no  inflammation) ;  /,  submucous 
follicle  (the  tissue  is  torn  apart  by  eft'used  blood  s'  ;  only  red  corpuscles  are  seen). 
Above  and  to  the  right  s",  the  heemorrhage  has  extended  beyond  the  capsule  ;  s,  red 
corpuscles  on  the  surface  of  the  normal  mucous  membrane. 

Academic  de  Medecine,  has  thus  expressed  his  opinion  :  "  Shall  I  not  admit 
with  Dieulafoy  that  commonplace  microscopic  lesions  may  be  found  in  the 
most  innocent  appendices,  and  that  their  discovery  after  section  in  an 
appendix  unnecessarily  removed  is  a  poor  excuse  for  the  surgeon  ?" 

Moreover,  sound  chnical  investigation  should  have  been  able  to  curtail 
the  faulty  practice  of  operating  on  so  many  persons  with  entero-colitis 
under  the  assumption  that  they  have  appendicitis  ;  it  is  sufficient  to  see 


DISEASES  OF  THE  INTESTINE  787 

what  happens  after  operations.  We  should  have  recognized  that  the 
operations  effect  neither  cure  nor  change  in  the  symptoms.  Apart  from 
certain  neurasthenics  who  expresr  reHef,  muco- membranous  tjrphlo- colitis 
runs  its  course  unaffected  by  removal  of  the  appendix.  My  own  inquiries 
on  this  point  leave  no  doubt  in  my  mind.  In  the  cases  mentioned  above 
the  symptoms  have  continued.  In  certain  cases  the  improvement  has 
been  temporary,  and  the  same  attacks  have  recurred  some  weeks  or  months 
later.  Wagner  mentions  the  case  of  a  child  classed  as  a  recovery  from  muco- 
membranous  entero-cohtis  after  the  ablation  of  the  appendix.     Esmonet 


mmw^di  F^^^-"Psfpsr 


,i 


J.\'t 


y 


~J 


Fig.  53. — SECxroN  THROfTGn  the  Meso- Appendix  (Letulle). 
L,  limit  of  the  ligature  ;  a',  a',  arteries  distended  by  blood  ;  v,  vein  engorged  with 
blood  ;  g,  g,  fat  cells  and  loose  connective-tissue  of  the  epiploon  free  from  any  inflam- 
matory lesion  ;  s,  s,  s,  hsemorrhagic  foci  between  the  meshes  of  adipose  tissue  in  the 
epiploon. 

treated  this  child  at  Chotel-Guyon  for  attacks  similar  to  those  which  pre- 
ceded the  operation.  Apert  saw  at  the  Tenon  Hospital  a  woman  suffering 
from  mucous  entero-colitis,  with  much  pain.  She  had  been  operated  on  for 
appendicitis  which  she  did  not  have,  and  the  old  symptoms  reappeared. 
Deleage  of  Vichy  had  under  his  care  a  lady  whose  attacks  of  muco-mem- 
Ijranous  typhlo-colitis  were  not  a  whit  better  after  removal  of  the  appendix. 
Bottentuit  of  Plombieres  has  recently  collected  twenty-eight  cases  of 
persons  suffering  from  muco-membranous  or  sabulous  typhlo-colitis  for  a 
more  or  le.ss  lengthy  period,  and  oj)erated  upon  for  appendicitis  which  they 
did  not  have.     1  have  studied  the  details  of  these  cases,  and  they  closely 

50—2 


788  TEXT-BOOK  OF  MEDICINE 

resemble  one  another  :  erroneous  removal  of  the  appendix ;  the  character 
of  the  attacks  not  changed  by  the  operation  ;  pain  and  passage  of  mucus 
and  membranes  still  persistent.  The  sufferers  all  came  to  Plombieres  in 
order  to  obtain  rehef  by  hydrotherapy, 

A  wrong  diagnosis  in  a  case  of  false  appendicitis  may  have  a  vicious 
action  upon  the  life  of  many  a  sufferer  from  muco-membranous  typhlo- 
colitis. Appendicitis  is  mentioned,  and  an  operation  is  suggested.  The 
patient  then  becomes  neurasthenic  and  fastidious  in  his  choice  of  food  ;  he 
grows  thin,  and  always  keeps  an  eye  on  his  right  iliac  fossse ;  constipation 
alarms  him. 

Sometimes  he  begs  for  an  operation,  at  other  times  he  dreads  it ;  his 
whole  existence  is  affected.  In  certain  instances  he  goes  to  a  surgeon 
and  asks  to  be  reheved  of  his  appendix.  This  is  done,  but  he  still  has  the 
same  attacks  of  pain,  and  he  finds  out  that  the  diagnosis  of  appendicitis  was 
wrong. 

If  I  speak  thus,  it  is  because  I  have  studied  this  question  carefully  for 
many  years.  I  have  often  prevented  an  operation  which  was  fixed  for  the 
following  day  or  for  the  following  week.  Years  have  passed,  and  time  has 
shown  that  my  diagnosis  was  correct. 

In  short,  recent  clinical  and  histological  knowledge  shows  that  many 
persons  with  typhlo-cohtis  undergo  a  futile  operation  for  appendicitis.  Cor- 
rect diagnosis,  then,  is  necessary  to  prevent  error  ;  we  must  get  rid  of  the 
idea  that  appendicitis  is  Hable  to  result  from  entero-oohtis. 

CUnical  study  teaches  us  that  in  muco-membranous  or  sabulous  entero- 
typhlo-colitis  it  is  typhhtis  which  is  responsible  for  the  symptoms  in  the 
right  iliac  fossa,  and  not  appendicitis.  This  view  is  confirmed  by  the 
pubhshed  cases,  and  by  the  anatomical  examination  of  many  appendices 
removed  owing  to  an  error  in  diagnosis.  If  by  chance  true  appendicitis 
does  supervene,  the  diagnosis  will,  I  admit,  present  difficulties,  but  these 
difficulties  are  not  insurmountable.     In  such  a  case  operation  is  imperative. 

VI.  INTESTINAL  TUBERCULOSIS— TUBERCULAE  ENTERITIS. 

etiology. — While  tubercular  enteritis  may  be  primary,  it  is,  as  a 
rule,  secondary  to  enteritis  in  chronic  pulmonary  phthisis.  In  some  cases 
it  results  from  auto-infection,  the  bacillus  entering  the  digestive  passages 
in  sputum  which  has  been  swallowed.  In  other  cases  the  bacillus  enters 
in  milk  from  tubercular  cows.  These  infections  enter  through  the  mucous 
membrane  of  the  intestine,  but  we  should  also  mention  infection  through  the 
deep  tissues,  the  bacillus  being  carried  by  the  lymph  and  bloodvessels, 
especially  in  the  case  of  mihary  tuberculosis.  According  to  Tchistovitch, 
when  infection  takes  place  through  the  surface  of  the  mucous  membrane, 


DISEASES  OF  THE  INTESTINE  789 

the  bacilli  traverse  the  epithelial  layer,  reach  the  walls  of  the  intestine  by 
means  of  the  lymphatics,  and  spread  in  the  submucous  adenoid  tissue  around 
the  bloodvessels.  The  transverse  direction  of  these  vessels  exphiins  the 
shape  of  certain  ulcerations  in  which  Koch's  bacilli  are  especially  numerous. 
Pathological  Anatomy.  —  On  opening  the  intestine,  two  kinds  of 
lesions  are  seen — ordinary  inflammation  and  tubercular  changes.  The 
latter  are  seated,  for  the  most  part,  in  the  terminal  portion  of  the  ileum  and 
in  the  caecum,  but  they  are  also  found  in  other  parts  of  the  intestine.  At 
the  post-mortem  examination  the  lesions  appear  as  granulations  and  ulcera- 
tions, which  vary  in  form  and  size.  The  latter  are  rounded  when  in  the 
isolated  folUcles,  but  longitudinal  or  oval  when  seated  in  Peyer's  patches. 
They  are  frequently  transverse,  and  surround  the  intestine  like  a  ring. 

The  tubercular  lesions  of  the  intestine  are  granulations  and  ulcers.  The 
granulations  arise  in  the  walls  of  the  vessels,  in  the  connective  tissue  around 
the  ends  of  the  tubular  glands,  or  in  the  connective  tissue  of  the  villi.  Their 
presence  induces  an  inflammatory  process  in  the  villi  and  glands. 

The  intestinal  villi,  infiltrated  with  round  cells,  unite  at  their  base  and 
form  an  excrescence,  which  looks  like  a  tubercular  nodule.     The  tubular 
glands  become  elongated  and  filled  with  cylindrical  cells.     The  small  tuber- 
cular mass  becomes  opaque  and  caseous,  and  commences  to  ulcerate.     This 
is  one  method  of  ulceration,  but  we  also  find  another  process,  in  which 
the   ulcerations   originate   in  the   tubercular  inflammation  of  the   closed 
follicles  and  Peyer's  glands.     At  the  commencement,  the  appearance  of  the 
affected  folUcles  does  not  differ  from  simple  psorenteria.     The  folhcle  is 
enlarged  and  infiltrated  with  lymphoid  cells.     Its  centre  soon  becomes 
opaque  and  greyish,  then  soft,  and  finally  converted  into  a  small  abscess, 
which  rapidly  ulcerates.     "  Often  several  of  these  altered  follicles  are  found 
on  a  Peyer's  patch  or  some  other  point  of  the  mucous  membrane,  sur- 
rounded by  diffuse  inflammation  of  the  submucous  connective  tissue,  the 
villi  and  the  glands,  and  united  to  form  a  prominent  patch,  which  ulcerates." 
This  is  another  method  of  ulceration  in  intestinal  tuberculosis,   but  no 
matter  whether  the  ulceration  begins  in  the  granulations  or  in  tubercular 
inflammation,  "  its  ulterior  development  and  its  consequences  are  the  same." 
The  ulcers  unite  and  often  assume  an  annular  form.     Segments  or  com- 
plete rings,  each  about  half  an  inch  wide  and  some  inches  from  one  another, 
are  then  found  on  the  mucous  membrane.     This  annular  disposition  is 
probably  due  to  the  fact  that  the  vessels  themselves  are  disposed  in  rings 
around  the  intestine,  their  walls  being  infiltrated  with  tubercular  granula- 
tions.   The  ulcerated  Peyer's  patches  are  not  swollen,  as  in  typhoid  fever, 
but  are  only  slightly  prominent,  and  studded  with  crater-like  ulcers.     These 
two  types — annular   ulcers  and   ulcerations  of   Peyer's   patches — may   be 
isolated  or  present  together  in  the  same  subject. 


790  TEXT-BOOK  OF  MEDICINE 

The  edges  and  the  floor  are  often  studded  with  tubercular  granulations, 
which  are  found  in  the  different  layers  of  the  connective  tissue  of  the  in- 
testinal walls,  between  the  muscular  fibres,  and  in  the  deep  submucous  tissue. 

The  lymphatic  system  participates  largely  in  the  process,  and  the 
lymphatic  vessels  which  start  from  the  ulcerated  Peyer's  patches  are  in- 
jected with  tubercular  matter.  The  areas  on  the  peritoneal  surface  of  the 
intestine  which  correspond  to  the  ulcers  of  the  mucous  membrane,  always 
show  numerous  tubercular  granulations,  standing  out  against  the  red 
ground  of  the  inflamed  serous  membrane.  The  lymphatic  vessels  passing 
to  the  mesenteric  glands  are  whitish,  nodular,  enlarged,  and  infiltrated  with 
tubercular  granulations. 

Tubercular  ulcers  of  the  intestines  sometimes  cause  stenosis,  and  in  rare 
cases  perforation.  They  are  sometimes  found  in  the  caecum  in  cases  of 
hypertrophic  tuberculosis.  The  ulceration  may  be  so  extensive  in  the  large 
intestine  that  at  fijst  sight  the  lesions  of  tubercular  colitis  resemble  those 
of  dysentery. 

Tubercular  ulceration  may  also  occur  in  the  appendix,  and  generally 
coexists  with  similar  lesions  in  the  small  intestine,  the  csecum,  and  the 
colon.  I  have  seen  a  case  of  this  kind  at  the  Hotel-Dieu,  and  the  lesions 
were  very  marked.*  The  ulcers  burrowed  deeply  into  the  walls  of  the 
appendix,  but  the  lumen  was  quite  free,  and  therefore  no  symptoms  of 
appendicitis  had  been  observed. 

Why  is  tuberculosis  of  the  appendix  latent  in  spite  of  the  marked  lesions 
in  the  walls,  whilst  in  appendicitis  very  small  lesions  can  cause  acute  toxi- 
infection  ?  In  tuberculosis  (so  long,  at  least,  as  the  appendix  remains 
permeable)  there  is  no  closed  cavity,  and,  consequently,  no  increase  in  the 
virulence  nor  migration  of  the  coli  bacillus  through  the  walls  of  the  appendix. 
In  the  sections  of  the  tubercular  appendix,  of  which  I  have  just  spoken, 
the  microbes  did  not  pass  beyond  the  superficial  layer  of  the  ulcer.  They 
had  not  increased  in  virulence,  because  the  lesions  had  not  given  rise  to 
a  closed  cavity.  In  this  case  the  intestinal  ulcers  had  not  caused  peritoneal 
mischief  ;  in  sections  of  them,  just  as  in  those  of  the  appendix,  the  microbes 
had  not  passed  beyond  the  surface.  Tubercular  lesions  of  the  appendix 
are  common.  Letulle  in  some  recent  statistics  has  noticed  the  frequency 
of  lesions  of  the  appendix  in  tubercular  patients.  One  fact  as  to  these 
patients  struck  us  both — viz.,  the  rarity  of  toxi-infection,  which,  clinically 
speaking,  alone  deserves  the  name  of  appendicitis. 

Description. — Enteritis  is  an  almost  constant  manifestation  of  tuber- 
culosis of  the  intestine.     Tubercular  enteritis  is  rarely  found  as  an  isolated 

*  This  case  has  heen  pubUshed  by  Apert  (Presse  Medicale,  1898,  No.  102  :  "  Tuber- 
culose  de  I'lntestin  et  de  I'Appendice  ;  Lesions  considerables  de  I'Appendice  ;  pas  da 
Cavite  close  ;   aucun  Symptome  d'Appendicite."). 


DISEASES  OF  THE  INTESTINE  791 

disease,  because  it  is  almost  always  associated  with  pulmonary  plithisis. 
The  severity  of  the  symptoms  depends  on  the  extent  of  the  lesions.  Some- 
times the  enteritis  is  transitory,  and  is  characterized  by  curable  diarrhoea ; 
more  frequently  the  diarrhoea  is  profuse,  obstinate,  and  accompanied  by 
abdominal  pains.  Blood  may  be  found  in  the  stools,  which  have  a  blackish 
or  brownish  tint,  similar  to  the  black  vomit  of  gastric  carcinoma.  Thia 
black  diarrhoea  may.  persist  for  several  weeks  without  the  slightest  modifi- 
cation. It  is  foetid  and  as  a  rule  appears  only  at  an  advanced  stage  of  the 
disease.  When  the  large  intestine  is  ulcerated,  dysenteric  symptoms,  with 
tenesmus,  may  be  seen,  as  well  as  the  usual  symptoms  of  enteritis.  In 
tubercular  patients  enteritis  is  a  sign  of  evil  augury.  It  often  ushers  in  the 
cachectic  period,  leading  to  malnutrition,  and  hastening  a  fatal  ending. 

Haemorrhage  from  the  bowel  is  very  rarely  fatal,  though  in  Chandeze's 
case  the  patient  had  several  attacks  of  haemorrhage,  which  were  so  profuse 
that  he  succumbed  in  twelve  hours.  The  post-mortem  examination  re- 
vealed ulceration  of  the  vessels.  In  Valhn's  case  intestinal  hsemorrhage 
killed  the  patient  in  a  few  hours  ;  in  Honot's  case  the  intestinal  haemorrhages 
followed  in  quick  succession,  and  the  patient  succumbed  in  two  days. 

In  children  tubercular  enteritis  is  always  associated  with  lesions  in 
the  mesenteric  glands  (Parrot).  This  entero-mesenteric  tuberculosis  was 
long  known  under  the  name  of  tabes  mesenterica.  It  is  characterized 
by  symptoms  of  enteritis,  and  also  by  distension  of  the  abdomen,  dilatation 
of  the  veins  of  the  abdominal  wall,  and  effusion  into  the  peritoneum. 

Perforation  of  the  bowel  with  peritonitis  is  exceedingly  rare.  It  would 
seem  at  first  sight  that  tubercular  ulcerations  of  the  gut  might  cause 
perforation,  but  this  is  not  the  case. 

In  chronic  ulcerative  tuberculosis  Koch's  bacilli  may  pass  into  the 
tributaries  of  the  portal  vein  and  reach  the  liver,  where  they  cause  inter- 
stitial hepatitis.  The  lesion  is  periportal,  and  is  accompanied  by  secondary 
cirrhosis  and  perilobular  fatty  infiltration. 

Diagnosis. — In  some  cases  of  miliary  tuberculosis,  the  intestinal  troubles 
and  the  general  symptoms  resemble  the  clinical  picture  of  enteric  fever.  In 
chronic  tubercular  enteritis  the  diagnosis  is  the  more  difficult,  in  that  the 
case  does  not  always  look  like  one  of  tuberculosis.  For  months  and 
years  phases  of  improvement  occur,  and  the  intestinal  troubles  are  ascribed 
to  gastro-intestinal  dyspepsia  or  to  the  arthritic  diathesis.  We  must,  how- 
ever, be  always  on  our  guard.  Cases  of  interminable  diarrhoea  or  enteritis 
which  seem  to  recover  at  Plombieres  or  elsewhere,  and  then  relapse,  are 
most  often  the  result  of  tuberculosis.  In  exceptional  cases  the  tubercle 
bacillus  has  been  found  in  the  stools. 

Tubercular  enteritis  is  often  rebellious  to  treatment.  Subnitrate  of 
bismuth  in  large  doses,  lime-water  with  morphia  in  very  small  doses,  albumin- 


792  TEXT-BOOK  OF  MEDICINE 

water,  and  nitrate  of  silver  in  pills,  are  the  means  usually  employed.  A  diet 
in  which  raw  meat  is  the  chief  ingredient  is  generally  associated  with  these 
medicines  to  advantage.  Lactic  acid  (Hayem)  and  powdered  talc  (1  ounce 
a  day)  (Debove)  have  been  recommended.  The  cure  at  Plombieres  is  of 
great  service. 


VII.  HYPERTROPHIC  TUBERCULOMA  OF  THE  C^CUM— 
DIAGNOSIS   OF  THE  TUMOURS  OF  THE  RIGHT   ILIAC   FOSSA. 

This  variety  of  tuberculosis  commences  in  the  caecum  or  the  ileo-caecal  angle,  and 
runs  a  chronic  course.  It  is  often  primary  ;  it  produces  tumours  which  simulate 
lymphadenoma,  and  is  often  curable  by  operation. 

This  malady  was  described  by  Duguet  in  1869.  Surgeons  have  called  attention  to 
it  (Terrier),  and  in  the  earhest  operations  they  thought  they  were  dealing  with  lympho- 
sarcomata  of  the  csecum  (Bassini,  1887  ;  Bouilly,  1889).  I  may  quote  the  works  of 
Billroth  (1891),  Hartmann,  PilUet  and  Broca  (1891),  of  Roux  (1892),  and  the  theses 
of  Le  Bayon  (1892)  and  Benoit  (1893). 

I  have  collected  a  great  number  of  cases  in  my  clinical  lectures,*  and  I  have  proposed 
the  name  of  hypertrophic  tuberculoma  of  the  caecum  for  this  disease. 

Hartmann  and  Pilliet  had  described  it  under  the  name  of  "  chronic  tubercular 
typhlitis  and  csecal  tuberculosis."  This  name  has  the  advantage  of  assigning  the  chief 
importance  to  the  lesion  of  the  caecum.  Other  authors  have  described  it  under  the  name 
of  "chronic  ileo-csecal  tuberculosis,"  but  this  name  is  not  exact,  because  it  induces  a 
belief  that  the  lesion  commences  in  the  ileum,  and  then  spreads  to  the  caecum,  which 
is  by  no  means  always  the  case.  Sometimes,  indeed,  the  walls  of  the  ileum  are  hyper- 
trophied,  and  this  fact  might  at  first  sight  induce  a  belief  in  a  tubercular  lesion  of  this 
portion  of  the  gut ;  but  closer  inspection  shows  that  it  is  only  a  compensating  hyper- 
trophy caused  by  the  stenosis  of  Bauhin's  valve  or  of  the  caecal  cavity,  and  that  this 
hypertrophy  must  not  be  confounded  with  a  tubercular  lesion.  In  short,  hypertrophic 
tuberculosis  does  not  commence,  as  a  rule,  in  the  ileum,  but  in  the  caecum,  close  to  the 
ileo-caecal  valve  (Hartmann,  Broca).  The  lesions  are  most  pronounced,  and  the  caecal 
walls  attain  their  greatest  thickness  at  this  point,  so  that  the  term  hypertrophic  tuber, 
culoma  of  the  caecum  seems  to  me  to  apply  in  the  majority  of  cases. 

The  tuberculoma  may  remain  hmited  to  the  caecum  without  invading  the  colon, 
as  in  one  of  my  cases.  In  most  of  the  pubhshed  cases,  however,  the  caecal  tuberculoma 
spreads  along  the  intestine,  and  finally  reaches  the  ascending  or  even  the  transverse 
colon.  In  one  of  my  i:)atients,  operated  on  by  Legueu,  the  lesion  began  in  the  caecum, 
invaded  the  ascending  colon  and  part  of  the  transverse  colon.  In  Broca's  case  the 
lesion  affected  the  colon,  the  mucous  membrane  being  polypoid  for  about  3  inches. 
In  Marion's  case  the  lesion  started  in  the  caecum,  and  spread  into  the  ascending  and 
transverse  colons.  In  Bouilly's  case  the  caecal  lesion  had  encroached  on  the  ascending 
colon.  In  Roux's  case  the  lesion  started  in  the  caecum,  and  invaded  the  whole  of  the 
ascending  and  transverse  colons.  Hypertrophic  tuberculoma  does  not,  then,  remain 
confined  to  the  caecum  in  the  great  majority  of  cases  ;  it  finally  invades  the  colon.  This 
distinction  is  important,  as  we  may  think  that  the  operation  should  be  limited  to  the 
caecum,  and  then  find  a  lesion  which  has  invaded  the  ascending  and  the  transverse 
colons,  so  that  it  is  necessary  to  remove  10  or  12  inches  of  bowel. 

*  Dieulafoy,  "  Tuberculome  Hypertrophique  du  Caecum  ;  Diagnostic  des  Tumeurs  de 
la  Fosse  Iliaque  Droite  "  {Clinique  Medicale  de  V Hotd-Dieu,  1903,  14™^  et  15'"'=  le§ons). 


DISEASES  OF  THE  INTESTINE  793 

Pathological  Anatomy. — Let  us  suppose  a  case  in  which  the  surgeon 
has  just  performed  the  operation.  It  is  often  tedious  because  the 
tumour  is  adherent  to  the  organs  in  the  iliac  fossa,  to  the  peritoneum,  or  to 
the  anterior  abdominal  wall ;  chains  of  glands  start  from  the  tumour  and 
reach  towards  the  spine  or  spread  out  into  the  iliac  fossa. 

The  tumour  at  first  sight  might  be  taken  for  a  lymphosarcoma  or  cancer, 
on  account  of  its  external  and  also  of  its  internal  appearance.  When  we 
handled  the  tumour  removed  by  Bouilly,  we  thought  it  a  cancer  of  the 
caecum.  At  the  first  microscopic  examination  PilUet  considered  the  mass 
to  be  a  lymphosarcoma,  and  it  was  only  later,  on  a  second  examination,  that 
he  recognized  the  case  as  hypertrophic  tuberculoma.  In  a  case  reported  by 
Chavannaz  and  Carriere  they  thought  of  cancer  of  the  caecum,  even  when 
they  saw  the  tumour.  The  tubercular  nature  of  the  tumour  was  shown 
later  on  microscopic  examination.  Dr.  Antipas  recently  sent  me  the  csecum 
of  a  patient  whom  he  had  cured  by  operation.  According  to  his  idea,  it 
was  a  case  of  hypertrophic  tuberculoma.  We  thought  that  it  was  a 
l3anphosarcoma,  but  the  microscopic  examination  made  by  Nattan-Larrier 
showed  that  it  was  really  a  tuberculoma  with  bacilli.  It  is  probable  that 
many  cases  formerly  called  cancer  of  the  csecum  were  really  cases  of  hyper- 
trophic tuberculoma. 

The  tumour  is  formed  by  the  caecum,  which  is  much  thickened,  nodular, 
surrounded  by  caseous  glands,  and  embedded  in  a  thick  mass  of  fibro-adipose 
tissue.  The  condition  is,  therefore,  a  true  fibro-adipose  perityphlitis,  quite 
comparable  to  the  fibro-adipose  perinephritis  which  accompanies  a  tuber- 
cular kidney.  This  envelope  was  enormous  in  my  specimens.  It  has 
been  found  in  several  cases,  and  Hartmann  and  Pilhet  have  given  an 
excellent  description  of  it  in  their  work  published  in  1891. 

The  walls  of  the  caecum  are  sometimes  enormous.  They  are  lardaceous 
or  fibroid,  and  creak  under  the  scalpel.  In  my  patients  they  were  about 
1  inch  in  thickness,  while  their  thickness  was  half  an  inch  in  Marion's  case 
and  2  inches  in  Gussenbauer's  case.  This  hypertrophy  is  in  part  due  to 
the  fibroid  tubercular  change  in  the  walls. 

When  the  caecum  is  opened,  the  internal  surface  projects,  in  the  form 
of  pillars  and  columns,  as  in  one  of  my  patients.  Vegetations  of  a  poly- 
poid or  papillomatous  appearance  may  be  seen,  and  resemble  the  tuber- 
cular vegetations  found  in  the  larynx.  Ulcers  are  seen  in  places.  The 
ileo-csecal  valve  is  sometimes  ulcerated  and  destroyed,  or  at  other  times 
indurated  and  rigid,  with  a  much  constricted  orifice.  These  lesions  may 
cause  stenosis  of  the  intestine  at  the  valve  and  in  the  cavity  of  the  caecum 
itself.  This  stenosis  induces  constipation  and  intestinal  obstruction.  In 
severe  ileo-caecal  stenosis  the  last  portion  of  the  ileum  is  much  dilated, 
and  the  ascending  colon  is  contracted. 


794  TEXT-BOOK  OF  MEDICINE 

Microscopic  examination  shows  that  the  thickening  is  due  to  a  con- 
siderable infiltration  of  embryonic  cells,  which  resembles  sarcomatous 
tissue.  This  infiltration  replaces  the  tunica  mucosa,  and  invades  the 
tunica  muscularis,  pushing  aside  the  fibres.  Tubercular  granulations  and 
large  tubercles  may  be  found  in  the  cellular  layer,  but  this  process  does  not 
end  in  caseation,  but  in  fibroid  change,  which  makes  the  wall  rigid  and 
thick.  Koch's  bacilli  were  very  numerous  in  the  preparations  from  the 
caecum  of  one  of  my  patients. 

Tuberculosis  of  the  csecum  always  produces  enlargement  of  the  glands. 
They  are  more  or  less  numerous  and  enlarged,  and  indurated  or  caseous. 
They  are  usually  found  in  the  ileo-caecal  angle,  but  some  may  be  met  with 
in  the  mesentery,  near  the  pancreas,  in  the  supraclavicular  region,  and 
in  the  groin. 

Ileo-Caecal  Appendix. — In  these  cases  the  walls  of  the  appendix  are 
almost  always  hypertrophied,  and  show  tubercles,  and  yet  the  patient  has 
not  appendicitis  in  the  clinical  sense  of  the  word.  He  has  tubercular  lesions 
in  the  appendix,  but.  they  do  not  give  rise  to  the  closed  cavity,  and  conse- 
quently to  the  toxi-infectious  symptoms  which  alone  deserve  the  name  of 
appendicitis. 

I  do  not  say  that  such  a  result  is  impossible,  but  I  can  find  no  mention  of 
purulent  peritonitis,  remote  abscesses,  subphrenic  empyema,  purulent  infec- 
tion of  the  liver,  putrid  pleurisy,  or  toxic  lesions  in  the  kidneys,  liver,  and 
stomach,  which  are  the  appanage  of  appendicitis.  An  individual  may, 
therefore,  have  tubercular  lesions  in  the  caecum,  and  the  appendix  may 
be  involved  in  the  tubercular  mass,  but  the  terrible  effects  of  appendicitis 
do  not  occur. 

What  is  true  of  hypertrophic  tuberculoma  is  equally  true  of  ulcerative 
ileo-csBcal  tuberculosis.  I  remember  a  phthisical  patient  who  suffered 
from  ulcerative  tuberculosis  of  the  intestine.  The  appendix  was  much 
affected  by  tubercular  lesions,  but  they  were  parietal,  and  had  not  caused 
the  formation  of  a  closed  cavity.  Furthermore,  the  patient  had  never  had 
any  symptoms  of  appendicitis,  and  the  histological  and  bacteriological 
examinations  confirmed  the  absence  of  any  toxi-infectious  focus  in  the 
appendix.  In  other  words,  tuberculosis  of  the  appendix  and  appendicitis 
are  two  very  different  things,  and  it  would  be  wrong  to  include  them  in  one 
classification.  Tuberculosis  of  the  walls  of  the  appendix  is  fairly  common, 
whilst  tubercular  appendicitis  is  exceedingly  rare.  This  is  also  the  opinion 
of  Letulle,  whose  authority  in  this  matter  is  great.  As  a  general  rule,  the 
lesions  of  the  appendix  (tuberculosis,  actinomycosis,  cancer)  which  remain 
limited  to  the  walls  of  the  appendix  do  not  cause  appendicitis.  These 
lesions  may  also  be  present  in  the  tissues  around  the  appendix,  but  they  are 
incapable  of  poisoning  the  system,  like  the  focus  of  appendicitis,  which  is 


DISEASES  OF  THE  INTESTINE  795 

closed,  and  contains  organisms.  It  is  certain  that  patients  suffering  from 
hypertrophic  tuberculoma  of  the  caecum  do  not  succumb  to  appendicitis, 
and  the  prognosis  is  at  least  free  from  this  compHcation. 

Clinical  Cases. — Two  years  ago  I  admitted  into  the  Hotel-Dieu  a  woman,  of  thirty- 
nine  years  of  age,  who  had  suffered  for  eighteen  months  from  chronic  diarrhoea  and 
acute  abdominal  pains,  especially  in  the  right  ihac  region.  From  the  commencement 
of  the  disease  she  had  passed  six  or  eight  stools  daily.  The  diarrhoea  was  not  always 
preceded  by  colic,  and  had  no  special  characters,  as  blood,  mucus,  and  membranes 
were  not  present. 

The  pains  were  exceedingly  acute  and  continuous  or  paroxysmal,  but  we  noticed 
no  special  time  of  onset,  which  might  have  helped  us  to  localize  the  intestinal  lesion. 
They  were  most  marked  in  the  right  iliac  fossa. 

She  did  not  look  ill,  in  spite  of  the  diiration  of  the  disease.  Nevertheless,  she  had 
lost  flesh  for  the  past  two  months,  and  the  diarrhoea  had  been  incessant.  Treatment 
had  given  no  relief. 

What  disease  had  caused  so  much  pain  and  diarrhoea  for  eighteen  months  ?  There 
was  no  fever  ;  the  uterus  and  its  adnexa  were  normal.  Examination  of  the  abdomen 
disclosed  a  tumour  of  the  size  and  shape  of  a  pear  in  the  right  ihac  fossa.  The  tumour, 
which  was  painful  on  pressure,  was  fairly  mobile  and  indurated,  but  not  nodular. 
Its  lower  portion  was  wider,  and  reached  nearly  to  Poupart's  ligament,  and  its  upper 
more  narrow  portion  reached  up  in  the  direction  of  the  ascending  colon.  Internally 
it  did  not  reach  the  middle  b'ne.  These  signs  and  this  locaUzation  being  given,  we  could 
think  only  of  the  caecum.  It  was  still  necessary  to  know  its  nature,  because  many 
tumours  occur  in  the  right  iliac  fossa. 

I  diagnosed  hypertropliic  tuberculoma  of  the  caecum,  and  not  cancer,  because  the 
wasting  was  only  of  two  months'-  duration.  Furthermore,  the  sero -diagnosis  of 
tuberculosis  was  positive,  and  confirpied  the  clinical  diagnosis.  The  lungs  were 
sound,  and  the  case  was,  therefore,  primary  tuberculoma  of  the  caecum.  Under  these 
conditions,  operation  seemed  to  me  to  be  imperative,  and  I  requested  Legueu  to 
perform  it. 

An  incision  6  inches  long  was  made  at  the  outer  border  of  the  rectus  muscle.  When 
the  peritoneum  was  opened,  the  indurated  portion  of  the  intestine  was  exposed.  Ex- 
amination showed  that  the  chief  trouble  was  in  the  caecum,  which  formed  a  large  tumour. 
Legueu  also  found  that  the  induration  of  the  intestinal  wall  extended  as  far  as  the 
hepatic  flexure.     The  ileum  was  healthy. 

The  diseased  intestine  was  removed,  and  the  two  ends  of  healthy  bowel  (ileum  and 
transverse  colon)  were  joined  by  end-to-end  anastomosis. 

Some  enlarged  glands  were  removed  from  the  mesentery.  A  catgut  suture  was 
applied  to  the  free  edge  of  the  mesentery,  so  as  to  unite  the  two  layers.  The  operation 
was  concluded  by  the  suture  of  the  abdominal  wall  and  the  insertion  of  a  single  drainage- 
tube. 

The  patient  had  a  motion  on  the  third  day.  We  commenced  to  feed  her  with  milk 
and  broth.  The  drainage-tube  was  removed,  and  from  the  eighth  day  onwards  the 
progress  was  rapid. 

Five  weeks  after  the  operation  she  was  fat  and  well.  Some  10  inches  of  intestine 
were  resected,  thus  removing  a  tubercular  lesion  of  eighteen  months'  duration,  which 
would  have  had  a  fatal  ending.  At  the  present  time  her  appetite  is  excellent,  and 
lier  digestion  is  normal.  The  abdominal  pain  and  the  diarrhoea  have  completely  dis- 
ap])cared. 

Eight  months  later  she  camo  back  to  see  us  at  the  Hotel-Dieu.  She  had  gained 
about  20  pounds  in  weight,  and  had  not  felt  the  least  malaise  since  the  operation — n 
proof  that  the  lesion  had  been  taken  away  in  toto.     Although  the  caecum,  ileo-ctecal 


796 


TEXT-BOOK  OF  MEDICINE 


valve,  ascending  colon,  and  a  portion  of  the  transverse  colon  were  removed,  her  diges 
tion  was  as  regular  as  with  a  normal  intestine. 

Immediately  after  the  operation  we  examined  the  specimen.  The  portion  resected 
by  Legueu  comprised  the  end  of  the  ileum,  the  caecum,  the  ascending  colon,  the  hepatic 
flexure,  and  a  part  of  the  transverse  colon — in  all,  about  10  inches  of  gut.  The  following 
figure  shows  the  intestinal  lesion  in  detail. 

The  ileum  was  quite  normal. 

The  caecum  formed  a  large  tumour,  the  size  of  which  has  been  increased  by  an 
adherent  fibro -fatty  sheath  (/).  Its  nodular  surface  gave  at  first  sight  the  impression 
of  a  sarcoma.     Caseous  glands  were  found  at  various  points. 

After  opening  the  specimen  we  found  the  following  details  : 

The  walls  of  the  caecum  were  hard  ^nd  fibroid,  being  1  inch  thick  at  the  bottom  (e), 
and  I  inch  a  little  higher.  The  walls  of  the  ascending  colon  were  i  inch  thick,  and  those 
of  the  hepatic  flexure  (6)  were  J  inch.  The  lesion  began  at  the  bottom  of  the  caecum, 
and  became  less  marked  as  it  extended  towards  the  colon.  The  caecal  cavity  was  con- 
stricted by  the  thickening  of  the  walls.     Concentric  hypertrophy  was  present. 


The  internal  surface  of  the  caecum  was  irregularly  corrugated.  The  ileo -caecal  valve 
(d)  was  indurated,  open,  and  constricted.  Two  sui^erficial  ulcers  were  found — one  (c) 
in  the  ascending  colon,  and  the  other  in  the  transverse  colon.  The  appendix  was 
slightly  indurated  and  hypertrophied. 

The  histological  examination  by  Nattan-Larrier  showed  the  following  details : 

The  hypertrophy  of  the  walls  of  the  caecum  was  confined  principally  to  the  sub- 
peritoneal cellulo -fibrous  layer  and  to  the  submucous  layer,  where  the  tubercular 
lesions  attained  their  maximum. 

The  epithelium  of  the  surface  was  preserved  everywhere  without  a  trace  of  ulcera- 
tion. The  glands  of  the  mucous  membrane  were  very  much  hypertrophied.  In  the 
submucous  layer  marked  infiltration  of  leucocytes  and  a  considerable  number  of  small 
isolated  or  agglomerated  tubercles  were  present.  The  muscular  layer  was  separated  by 
abundant  oedema,  and  embryonic  infiltration  was  found  at  certain  points.  The  serous 
layer  was  very  rich  in  adipose  tissue,  and  patches  of  very  dense  fibrous  tissue  and  some 
small  tubercles  were  also  found.     Films  on  slides  revealed  the  presence  of  Koch's 


DISEASES  OF  THE  INTESTINE  797 

bacilli.  The  histological  examination  of  the  appendix  showed  non-tubercular  hyper- 
trophy of  the  walls,  with  obUteration  of  the  canal  throughout  its  whole  length. 

Another  patient  suffered  from  continual  diarrhoea,  and  could  not  take  food.  He 
had  lost  50  pounds  in  weight  in  three  years.  In  the  right  iliac  fossa  he  had  a  tumour 
which  was  easily  felt,  because  the  walls  of  the  abdomen  were  very  thin.  Examination 
of  the  region  did  not  cause  pain.  The  tumour  was  of  ligneous  consistency,  and  as  big 
as  a  large  orange.  It  seemed  to  be  adlierent  to  the  pelvis.  It  was  2  inches  from  the 
linea  alba,  and  3  inches  from  the  false  ribs.  Below,  it  did  not  reach  Poupart's  ligament. 
The  inguinal  glands  were  hard,  but  not  painful. 

The  tumour  was  evidently  in  the  caecum,  but  how  were  we  to  know  whether  it  was 
cancerous  or  tubercular  ?  Induration  of  the  tumour,  glands  in  the  groin,  loss  of  flesh, 
and  cachexia  were  not  sufficient  to  establish  the  differential  diagnosis.  The  course  of 
the  disease,  however,  was  important.  The  patient  had  been  ill  for  three  years.  At 
this  period  an  abundant  bloody  diarrhoea  came  on,  and  had  never  disappeared. 
It  came  on  immediately  after  the  ingestion  of  food.  Diarrhoea,  abdominal  pains, 
anorexia,  loss  of  flesh,  and  cachexia  might  be  present  in  tuberculosis  or  in  cancer  of 
the  caecum.  I  nevertheless  put  aside  the  idea  of  cancer,  on  account  of  the  long  duration 
of  the  disease.  Besides,  we  had  another  argument  in  favour  of  tuberculosis — the  patient 
was  suffering  from  pulmonary  tuberculosis.  The  lung  trouble  was  not  the  primary 
disease,  because  the  patient  had  been  examined  several  times  at  the  Hotel-Dieu,  and 
the  lungs  had  always  been  foxmd  healthy.  Two  years  and  a  half  before  he  was  treated 
for  intestinal  troubles,  but  we  found  nothing  the  matter  with  his  lungs.  As  the  disease 
became  worse,  he  returned  for  advice  a  year  later,  and  we  again  found  intestinal  symp- 
toms, but  no  indication  of  phthisis.  I  therefore  diagnosed  hypertrophic  tuberculoma 
of  the  caecum,  with  secondary  disease  in  the  lungs. 

If  this  man  had  come  to  us  earlier,  before  the  onset  of  the  lung  trouble  and  of  the 
cachexia,  I  should  not  have  hesitated  as  to  operation.  In  his  actual  condition  there 
could  be  no  thought  of  surgical  intervention.  We  tried  in  vain  to  feed  the  patient  up, 
but  he  succumbed  six  weeks  after  admission. 

The  results  of  the  post-mortem  examination  were  as  follows  :  It  was  a  case  of  hyper- 
trophic tuberculoma  of  the  caecum.  There  was  a  nodular  tumour  of  the  size  of  an 
orange,  which  at  first  sight  simulated  a  lymphosarcoma.  The  caecal  tumour  was  en- 
larged by  a  fibro-fatty  covering.  When  this  envelope  was  removed,  the  walls  of  tha 
caecum  (b)  were  greatly  hypertrophied,  fibroid,  and  lardaceous,  as  Avill  be  seen  from 
Fig.  55.  The  lesion  was  absolutely  confined  to  the  caecum.  The  ileum  (d)  and  the 
colon  (a)  were  not  affected.  The  delimitation  of  the  lesion  was  as  clear  internally  as 
externally.  A  large  ulcer  (c)  had  destroyed  the  valve,  and  occupied  the  bottom  of  tlie 
caecal  cavity.  Elsewhere  the  internal  surface  of  the  caecum  was  closely  set  with  folds, 
forming  bridles,  pillars,  and  columns.  Glands  were  not  numerous.  The  appendix, 
though  thickened  and  embedded  in  the  fatty  tissue  around  the  caecum,  had  preserved 
its  normal  calibre.  In  the  histological  preparations  Koch's  bacilli  were  found  in 
aljundance. 

Bouilly's  case  (the  first  case  operated  on  in  France) :  A  woman  had  been  suffering 
from  gastro-intestinal  troul)les  for  five  years.  An  immovable  painful  tumour  of  the 
size  of  an  orange  was  found  in  the  right  iliac  fossa,  and  was  supposed  to  be  an  ileo-coecal 
cancer.  The  tumour  was  removed.  On  examining  the  specimen,  thickening  of  the 
walls  was  found ;  the  ileo-ca^cal  valve  was  unrecognizable,  and  the  mucous  membrane 
of  the  caecum  was  covered  with  vegetations,  which  projected  into  the  cavity.  The  case 
was,  therefore,  a  tuberculoma.  The  appendix  was  large,  but  the  canal  was  patent. 
Glands  were  present  at  the  junction  of  the  ileum  and  of  the  c;ecuin.  Tiie  patient  was 
in  good  healtli  four  years  after  this  operation. 

One  of  BiHroth'a  cases  refers  to  a  ciiild  of  ten  years  of  age  who  liad  suffered  from 
intestinal  troubles  for  two  years.     A  tumour  of  the  size  of  an  apple,  which  wiw  tender 


798  TEXT-BOOK  OF  MEDICINE 

on  pressure,  mobile  in  all  directions,  and  of  a  ligneous  consistency,  was  felt  in  the  csecal 
region.  In  order  to  clear  up  the  diagnosis,  an  injection  of  tuberculin  was  given,  and 
caused  a  reaction  of  104°  F.  The  case,  therefore,  was  held  to  be  tubercular.  An 
operation  was  performed.  The  tumour  was  4  inches  in  length  ;  the  ileo-cgecal  valve 
was  much  constricted  ;  the  mucous  membrane  of  the  caecum  was  covered  with  polypoid 
vegetations,  surrounded  by  a  callous  zone.  Microscopic  examination  showed  an 
infiltration  of  small  cells,  grouped  in  tubercles  and  giant  cells.  The  operation  was 
followed  by  recovery. 

Description. — The  onset  is  generally  slow  and  insidious.  The  patient 
complains  of  abdominal  pains,  with  alternate  diarrhoea  and  constipation. 
The  pains,  which  are  at  times  very  sharp,  may  affect  the  form  of  colic,  and 
be  most  severe  in  the  right  iUac  fossa.  The  diarrhoea  is  sometimes  inter- 
mittent, or  at  other  times  as  obstinate  as  in  ordinary  tubercular  enteritis. 
Blood  is  rarely  present,  contrary  to  what  is  noticed  in  ordinary  tubercu- 
losis of  the  intestine.  During  this  first  period  the  patient  loses  but  little 
flesh. 


FlQ.  55. 

The  stationary  stage,  during  which  the  lesions  become  definite,  varies 
from  a  few  months  to  several  years.  During  this  period  the  symptoms  are 
almost  invariable,  and  comprise  intestinal  troubles,  pains  predominating 
in  the  right  iliac  fossa,  diarrhoea,  constipation,  vomiting,  and  loss  of  flesh. 
The  examination  should  be  preceded  by  an  aperient.  Exploration  of  the 
abdomen  reveals  hypersesthesia  in  the  right  iliac  fossa,  where  an  induration 
or  a  tumour,  varying  in  size  from  a  nut  to  an  orange,  is  found.  The  indura- 
tion sometimes  appears  diffuse,  uneven,  and  nodular ;  at  other  times  we 
find  a  tumour  fairly  circumscribed,  mobile  in  every  direction  or  only  in  a 
transverse  direction,  or  immobile,  on  account  of  adhesions  in  the  iliac  fossa 
and  to  the  abdominal  wall.  One  or  more  fistulous  tracks  may  open  on  the 
skin  of  the  iliac  region.  What  does  the  general  examination  of  the  patient 
teach  us  ?  In  a  woman  vaginal  touch  reveals  the  integrity  of  the  pelvic 
organs.     The  lungs  are  generally  healthy,  and  pulmonary  tuberculosis  has 


DISEASES  OF  THE  INTESTINE  799 

been  noticed  only  five  times  in  thirty  cases  (Benoit),  and  even  then 
the  signs  were  fairly  discrete.  Fever  is,  as  a  rule,  absent,  or  only  super- 
venes in  acute  complications.  Appendicitis  is  practically  never  seen.  The 
gravity  of  the  prognosis  does  not  arise  solely  from  the  tuberculoma,  but  is 
especially  dependent  on  primary  or  secondary  pulmonary  tuberculosis. 

Diagnosis. — The  diagnosis  of  hypertrophic  tuberculoma  of  the  caecum 
comprises  the  diagnosis  of  tumours  of  the  right  iliac  fossa.  During  the  first 
phase  of  the  disease,  when  there  is  no  tumour,  the  diagnosis  is  extremely 
difl&cult,  because  it  rests  on  two  symptoms  alone — pain  and  diarrhoea, 
which  are  common  to  several  lesions  in  this  region.  Later,  when  a  tumour 
has  formed  in  the  right  iUac  region,  the  diagnosis  is  not  less  difficult,  because 
tumours  of  every  kind  may  occupy  this  region.  Nevertheless,  let  us  discuss 
tumours  arising  in  situ,  without  troubling  ourselves  about  those  which 
have  come  from  neighbouring  regions. 

1.  Glandular  Lesions  of  the  Right  Iliac  Fossa. — I  saw  a  young  girl  who  had 
suffered  from  intestinal  troubles  for  several  months  past.  She  complained  of  abdominal 
pains,  principally  in  the  right  iliac  fossa.  At  various  times  the  crises,  which  were 
accompanied  by  vomiting,  had  awakened  the  idea  of  appendicitis.  Diarrhoea  was 
frequent,  and,  indeed,  formed  the  chief  symptom  in  the  interval  between  the  crises. 
Mela?na  had  never  been  noticed.  Digestion  was  painful,  and  alimentation  imperfect. 
She  had  no  fever,  but  she  often  kept  her  bed,  because  any  movement  brought  on  the 
abdominal  pains. 

On  exploring  the  abdomen  I  found  a  tumour  of  the  size  of  a  nut  in  the  right  iliac 
fossa.  This  tumour  was  indurated,  mobile,  and  very  painful,  and  from  its  situation 
seemed  to  form  part  of  the  caecum.  The  girl's  father  had  died  from  tuberculosis,  and 
though  she  showed  no  sign  of  disease  in  the  lung,  she  looked  like  a  consumptive.  I 
had  grave  doubts  about  the  diagnosis.  I  thought  of  the  possibility  of  hypertropliic 
tuberculoma  of  the  caecum,  and  advised  the  family  to  call  in  Gerard  Marchant. 

He  gave  the  following  report  at  the  Societe  de  Chirurgio  :  "  When  the  peritoneum 
was  opened  and  the  caecum  laid  bare,  I  was  especially  struck  by  the  existence  of  two 
juxtaposed  masses  of  glands,  one  of  which  was  larger  than  the  other,  on  the  caecum, 
near  its  internal  surface  and  close  to  its  junction  with  the  small  intestine — that  is  to 
say,  where  normal  anatomy  shows  glands.  One  of  these  glands  showed  a  yellowish 
point  near  its  surface.  No  adhesions  were  present,  and  I  was  able  to  enucleate  these 
glands  without  disturbing  the  coats  of  the  ciecum.  Though  the  appendix  appeared 
healthy,  it  was  resected." 

The  glands  and  the  appendix  were  examined.  The  appendix  sliowed  no  lesion. 
The  glands  were  caseous.  The  operation  was  followed  by  rapid  improvement,  the 
pains  and  the  diarrhcea  disappeared,  and  five  years  later  I  saw  the  patient,  in  perfect 
health. 

I  quote  two  more  cases  of  precaecal  adenitis,  reported  by  Gerard  Marchant :  On 
November  14,  1899,  ho  oporatc^d  on  a  young  girl  who  suffered  every  two  or  tliroo  months 
from  sliarp  pain  in  the  right  iliac  fossa,  vvitliout  vomiting.  The  pain,  as  a  rule,  sub.sided 
after  a  few  liours'  rest.  The  first  severe  crisis  occurred  in  July,  1899,  witli  liigii  fever, 
vomiting  whicli  lasted  four  days,  and  violent  pains  at  the  usual  spot.  Tliis  crisis  lasted 
for  a  fortnight,  and  yielded  to  ico,  opium,  and  starvation  diet.  The  patient,  however, 
always  felt  pain  in  the  riglit  iliac  fossa.  The  second  crisis  occurred  during  the  night 
of  Novcmljcr  2  —nausea,  lipothyniia,  and  extreme  distress,  but  no  fever.  Ten  "days 
later  Marchant  noticed  a  well-marked  swelling  in  the  caecal  region.     He  thought  it  was 


800  TEXT-BOOK  OF  MEDICINE 

a  case  of  appendicitis,  but  he  was  surprised  at  the  operation  to  find  the  appendix  normal. 
On  the  anterior  surface  of  the  caecum,  however,  there  was  a  large  suppurating  gland, 
which  was  so  adlierent  to  the  caecum  that  extirpation  had  to  be  abandoned.  The  gland 
was  treated  by  scraping  and  cauterization.  The  septic  focus  was  then  isolated  from 
the  general  peritoneal  cavity  by  suture  of  the  csecum  to  the  edge  of  the  peritoneum. 
The  patient  had  a  sister  suffering  from  coxalgia,  and  a  brother  who  was  phthisical. 
The  operation  resulted  in  cure.  Histological  examination  of  the  appendix  showed 
follicular  inflammation  of  the  walls,  but  there  was  no  appendicitis. 

In  another  case  reported  by  Gerard  Marchant  appendicitis  had  been  diagnosed. 
There  were  persistent  pains  over  the  csecum  and  rapid  loss  of  flesh. 

The  operation  showed  the  integrity  of  the  appendix,  which  was,  however,  resected ; 
but  the  operator  found  a  quantity  of  small,  hyperplastic,  indurated  glands,  which  were 
not  limited  to  the  csecum,  but  were  also  present  in  the  meso-ajDpendix,  the  great  omen- 
tum, and  the  right  layer  of  the  mesentery.  None  of  these  glands  were  touched.  The 
abdomen  was  sutured,  and  the  patient  got  better  under  the  influence  of  general  treat- 
ment. 

In  his  commentary  on  these  cases  Marchant  thinks  justly  that  pre- 
csecal  adenitis  may  be  consequent  on  pre-existing  tubercular  or  infectious 
lesions  of  the  csecum,  or  of  the  ileo-csecal  valve.  I  think  that  precsecal 
adenitis  may  become  the  chief  lesion,  the  caecal  or  ileo-csecal  lesion  remaining 
in  statu  quo.  The  history  of  cervical  or  mediastinal  tubercular  adenitis  fur- 
nishes us  with  similar  examples.  An  apparently  insignificant  tubercular 
lesion  in  an  organ  may  cause  infection  in  the  adjacent  or  remote  lymphatic 
glands.  Adenoid  growths  and  tonsillar  lesions,  which  I  have  already 
described  under  Masked  Tuberculosis  of  the  Tonsils,*  may  lead  to  enlarge- 
ment of  the  glands  in  the  neck,  whilst  the  primary  lesion  becomes  stationary, 
and  passes  almost  unnoticed. 

Similar  considerations  seem  to  me  to  be  apphcable  to  csecal  tuberculosis. 
In  studying  the  classical  form  of  hypertrophic  tuberculoma  of  the 
caecum,  we  have  seen  that  it  is  always  accompanied  by  adenitis,  which 
may  spread  far,  though  its  seat  of  election  is  the  anterior  surface  of  the 
csecum  and  the  ileo-csecal  junction.  Now,  side  by  side  with  the  classical 
form  which  is  revealed  by  the  symptoms  enumerated  in  this  chapter,  we  may 
ask  whether  a  masked  form  of  csecal  tuberculosis  may  not  occur,  and  declare 
itself,  not  by  the  classical  symptoms,  but  by  pain  and  caseation  or 
suppuration  of  the  glands  in  the  right  iliac  fossa,  attacking  especially  those 
on  the  anterior  surface  of  the  csecum  and  the  ileo-csecal  junction. 

The  enlarged  glands,  which  are  more  or  less  appreciable  on  palpation, 
according  as  they  form  a  tumour  or  not,  occupy  the  cseco-appendicular 
region,  in  which  chronic  lesions  of  the  appendix  and  the  csecum  are  also 
found.  Besides,  these  precsecal  cases  borrow  symptoms  from  the  neigh- 
bouring organs  (peritoneum  and  intestine),  and  thus  cause  difficulty  in 
diagnosis.     They  are  accompanied  by  continuous  or  paroxysmal  pains, 

*  Dieulafoy,  "  Tuberculose  Larvee  des  Trois  Amygdales  "  {^Academic  de  Medecine, 
seance  du  30  A\Til,  1895). 


DISEASES  OF  THE  INTESTINE  801 

which  somewhat  resemble  the  pains  of  chronic  appendicitis.  They  cause 
diarrhoea,  which  diverts  the  attention  to  the  intestine,  and  they  form  a 
painful  tumour  in  the  right  iliac  fossa,  just  as  hypertrophic  tuberculoma 
of  the  caecum  does,  so  that  we  find  three  kinds  of  lesions — \'iz.,  csecal  tuber- 
culoma, chronic  appendicitis,  and  precsecal  adenopathy.  They  occupy 
the  same  region,  and  have  common  symptoms.  Differential  diagnosis 
between  these  three  lesions  is,  then,  extremely  difficult  before  the  opera- 
tion. The  differential  diagnosis  is  not  of  prime  importance,  because  in  all 
three  cases  surgical  intervention  is  imperative. 

2.  Hypertrophic  Tuberculosis  of  the  Ileum.— We  must  nest;  con- 
sider the  diagnosis  between  hypertrophic  tuberculoma  of  the  caecum  and 
hypertrophic  tuberculosis  of  the  small  intestine  in  the  right  iliac  region. 
Bernay  classes  tubercular  stenoses  of  the  small  intestine  in  three  groups, 
according  as  the  constriction  is  fibrous,  cicatricial,  or  hypertrophic.  The 
fibrous  and  cicatricial  constrictions  are  almost  always  found  in  the  upper 
three-quarters  of  the  small  intestine,  whereas  the  hypertrophic  constriction 
is  principally  met  with  in  the  lower  fourth.  This  last  form  is  much  less 
common,  since  it  only  existed  eight  times  in  seventy  cases  of  tubercular 
con.striction.     Even  then  it  does  not  always  extend  to  the  cgecum. 

A  very  clear  case  has  been  published  by  Tuflfier. 

A  woman  who  was  neither  consumptive  nor  syphilitic  had  suffered  from  colic  for 
about  two  years.  The  attacks  of  colic  made  their  appearance  four  or  five  hours 
after  meals,  and  ended  in  liquid  stools  wathout  a  trace  of  melaena.  Although  her 
appetite  was  good,  she  ate  little,  for  fear  of  the  intestinal  pains,  and  she  had  lost  flesh 
considerably.  On  exploring  the  abdomen  a  tumour  of  the  size  of  a  small  tangerine 
orange  was  found  in  the  right  iliac  fossa.  The  tumour  was  painless,  mobile,  and  of  a 
renitent  consistency.  The  diagnosis  of  tubercular  stenosis  of  the  small  intestine  was 
made,  and  Tuffier  operated.  It  turned  out  to  be  a  case  of  hypertrophic  tuberculosis 
of  the  small  intestine.  Thirteen  inches  of  the  intestine  were  resected,  and  in  a  few 
weeks  later  the  patient  had  recovered.  On  examining  the  specimen  it  was  found  that 
the  tuberculosis  was  at  once  ulcerative,  hypertrojjhic,  and  constricting.  The  stenosis 
was  the  result  of  fungoid  enteritis.  The  histological  preparations  showed  considerable 
hypertrophy  of  the  different  layers  of  the  intestine,  but  principally  of  the  submucous 
one.  In  tlie  deep  layers  of  tlic  submucosa  large  tubercular  follicles  with  giant  cells 
and  tubercle  bacilli  were  found. 

In    other    words,    hypertrophic    tuberculosis    of    the    ileum    may 

give  rise  to  a  tumour  resembling  hypertrophic  tuberculoma  of  the 
caecum. 

3.  Chronic  Appendicitis. — Let  us  now  consider  tumours  of  the  right 
iliac  fossa  consecjuent  on  previous  appendicitis.  I  do  not  speak  here  of 
the  iliac  abscesses  which  occur  in  suppurative  appendicitis,  but  I  allude  to 
fibroid  raas.ses  of  slow  and  progressive  growth  and  to  tumours  of  a  neo- 
plastic aspect,  which  form  a  chapter  in  chronic  appendicitis  as  yet  but 
little  studied. 

t  51 


802  TEXT-BOOK  OF  MEDICINE 

In  its  extra-appendicular  migration  the  infection  may  remain  limited 
to  the  right  iliac  fossa,  and  does  not  always  cause  the  formation  of  pus 
(suppurative  perityphlitis).  It  sometimes  gives  rise  to  an  inflammatory 
tumour,  or  produces  false  membranes  and  adhesions  which  have  the  look 
and  the  consistency  of  fibroid  and  lardaceous  tissue.  This  process  may 
reach  the  mesentery,  and  extend  beyond.  "  Fibrous,  hard,  resistant,  and 
irregularly  distributed  bands  fix  the  appendix  to  the  caecum,  ileum, 
mesentery,  or  iHac  peritoneum."  Thick  adhesions  may  bend  the  termina- 
tion of  the  small  intestine  at  its  junction  with  the  csecum,  and  compress  the 
ileo-caecal  valve.  The  csecum,  embedded  in  the  inflammatory  tissue,  is 
at  times  unrecognizable,  the  portion  of  the  large  intestine  being  replaced 
by  a  mass  of  fibroas  tissue,  in  which  ileum  and  ascending  colon  are  matted 
together.  On  palpation  of  the  right  iliac  fossa,  a  pericsecal  or  ileo-csecal 
tumour  may  be  felt. 

This  extra-appendicular  process  is  slow  in  its  evolution,  and  the  symp- 
toms closely  resemble  those  of  hypertrophic  tuberculoma  of  the  csecum. 
The  patient  complains  of  heaviness,  twitchings,  and  pains  in  the  right  iliac 
fossa.  These  pains  may  only  amount  to  a  feehng  of  numbness,  or  may 
occur  in  acute  crises  analogous  to  those  of  appendicitis.  They  then  can 
only  be  due  to  bridles  and  to  adhesions.  Here,  as  in  fibrous  peri- 
cholecystitis, the  adhesions  may  give  rise  to  attacks  of  severe  pain.  The 
patient  sometimes  complains  of  dyspepsia,  anorexia,  or  vomiting.  Diarrhoea 
is  frequent ;  constipation  may  be  obstinate,  and  accompanied  by  symptoms 
of  intestinal  occlusion.  The  patient  grows  thinner.  I  have  also  seen  reflex 
cardiac  troubles  and  palpitation,  which  may  obscure  the  diagnosis,  by 
directing  the  attention  to  the  heart,  while  the  trouble  reaUy  arises  from  the 
appendicular  lesion. 

When  we  examine  the  right  iliac  fossa,  we  may  find  an  induration  or 
a  painful  tumour,  which  on  removal  presents  at  first  sight  the  appearance 
of  a  neoplasm.  This  tumour  occupies  the  situation  of  csecal  or  pericsecal 
tumours.  If  the  onset  of  the  disease  has  been  clearly  characterized  by  one 
or  more  attacks  of  appendicitis,  chronic  lesions  of  the  appendix  will  be 
thought  of,  and  the  diagnosis  made.  If  this  guide  is  absent,  we  can  only 
make  a  provisional  diagnosis  of  csecal  tuberculoma  or  cancer  of  the  csecum  ; 
but  in  any  case  we  advise  an  operation.  The  surgeon  may  fijid  a  shapeless 
mass,  in  which  the  ileum  and  the  ascending  colon  are  matted  together ; 
kinking  of  the  ileum  at  its  entrance  into  the  csecum,  constriction  of  the  ileo- 
csecal  valve,  hypertrophic  infiltration  of  the  intestinal  walls,  caseous  magma, 
purulent  collections,  adhesions,  enlarged  glands,  or  a  neoplastic  tumour, 
which  all  result  from  previous  appendicitis.  The  operation  is  often  suc- 
cessful. The  above  description  shows  how  chronic  lesions  consequent  on 
appendicitis  give  rise  to  a  tumour  in  the  right  iliac  fossa. 


DISEASES  OF  THE  INTESTINE  803 

4.  So-called  Inflammatory  Tumours. — Besides  the  tumours  due  to 
hypertrophic  tuberculoma  of  the  caecum  and  ileum,  to  pericaecal  adenitis, 
and  to  sequelae  of  appendicitis,  there  are  other  tumours  of  the  right 
iliac  fossa — much  rarer,  it  is  true — the  cause  of  which  escapes  us.  We  find 
neither  tuberculosis  nor  appendicitis,  and  for  want  of  a  better  name  the 
ileo-caecal  tumour  is  called  "  purely  inflammatory."  In  this  acceptation  of 
the  term,  Marchant  and  Demoulin  quote  the  cases  of  Hartmann,  Boiffin,  and 
Julliard  ;  but  some  of  these  cases  leave  a  doubt  as  to  their  "  purely  inflam- 
matory "  origin.  Thus,  in  Boifiin's  case  there  was  no  examination  of  the 
tumour.  It  therefore  cannot  be  said  that  it  was  not  a  case  of  tuberculoma. 
In  JuUiard's  case  "  the  appendix  was  deformed  and  almost  unrecognizable," 
which  leads  us  to  suppose  that  the  so-called  inflammatory  tumour  had  its 
origin  in  an  infection  of  the  appendix.  Marchant  has  cited  a  case  of  these 
so-called  inflammatory  tumours.  A  lateral  tumour  of  the  caecum  was 
present,  and  was  of  the  size  of  a  nut.  The  appendix  was  healthy.  The 
histological  examination  proved  that  this  was  neither  a  neoplasm,  tuber- 
culosis, nor  lymphadenoma,  but  simply  a  so-called  inflammatory  thickening 
of  the  submucous  coat. 

Schwartz  has  communicated  the  following  case  : 

A  young  woman  was  suffering  from  a  tumour  in  the  right  iliac  fossa.  This  tumour, 
which  had  been  painful  for  a  long  time,  was  hard  and  relatively  mobile.  An  operation 
was  performed,  and  a  tumour  of  the  size  of  tlie  fist  was  removed.  It  was  formed  by 
the  caecum  and  the  terminal  portion  of  the  ileum.  On  incising  the  specimen,  the  resist- 
ance of  the  tissues  was  marked.  The  caecum  was  hypertrophied  to  such  an  extent 
that  its  walls  measured  1  inch.  The  ileo-caecal  valve  was  thickened,  but  not  con- 
stricted. The  mucous  membrane  was  normal,  and  showed  no  trace  of  ulceration. 
This  tumour  was,  so  it  appears,  neither  tubercular  nor  cancerous.  It  had  not  an 
appendicular  origin.  In  what  category  should  it  be  placed  ?  The  histological  examina- 
tion by  Cornil  revealed  considerable  hypertrophy  of  the  musculature  of  the  intestine. 

5.  Actinomycosis. — Actinomycosis  of  the  appendix  and  caecum  may 
cause  a  tumour  in  the  right  iliac  fossa.  I  had  recently  the  opportunity  of 
seeing  a  case  with  Widal  and  Segond. 

The  patient  for  a  year  past  had  had  intermittent  attacks  which  resembled  recurrent 
appendicitis.  They  began  with  pain,  tympanites,  and  obstinate  constipation.  Tho 
pains,  though  general  over  the  whole  abdomen,  had  been  most  severe  in  the  right  ihac 
region.  In  spite  of  the  intensity  of  tho  pain,  there  had  been  neither  vomiting  nor  fever. 
These  attacks  lasted  for  some  days,  and  ended  without  leaving  any  trace  of  pain  in  the 
cajco-appendicular  region.  In  the  interval  between  these  acute  episodes  the  health 
had  been  good. 

Though  the  attacks  somewhat  resembled  appendicitis,  they  differed,  nevertheless, 
in  several  points.  Appendicitis  is  not  ushered  in,  as  a  rule,  by  tympanites,  and,  in 
addition,  we  never  see  a  severe  attack  of  appendicitis  which  is  not  accompanied  by 
fever  and  vomiting.  Finally,  very  severe  attacks  of  appendicitis  leave  beiiind  for 
some  time  a  painful  feeling  in  tho  right  iliac  fossa.  The  patient  sliowed  an  absence  of 
all  these  sym{)toms,  and  I  was,  therefore,  unwilling  to  admit  appendicitis.  I  had 
thought  of  typhlo-coUtis,  but  this  diagnosis  had  to  bo  abandoned,  for  in  these  cases  tho 

51— li 


804  TEXT-BOOK  OF  MEDICINE 

attficks  are  followed  by  the  expulsion  of  mucus,  membranes,  or  intestinal  sand.  Several 
hypotheses  were,  therefore,  possible,  and  precaecal  adenitis,  tuberculosis,  or  cancer  was 
suggested.     I  admit  that  I  did  not  think  of  actinomycosis. 

A  tumour,  however,  appeared  in  the  ileo-C£ecaI  region.  The  tumour,  which  was 
hard,  elongated,  mobile,  and  tender  on  pressure,  shed  no  light  on  the  diagnosis,  and 
it  might  have  been  a  case  of  cancer.  The  general  condition  remained  good.  Surgical 
intervention  became  inevitable.  Segond  operated,  and  removed  an  enormous  appendix, 
surrounded  by  membranes  and  adhesions,  though  no  traces  of  suijpiiration  or  peri- 
tonitis were  foujid.  The  walls  of  the  appendix  were  very  thick,  hard,  and  lardaceoiis. 
The  mucous  membrane  was  healthy,  and  the  lesion  did  not  deserve  the  name  of  appen- 
dicitis in  the  true  sense  of  the  word.  Microscopic  examination  showed  actinomycosis 
of  the  appendix. 

Actinomycosis  of  the  appendix  has  been  accurately  described  in  recent 
years,  notably  in  the  treatise  of  Poncet  and  Berard.  During  the  first 
phase,  which  lasts  from  one  to  two  years,  the  disease  closely  resembles  re- 
current appendicitis.  The  patient  suffers  from  continuous  or  paroxysmal 
pains,  which  are  most  marked  in  the  right  iliac  fossa.  There  are  attacks  of 
gastro -intestinal  tympanites  and  constipation,  or  more  frequently  diarrhoea, 
with  blood-stained  stools  and  tenesmus.  Later,  in  the  cseco-appendicular 
region  a  ligneous  swelling  or  an  induration,  giving  the  sensation  of  a 
deep  fibroma,  with  ill-defined  edges,  is  felt.  This  condition  may  remain 
stationary  for  months,  until  the  actinomycosis  comes  in  contact  with  the 
peritoneum  and  the  abdominal  wall,  which  it  infiltrates  hke  a  breast- 
plate, when  softening,  ulceration,  and  fistulse  supervene. 

It  must  be  admitted  that  the  diagnosis  is  most  difficult  in  the  first  phase 
of  the  disease.  There  are  only  two  cardinal  symptoms  to  serve  as  guides — 
viz.,  the  localization  of  the  pain  and,  later,  the  appearance  of  the  tumour. 
Chronic  disease  of  the  appendix,  early  csecal  tuberculoma,  or  some  other 
lesion,  is  then  thought  of,  but  nothing  as  yet  points  to  the  existence  of 
actinomycosis.  In  a  case  of  chronic  diarrhoea  the  parasite  may  be  found  in 
the  stools. 

6.  Cancer  of  the  Caecum. — We  must  make  the  diagnosis  of  tubercu- 
loma of  the  caecum  from  ileo-csecal  cancer.  The  patient  is  more  or  less 
cachectic,  and  has  been  suffering  from  abdominal  pains  and  diarrhcsa  for  a 
long  time.  A  small,  irregular,  mobile  tumour  is  felt  in  the  right  iHac  fossa. 
Has  the  patient  cancer  or  chronic  tuberculosis  ?  Upon  what  signs  are  we 
to  base  our  diagnosis  ?  Obstinate  constipation  and  intestinal  obstruction 
may  exist  in  both  cases.  Diarrhoea,  with  or  without  intestinal  haemorrhage, 
is  also  common  in  each  condition.  Nevertheless,  melaena  is  very  rare  in  hyper- 
trophic tuberculoma,  and  more  frequent  in  cancer.  Spontaneous  or  provoked 
pain  does  not  furnish  adequate  information.  The  dimensions,  form,  and 
mobihty  or  immobility  of  the  tumour  tell  us  nothing  positive.  Indurated  and 
enlarged  glands  in  the  groin  and  in  the  supraclavicular  hollow  may  be 
present  in  both  cases.     The  appearance  of  phlegmasia  alba  dolens  may  also 


DISEASES  OF  THE  INTESTINE  805 

be  seen  in  either  condition.  The  search  for  pulmonary  tuberculosis  is  only 
of  secondary  interest,  for  five  times  out  of  six  chronic  tuberculosis  of  the 
csecum  is  primary  and  local,  supervening  in  patients  who  are  free  from  any 
other  tubercular  lesion.  In  favour  of  tuberculosis  there  is,  then,  only  the 
long  duration  of  the  disease,  which  is  more  compatible  with  the  hypothesis 
of  tuberculoma,  and  the  recognition  of  the  bacillus  in  the  faeces.  Billroth 
once  made  a  correct  diagnosis  by  inducing  a  reaction  of  104°  F.  with  tuber- 
culin, but  I  would  rather  have  recourse  to  sero-diagnosis. 

7.  Finally,  we  may  see  a  patient  who  has  one  or  more  discharging  fistulas 
in  the  iUac  region.  Whence  comes  the  pus,  and  what  is  the  nature  of  the 
lesion  ?  Have  we  to  do  with  a  bone  lesion  or  not  ?  Even  if  the  tubercle 
bacillus  be  found  in  the  pus,  and  even  if  the  tubercular  nature  of  the 
lesion  be  proved  by  experimental  means  or  by  the  reaction  of  tuberculin, 
we  should  know  only  one  thing — viz.,  that  we  have  to  deal  with  a  tubercular 
lesion.  The  passage  of  fsecal  matter  through  the  fistulae  would  remove  all 
doubts,  and  prove  that  the  caecum  is  the  origin  of  the  lesions. 

Termination. — Chronic  tuberculosis  of  the  caecum  may  end  in  different 
ways.  It  may  recover  without  operation  by  a  curative  fibrous  process, 
analogous  to  the  curative  fibroid  process  in  pulmonary  tuberculosis.  In  some 
cases  the  constriction  of  the  ileo-caecal  valve  and  of  the  caecum  attains  such 
a  degree  that  the  patient  succumbs  to  intestinal  obstruction.  Iliac  phleg- 
mon and  fistulae,  burrowing  into  the  ischio -rectal  fossa,  the  edge  of  the  anus, 
or  the  right  groin,  are  possible  complications. 

etiology. — Chronic  tuberculosis  of  the  caecum,  as  I  have  already 
remarked,  is  most  often  primary.  It  is  a  local  tuberculosds  such  as  we  find 
in  the  joints  or  bones.  All  the  hypotheses  made  to  explain  primary  tuber- 
culosis of  the  digestive  passages  may  here  find  their  place.  It  is  probable 
that  the  ileo-caecal  region,  by  its  natural  constriction,  offers  a  favourable 
asylum  for  the  tubercle  bacillus. 

Treatment. — The  prognosis  of  hypertrophic  tuberculoma  of  the  caecum 
has  been  completely  modified  during  the  past  few  years.  A  patient  suffer- 
ing from  caecal  tuberculosis  was  formerly  considered  to  be  stricken  with  a 
fatal  disease.  At  present  the  mischief  can  often  be  cured  by  operation. 
Cure,  however,  can  only  be  obtained  on  certain  conditions.  It  is  necessary 
to  operate  as  early  as  possible,  before  the  subject  is  cachectic,  and  as  soon  as 
the  disease  is  recognized  or  even  suspected.  The  coexistence  of  pulmonary 
tuberculosis  makes  the  prognosis  far  worse,  because  this  complication  is  a 
counter-indication  against  operation.  Do  not  let  us  forget,  however,  that 
pulmonary  tuberculosis  is  rarely  the  source  of  tuberculosis  of  the  caecum.  It 
is  sometimes  the  consequence  thereof,  which  is  another  reason  for  not 
delaying  surgical  intervention  too  long.  Timely  operation  gives  nuraeroua 
successes. 


806  TEXT-BOOK  OF  MEDICINE 


VIII.  ANO-RECTAL  TUBERCULOSIS. 

Lupus  of  the  Anal  Region. — Lupus,  whicli  is  relatively  frequent  in 
the  face,  is  extremely  rare  at  the  anus.  It  is  generally  associated  with  lupus 
of  the  genital  organs  in  women.  In  two  cases  lupus  developed  at  the 
external  orifice  of  a  fistula.  One  of  these  cases,  communicated  by  Besnier, 
is  described  as  follows  :  The  lupus  consisted  of  an  extensive  cicatricial 
surface,  fibroid  at  the  centre,  papillomatous  at  the  circumference,  and  bor- 
dered with  ulcerated  tubercles,  which  formed  large  festoons  around  it. 
The  diagnosis  of  lupus  could  not  be  doubted  :  chronic  cutaneous  affection 
evolving  in  situ  for  the  last  eighteen  years  around  an  anal  fistula  ;  fibroid 
cicatrization  of  the  points  first  attacked,  and  peripheral  extension  by  slowly 
growing  crops  of  tubercles. 

Neither  syphiloderma  nor  epithelioma  runs  this  course,  nor  have  they  the 
slowness  of  this  process.  One  objective  point  alone  might  have  pointed  to 
syphilis,  and  that  was  the  polycyclical  border  ;  but  this  formation  is  met 
with  in  some  cases  of  lupus. 

Warty  Tuberculosis  of  the  Anus. — It  is  probable  that  the  warty 
form  of  tuberculosis  was  formerly  confounded  with  epithelioma  and  papil- 
loma. It  has  been  recognized  since  the  work  of  Hartmann,  Routier,  and 
Toupet.  The  lesion  commences  around  the  anus,  and  encroaches  on  the 
buttock  in  the  shape  of  a  patch  studded  with  non-ulcerative  mammillae  and 
crusts.  Between  the  mammillse,  eroded  oozing  furrows  are  seen.  The 
inguinal  glands  are  sometimes  healthy,  sometimes  enlarged.  Histological 
examination  reveals  giant  cells  in  the  midst  of  the  cell  mass,  and 
bacteriological  examination  proves  the  presence  of  the  tubercle  bacillus. 
Except  by  bacteriological  examination  or  inoculation  of  guinea-pigs,  it  is 
scarcely  possible  to  differentiate  warty  tuberculosis  from  papilloma  or 
epithelioma. 

Anal  Tubercular  Ulcerations. — Hartmann  has  collected  about  thirty 
cases.  After  several  months  of  itching,  oozing,  and  pains  on  defaecation,  a 
superficial  sore  appears  around  the  anus,  and  forms  an  ulcerated  scrofuloma 
en  cuirasse.  The  ulcer  is  confined  to  the  edge  of  the  anus,  and  does  not 
encroach  on  the  buttocks,  but  it  often  extends  inside  the  anal  canal  as  far 
as  the  lower  extremity  of  the  rectum.  The  ulceration  bleeds  shghtly ;  its 
edges  are  often  polycyclical,  sometimes  undermined,  sometimes  clean-cut. 
The  floor  of  the  ulcer  is  anfractuous,  granulating,  and  often  studded  with 
yellow  granules.  The  ulcer  secretes  a  muco-purulent  hquid,  and  is  some- 
times covered  with  a  crust.  Prominent  tubercles  may  be  seen  around  the 
ulcerated  surface. 

On  examining  the  anus  with  a  speculum,  lesions  are  seen  on  the  mucous 


DISEASES  OF  THE  INTESTINE  807 

membrane  analogous  to  those  of  the  skin.  Digital  examination  reveals  the 
limits  of  the  disease.  The  inguinal  glands  are  almost  always  enlarged. 
These  ulcerations  are  the  more  painful  because  the  pain  is  repeatedly- 
excited  by  the  passage  of  fsecal  matter,  walking,  and  rubbing.  In  some 
cases,  however,  they  are  almost  painless. 

Tubercular  ulceration  of  the  anus  has  an  exceedingly  slow  course,  and 
shows  no  tendency  to  cicatrization.  It  coincides  sometimes  with  tuber- 
cular ulcerations  of  the  other  parts  of  the  intestine.  The  search  for  bacilli, 
in  the  secretions  of  the  ulcerated  surface  is  the  most  certain  means  of 
diagnosis. 

Abscess  and  Anal  Fistula. — Fistula  of  the  anus  of  tubercular  origin 
always  follows  on  an  abscess,  and  is  not  the  result  of  burrowing  ulcer- 
ation. In  twelve  abscesses  of  the  anal  region  Hartmann  and  Lieffring 
found  the  tubercle  bacillus,  with  other  microbes,  in  seven  cases. 

The  subcutaneous  tubercular  abscess  opens  externally  on  the  skin, 
or  internally  in  the  ano-rectal  canal,  but  it  may  open  both  on  the  skin  and 
into  the  intestine.  If  the  track  formed  by  the  abscess  becomes  persistent, 
a  fistula  results.  A  fistula  is  a  canalicular  ulcer  which  shows  no  spontaneous 
tendency  to  heal.  It  commences  when  the  process  of  repair  ceases.  A 
complete  fistula  supposes  a  passage  with  two  orifices — the  one  cutaneous, 
the  other  intestinal.  The  fistula  if^  said  to  be  a  blind  external  one  if  there 
is  only  a  cutaneous  opening,  while  it  is  said  to  be  a  blind  internal  one  if 
there  is  only  an  intestinal  opening. 

The  symptoms  of  fistula  are  preceded  by  those  of  abscess.  In  the 
external  fistula  the  disease  only  causes  pruritus,  oozing,  suppuration,  and 
.soiling  of  the  underclothing.  In  the  case  of  a  complete  fistula  soiling  of  the 
linen  by  fa?cal  matter,  fsecal  odour,  and  tenesmus,  which  is  sometimes  painful, 
complicate  the  .situation.  At  certain  times  the  patient  has  attacks  of  in- 
flammation. As  soon  as  there  is  any  obstruction  to  the  exit  of  the  infective 
liquid,  and  as  soon  as  the  fistulous  passage  is  transformed  into  a  closed 
cavity,  the  microbes  increase  in  virulence  (coli  bacillus,  streptococcus). 
These  "  revivals  "  of  the  fistula  cause  fresh  abscesses,  with  fever,  pain  in  the 
anal  region,  etc. 

In  tubercular  patients  anal  fi.stula  exists  in  the  proportion  of  12  per 
cent.  (Cripps),  14  per  cent.  (Allingham),  16  per  cent.  (Geffrart),  50  per 
cent.  (Hartmann),  and  15  per  cent,  (personal  observations).  The  abscess 
and  the  fistula  which  results  generally  develop  during  the  course  of  pul- 
monary tuberculosis  or  at  an  advanced  stage  of  the  disease.  In  some  cases, 
however,  the  abscess  seems  to  precede  the  disease  in  the  lung,  and  it  is  by 
no  means  rare  to  find  people,  who  have  been  coughing  for  years,  under  the 
impression  that  they  are  .suffering  from  simple  emphysema  with  bronchial 
catarrh,  when  the  appearance  of  a  tubercular  absce.ss  of  the  anus  reveals 


808  TEXT-BOOK  OF  MEDICINE 

the  true  nature  of  the  bronchitis.  In  a  tubercular  family  it  is  not  rare 
to  find  one  of  the  members — perhaps  one  of  the  children — with  a  tuber- 
cular abscess  of  the  anus  as  the  only  sign  of  tuberculosis. 

An  important  question  presents  itself  in  regard  to  these  fistulas :  Can 
they  be  operated  upon  without  harm  to  the  patient  ?  Generally  speaking, 
anal  fistula  in  tubercular  patients  has  been  looked  upon  as  a  sort  of  conduit 
which  must  be  let  alone,  for  fear  of  causing  recrudescence  in  the  pulmonary 
disease.  This  assertion  is  exaggerated,  but  yet,  before  we  come  to  a  decision 
and  operate  on  the  fistula,  we  must  take  careful  stock  of  the  patient's  con- 
dition. The  operation  may  be  performed  unless  the  pulmonary  lesions  are 
too  far  advanced.  I  am  of  opinion  that  in  a  patient  with  advanced  phthisis 
we  ought  to  proscribe  an  operation  ;  in  all  other  cases  it  should  be  performed, 
for  I  have  never  seen  any  serious  inconvenience  result. 


IX.  SIMPLE  ULCER  OF  THE  DUODENUM— PERFORATION— 
SUPERACUTE  PERITONITIS. 

Pathological  Anatomy. — Simple  ulcer  of  the  duodenum  closely  re- 
sembles ulcer  of  the  stomach  and  oesophagus.  It  usually  affects  the 
first  portion  of  the  duodenum,  the  anterior  more  often  than  the  posterior 
surface,  and  at  times  encroaches  on  the  pylorus.  When  there  are  several 
ulcers,  they  become  fused,  and  give  an  irregular  form  to  the  ulceration.  It 
is  by  no  means  rare  to  find  both  ulcer  of  the  duodenum  and  of  the  stomach. 
The  pathogenesis,  course,  cicatrization,  and  perforation  of  the  duodenal 
ulcer,  as  well  as  the  pathogenesis  of  haemorrhage  and  peritonitis,  are  in  all 
points  comparable  with  the  same  processes  in  gastric  ulcer.  Adhesions  and 
fistulse  may  be  found  between  the  duodenum  and  the  neighbouring  organs. 

Symptoms. — Simple  ulcer  of  the  duodenum  generally  arises  in  an  almost 
latent  fashion,  hke  certain  ulcers  of  the  stomach.  It  is  even  more  often 
latent  than  ulcer  of  the  stomach.  Pain,  vomiting,  melsena,  and  haemate- 
mesis  are  the  usual  symptoms. 

The  pain  has  much  the  same  characteristics  as  have  been  mentioned 
under  Ulcer  of  the  Stomach,  but  it  has  a  slightly  different  seat.  The 
xiphoid  and  spinal  points  are  often  absent,  and  the  pain  appears  two  to 
three  hours  after  meals  in  the  pyloric  region  below  the  inferior  edge  of  the 
liver. 

The  intestinal  haemorrhages  may  be  fulminant  in  the  case  of  erosion  of 
a  large  vessel,  such  as  the  gastro-epiploic  artery  (Broussais),  the  pan- 
creatico-duodenal  artery  (Knecht),  the  aorta  (Stich),  or  the  portal  vein 
(Rayer).  In  ordinary  cases  melsena  recurs  at  more  or  less  close  intervals, 
with  or  without  pain,  and  is  accompanied  by  hsematemesis  if  the  blood  has 


DISEASES  OF  THE  INTESTINE  809 

regurgitated  into  the  stomach.  Pallor  of  the  face  and  of  the  body,  and 
tendency  to  fainting  or  syncope,  result  from  these  attacks  of  haemorrhage. 

Perforation  of  the  Ulcer. — Ulcer  of  the  duodenum  very  often  ende 
in  perforation,  and  in  262  ulcers  181  perforations  have  been  coimted.  The 
perforation  caused  general  peritonitis  125  times.  In  other  cases  the  peri- 
tonitis was  hmited  by  adhesions,  or  else  the  perforation  had  no  evil  result, 
because  the  liver  or  the  pancreas  formed  a  tampon. 

Partial  peritonitis  and  encysted  abscesses  due  to  adhesions  are  far  less 
common  in  the  case  of  perforating  ulcer  of  the  stomach.  They  may  open 
at  the  umbilicus  or  in  an  intercostal  space. 

Perforation  of  the  duodenal  ulcer,  with  superacute  peritonitis,  is  a 
terrible  complication.  The  reader  will  obtain  some  idea  of  it  from  the 
following  case,  taken  from  one  of  my  clinical  lectures  on  perforation  of 
simple  ulcer  of  the  duodenum  : 

A  patient  was  brought  into  the  Hotel-Dieu,  and  lay  groaning.  He  was  immediately 
put  to  bed,  and  Charrier  diagnosed  acute  peritonitis.  The  patient,  Avith  drawn  face 
and  hollow  eyes,  was  very  restless.  His  respiration  was  jerky  and  interrupted  from 
pain.  The  abdomen  was  very  distended,  excessively  painful,  and  resonant,  except  in 
the  hypogastrium  and  the  flanks. 

He  had  been  in  good  health  until  two  days  before  his  admission.  His  digestive 
functions  had  always  been  normal,  when  he  was  suddenly  seized  ^-ith  very  acute  pain 
which  he  compared  to  a  stab.  Beausse  \vas  at  once  called,  and  found  the  patient 
^vrithing  in  agony. 

Beausse  immediately  administered  an  injection  of  morphia,  which  gave  the  patient 
some  rehef,  and  he  was  then  carried  home.  It  was  now  possible  to  examine  him.  The 
abdomen  was  retracted  and  hard.  Palpation  was  very  painful,  particularly  in  the  right 
hypochondrium,  whence  the  pain  radiated  towards  the  pit  of  the  stomach  and  the 
spine.  Deep  palpation  was  not  po-ssible,  because  the  abdominal  walls  were  as  hard  as 
a  board.  As  the  pain  was  not  marked  at  McBurney's  point,  the  diagnosis  of  appen- 
dicitis was  discarded.  On  the  next  day,  Sunday,  the  abdomen  was  still  painful  and 
retracted,  but  the  patient  was  much  easier,  as  the  temperature  did  not  exceed  99"^  F. 

During  the  day  he  passed  a  motion,  and  seemed  better  in  the  evening.  The  pains 
were  less  sharp,  and  the  abdomen  was  still  retracted.  On  Monday  morning,  however, 
he  vomited  greenish  fluid,  the  eyes  became  hollow,  the  nose  pinched,  and  the  abdomen, 
which  was  previously  retracted,  now  became  distended.  He  was  then  brought  to  tho 
Hotel-Dieu. 

The  patient  was  taken  into  my  ward,  suff'ering  from  acute  peritonitis,  the  pain,  aa 
at  its  onset,  being  most  acute  under  the  ribs  on  the  right  side,  between  the  hypochon- 
drium and  epigastrium.  Although  the  prognosis  was  almost  hopeless,  and  the  peri- 
tonitis was  general,  surgical  intervention  was  necessary  as  a  last  resource.  The  opera- 
tion was  performed  by  Cazin  within  an  hour  of  his  admission  into  hospital.  The 
peritonitis  was  general,  and  the  pelvis  was  full  of  pus,  but  there  was  no  appendicitis. 
As  the  operation  had  already  lasted  some  time,  and  as  tho  patient's  condition  was  most 
serious,  it  was  very  wi.sely  decided  not  to  continue  the  exploration.  The  patient 
succumbed  a  few  hours  later. 

Next  morning,  on  arriving  at  the  Hotel-Dieu,  I  heard  the  details  of  the  case,  and  I 
am  sure  nothing  more  could  have  been  done.  When  a  patient  is  attacked  with  acute 
peritonitis,  ho  must  be  given  the  only  chance  of  salvation,  which  lies  in  operation.  It 
is  true  that  we  are  not  always  successful,  but  I  can  quote  desperate  cases  in  which 


810  TEXT-BOOK  OF  MEDICINE 

surgical  intervention  has  been  a  complete  success.  After  hearing  the  report  of  the 
case,  I  gave  my  opinion  as  to  the  cause  of  the  peritonitis,  and  I  felt  justified  in 
affirming  that  he  had  died  from  the  perforation  of  a  latent  ulcer  of  the  duodenum  or 
stomach. 

Post-mortem  examination  :  General  peritonitis.  Methodical  examination  of  the 
intestine  revealed  the  cause  of  the  peritonitis.  On  the  posterior  surface  of  the  duodenum, 
1  inch  below  the  pylorus,  we  found  a  simple  ulcer,  which  had  perforated  at  its  centre. 

On  the  intestinal  surface  the  ulcer  had  a  funnel-like  shape,  and  its  base  measured 
|.  inch  in  diameter.  The  walls  were  steep,  and  formed  two  steps.  At  the  bottom  of 
the  ulcer  there  was  a  perforation  J  inch  in  diameter,  Avith  circular,  indurated,  thick 
outhnes  formed  by  the  rounded  edges.  On  the  serous  surface  the  perforation  was  so 
clean  that  it  seemed  to  have  been  punched  out  of  healthy  tissue.  The  remainder  of 
the  duodenum  was  absolutely  normal.  On  the  anterior  surface  of  the  stomach  the 
radiating  cicatrix  of  an  old  healed  ulcer  was  present. 

To  sum  up,  the  patient  succumbed  in  less  than  three  days  from  superacute  peri- 
tonitis, due  to  perforation  of  a  duodenal  ulcer  which  had  been  absolutely  latent. 

Analysis  of  the  Symptoms. — The  first  point  to  be  noticed  is  that  in 
the  very  great  majority  of  cases  the  ulcer  is  latent.  In  all  the  cases  men- 
tioned in  my  clinical  lecture  the  duodenal  ulcer  had  been  absolutely  latent. 
During  its  course  it  caused  neither  pain  nor  haemorrhage.  It  revealed 
itself,  suddenly,  by  perforation  in  healthy  persons,  who  had  never  felt  any 
symptom  pointing  to  the  presence  of  such  a  terrible  lesion.  It  is  by  perfora- 
tion, then,  that  duodenal  ulcer  generally  announces  itself.  The  perforation 
causes  the  sudden  agonizing  pain  which  I  have  named  the  peritoneal 
dagger-thrust.     All  the  cases  in  my  clinical  lectures  came  on  in  this  way. 

My  patient,  when  he  was  about  to  mount  guard  at  the  police-station,  was 
suddenly  seized  with  agonizing  pain  in  the  subhepatic  region.  Nothing  could  have 
been  more  sudden.  Dutil's  patient  was  taken  unawares  at  seven  o'clock  in  the  evening 
witli  such  intense  abdominal  pains  that  he  fell  groaning  to  the  ground.  He  succumbed 
in  eighteen  hours,  and  at  the  post-mortem  examination  a  perforating  duodenal  ulcer 
was  found.  Vermorel  and  Marie's  patient  was  also  in  a  state  of  perfect  health  when 
he  experienced,  without  the  slightest  warning,  terrible  pain  due  to  perforation.  He 
died  in  twenty-seven  hours,  and  at  the  post-mortem  examination  a  perforating  ulcer 
of  the  duodenum  was  found.  Brouardel's  patient  had  gone  to  bed  the  evening  before 
in  excellent  health,  when  he  was  awakened  suddenly  at  three  o'clock  in  the  morning 
with  most  acute  pain  between  the  hver  and  the  stomach.  He  died  in  twenty-eight 
hours,  and  at  the  autopsy  a  perforating  ulcer  was  found. 

Another  important  point  is  the  state  of  the  abdomen  after  the  perfora- 
tion during  the  first  stage  of  the  peritonitis.  We  are  generally  too  much 
imbued  with  the  idea  that  peritonitis  due  to  perforation  is  followed  by 
meteorism.  This  is  not  always  the  case,  and  it  is  wrong  to  exclude  perito- 
nitis because  the  abdomen  is  hard,  flat,  and  retracted.  We  may  see  patients 
suffering  from  duodenal  perforation  in  whom  the  peritonitis  at  first  causes 
such  contraction  of  the  abdominal  muscles  from  reflex  action  that  the 
stomach  is  flat,  hard,  and  retracted.  The  stomach  was  hard  and  flat  in 
the  cases  of  Letulle,  Banzet,  and  Lardennois.     The  stomach  was  likewise 


DISEASES  OF  THE  INTESTINE  811 

retracted  and  as  hard  as  a  board  when  Beausse  was  called  in  to  the 
patient  whose  history  I  have  just  given.  This  point  is  important.  Never- 
theless, the  two  conditions  may  follow  one  another  in  the  same  case.  A 
patient  whose  stomach  is  hard  and  flat  in  the  early  stage  of  peritonitis  may 
present  a  tympanitic  and  distended  abdomen  some  hours  later. 

The  discussion  which  I  entered  into  with  regard  to  the  diagnosis  of  per- 
foration of  a  gastric  ulcer  is  absolutely  applicable  to  the  diagnosis  of  duo- 
denal ulcer.  The  suddenness,  the  intensity  of  the  pain,  and  the  peritoneal 
dagger-thrust  are  as  much  the  appanage  of  perforation  of  a  duodenal  ulcer 
as  of  an  ulcer  of  the  stomach.  This  symptom,  when  well  established,  is 
sufficient  to  eliminate  hepatic  coUc,  intestinal  occlusion,  appendicitis,  and 
other  morbid  states  with  peritoneal  symptoms,  which  never  begin  with  such 
violent  and  sudden  pains. 

The  pain  of  hepatic  colic  and  of  duodenal  perforation  commences  in  the 
same  neighbourhood,  but  still  the  pain  of  hepatic  coUc  (even  when  it  is 
severe)  is  not  so  sudden  and  severe  as  the  pain  from  perforation  of  the 
duodenum.  Furthermore,  a  man  suffering  from  hepatic  coHc,  in  spite  of 
the  pain  and  vomiting,  has  never  at  the  end  of  an  hour  or  two  the  peritoneal 
look  of  one  who  has  a  duodenal  perforation  with  early  superacute  peritonitis. 
The  features  are  drawn,  the  complexion  is  of  an  earthy  pallor,  and  the 
abdomen  is  hard  and  retracted  from  the  defensive  contraction  of  the 
abdominal  muscles,  or  tympanitic  from  the  distension  of  the  paralyzed  coils 
of  the  bowel  and  the  passage  of  gas  into  the  peritoneal  cavity.  The  least 
touch  causes  the  most  acute  pains.  The  pulse  is  small  and  rapid,  and 
perhaps  the  patient  already  has  hiccough.  Nothmg  of  this  kind  is  seen  in 
hepatic  colic.  I  am  not  speaking  of  the  icteric  tinge  and  of  the  presence  of 
bile  in  the  urine,  for  these  signs,  common  in  hepatic  colic,  do  not  occur  early  ; 
they  supervene  when  the  diagnosis  should  have  already  been  made. 

The  knowledge  furnished  by  the  temperature  is  not  of  much  diagnostic 
value.  We  are  too  liable  to  think  that  hepatic  colic  is  apyretic,  and  that 
peritonitis  due  to  perforation  is  febrile.  This  is  quite  true  in  some  cases, 
but  the  converse  is  also  true.  Peritonitis  may  be  seen  without  a  rise  in 
temperature,  and,  on  the  other  hand,  hepatic  colic  may  be  accompanied  by 
violent  rigors  and  a  temperature  of  102°  or  103°  F.  I  shall  describe  later 
this  hepatalgic  fever,  to  make  use  of  Charcot's  expression,  which  is  a 
satellite  fever  in  the  migration  of  ])iliary  calculi,  and  must  not  be  confounded 
with  bilio-septic  fever.  I  refer  the  reader  to  the  section  on  Appendicitis 
for  the  diagnosis  between  appendicitis  and  perforating  ulcer  of  the  stomach. 

In  a  patient  suffering  from  tympanites,  with  pain,  vomiting,  and  stoppage 
of  fa3cal  matter  or  gas,  peritonitis  from  perforation  has  sometimes  been  taken 
for  intestinal  occlusion.  This  error,  I  think,  should  be  avoided,  because 
occlusion   never   commences   with    tlie    peritoneal    dagger-thrust.      The. 


812  TEXT-BOOK  OF  MEDICINE 

symptoms  are  gradual  and  progressive,  and  a  period  of  constipation  has 
preceded  the  symptoms  of  occlusion  by  several  days.  Nothing  of  the  kind 
occurs  in  perforation  of  the  duodenum. 

It  is  almost  impossible  to  say  whether  the  ulcer  is  seated  in  the  duodenum 
or  the  stomach  ;  it  can  only  be  localized  in  the  stomach  if  the  perforation 
has  been  preceded  by  the  classical  signs  of  ulcer,  and  even  then  there  may 
have  been  two  ulcers — one  in  the  stomach,  which  has  cicatrized,  and  the 
other  in  the  duodenum,  which  has  perforated.  This  topographical  diagnosis 
is  only  of  minor  importance,  since  the  same  operative  indications  are 
applicable  in  both  cases. 

The  suddenness  and  the  violence  of  the  pain,  the  intensity  and  generaliza- 
tion of  the  peritonitis  in  perforation  of  a  duodenal  or  gastric  ulcer,  depend 
on  the  dimensions  of  the  perforation  and  on  the  rigidity  of  the  tissues  which 
form  the  wall.  If  the  hole  is  large  and  gaping,  the  indurated  edges  have  no 
tendency  to  close  the  void,  as  flabby  tissues  might  do.  Chyme,  microbes, 
and  toxines  are  rapidly  discharged  into  the  peritoneum  in  considerable 
quantity.  In  this  respect  the  duodenal  perforation  seems  to  me  more  to 
be  feared  than  that  of  the  stomach,  for  the  toxi-infectious  matter  of  digestion 
may  pass  into  the  peritoneum  in  the  form  of  chyme  from  the  stomach  and 
in  the  form  of  fsecal  matter  from  the  intestine  by  antiperistaltic  movements. 
The  peritoneum  suffers  such  an  attack  that  the  peritonitis  becomes  general 
in  less  than  twenty  hours,  and  death  may  be  very  rapid. 

What  a  difference  from  the  peritonitis  following  the  small  perforations 
in  typhoid  fever,  which  may  be  so  small  that  at  the  post-mortem  examina- 
tion it  is  often  necessary  to  distend  the  intestine  with  water  in  order  to 
discover  the  breach  of  surface  ! 

Treatment.  —  Surgical  intervention  is  the  only  treatment  in  super- 
acute  peritonitis  consequent  on  perforation  of  a  duodenal  ulcer.  In  nine 
cases  published  in  the  Medical  News*  the  operation  was  followed  each  time 
by  death  ;  but  it  is  only  fair  to  say  that  all  these  patients  were  operated  on 
too  late.  The  case  of  cure  published  by  Landerer  and  Gliickmann  refers 
to  a  man  who  was  operated  on  twelve  hours  after  perforation.  The  con- 
clusion is  that  in  duodenal  perforation,  as  in  gastric  perforation,  it  is 
necessary  to  make  a  correct  diagnosis,  and  operate  at  once. 

I  have  just  spoken  of  cases  in  which  the  duodenal  ulcer  perforates  ;  in 
some  cases  it  cicatrizes,  like  ulcer  of  the  stomach.  The  cicatrix  may,  how- 
ever, cause  constriction  of  the  pylorus,  followed  by  dilatation  of  the  stomach, 
and  occlusion  of  the  bile-duct,  with  chronic  icterus  or  thrombosis  of  the 
portal  vein. 

*  The  Medical  News,  1895.  p.  460. 


DISEASES  OF  THE  INTESTINE  813 


X.  CANCER  OF  THE  INTESTINE. 

Cancer  of  the  intestine  ranks  next  to  cancer  of  the  stomach,  Hver,  and 
breast.     It  has  this  special  feature — that  it  is  fairly  common  in  adults. 

Pathological  Anatomy. — The  various  parts  of  the  intestine  invaded 
by  cancer  are,  in  order  of  frequency,  the  rectum,  sigmoid  flexure,  colon, 
caecum,  and  small  intestine,  or,  in  other  words,  cancer  becomes  less  common 
as  we  approach  the  upper  portion  of  the  intestine.  Cancer  of  the  bowel 
may  be  primary  or  secondary  to  cancer  of  the  stomach  or  uterus.  The 
following  varieties  are  found  :  cyhndrical  epithelioma,  encephaloid  and 
scirrhous.  It  may  arise  in  the  glandular  epithelium  of  the  mucous  mem- 
brane or  in  the  submucous  layer  ;  it  shows  itself  in  the  shape  of  a  patch, 
nodule,  or  ring.  The  patches  sometimes  convert  a  segment  of  the  in- 
testine into  a  rigid  tube,  and  the  rings  constrict  the  lumen,  so  that  a  goose- 
quUl  can  scarcely  be  passed  through  them.  The  internal  surface  of  the 
cancer  is  either  fungous,  ulcerated  and  bleeding,  or  hard  and  scirrhous. 
The  intestine  above  the  constricted  point  generally  shows  a  dilatation 
which  may  be  large  ;  the  muscular  layers  are  much  thickened  in  some  cases. 
Extension  to  the  peritoneum  and  mesenteric  glands  is  a  frequent  comphca- 
tion,  and  is  generally  associated  with  serous  or  hgemorrhagic  effusion  into 
the  peritoneum.  Perforations  of  the  intestine  and  communications  with 
the  neighbouring  organs  are  rarer  complications. 

Symptoms. — Intestinal  cancer  generally  rmis  the  following  course  : 
The  onset  is  insidious,  and  for  several  weeks  or  months  the  patient  experi- 
ences only  more  or  less  sharp  pains,  which  may  be  fixed  or  movable.  The 
digestive  functions  are  interfered  with.  Constipation  is  the  rule,  but  the 
evacuation  of  a  large  quantity  of  more  or  less  liquid  matter  often  alternates 
with  constipation.  If  the  growth  occupies  the  lower  portion  of  the  large 
intestine,  and  causes  appreciable  constriction,  the  motions  are  ribbon-like. 
Melsena  is  a  frequent  symptom,  and  the  blood  voided  in  the  stools  keeps 
its  red  colour  if  the  lesion  occupies  the  lower  part  of  the  intestine,  or  if  the 
htcmorrhage  is  abundant  and  rapidly  rejected.  The  blood  is  tarry  if  it  has 
remained  in  the  intestine  in  contact  with  the  excreta.  The  abdomen  is 
often  ballooned,  and  this  condition  is  unfavourable  to  the  search  for  a 
cancerous  tumour.  In  malignant  stricture  we  may  see  attacks  of  pain  in 
which  the  intestinal  coils  stand  out  in  rehef  and  are  visible  beneath  the 
abdominal  walls. 

The  growth  is  not  always  accessible  to  abdominal  palpation.  If  the 
patient  has  grown  thin,  or  if  the  abdomen  is  retracted,  the  tumour  can  be 
made  out,  and  is  generally  found  to  be  mobile  ;  if  the  stomach  is  distended, 
or  if  peritoneal  effusion  is  present,  the  tumour  may  be  difficult  to  find. 


814  TEXT-BOOK  OF  MEDICINE 

The  general  symptoms,  as  in  every  case  of  cancer,  are  progressive  anaemia 
and  gradual  loss  of  flesh.  The  pale  colour  of  the  skin  is  followed  by  the 
yellow  tint  of  cancer,  the  distaste  for  food  increases  daily,  emaciation  be- 
comes extreme,  and  cachexia,  with  oedema  and  dropsy,  ushers  in  the  end. 
Death  supervenes  from  cachexia  (dropsy,  thrush,  or  diarrhoea),  or  in 
consequence  of  some  complication  (peritonitis,  intestinal  obstruction,  per- 
foration, or  haemorrhage). 

Such  is  the  general  course  of  intestinal  cancer,  but  the  exceptions  are 
numerous.  The  development  of  cancer  is  latent  in  some  cases,  and  symp- 
toms of  obstruction  suddenly  appear  during  apparent  good  health.  The 
sudden  onset  of  the  complications  leads  us  to  think  of  some  'other  lesion. 
Laparotomy  reveals  a  cancerous  stricture  of  the  intestine.  In  other  cases 
before  the  cancer  of  the  intestine  has  caused  general  symptoms,  chronic 
peritonitis  with  effusion  shows  itself,  and  we  naturally  think  of  ascites 
due  to  disease  of  the  peritoneum  or  liver.  Abdominal  puncture,  however, 
3delds  blood-stained  fluid.  Palpation,  made  easier  by  the  withdrawal  of 
the  liquid,  shows  the  condition  of  the  peritoneum  and  of  the  intestine 
(cancerous  peritonitis),  although  the  diagnosis  was  impossible  prior  to  the 
evacuation  of  the  liquid. 

Cancer  of  the  rectum  belongs  rather  to  surgery  than  to  medicine, 
and  if  some  mistakes  are  made,  it  is  because  digital  examination  of  the 
rectum  is  too  often  neglected.  It  is  only  by  such  an  examination  that  we 
can  ascertain  the  existence  and  the  site  of  rectal  cancer. 

Diagnosis. — The  diagnosis  of  intestinal  cancer  is  easy  when  its  course 
is  classical.  The  abdominal  pains,  the  alternate  constipation  and  diarrhoea, 
the  presence  of  a  tumour,  and  the  invading  cachexia,  leave  no  room  for 
error.  The  diagnosis  is  more  difficult  when  the  lesion  is  masked  by  compli- 
cations (cancerous  peritonitis,  ascites)  which  accompany  or  hide  the  primary 
mischief. 

Treatment. — The  treatment  of  intestinal  cancer  is  purely  palliative. 
The  most  common  remedies  are  laxatives  or  purgatives  and  injections  of 
morphia  when  the  pains  are  severe.  In  cancer  of  the  rectum  surgical  inter- 
vention is  sometimes  useful. 


XI.  INTESTINAL  OCCLUSION. 

Definition. — The  names  ileus,  volvulus,  iliac  passion,  or  miserere  colic,  were  employed 
to  describe  a  morbid  condition  characterized  by  absolute  constipation,  ballooning 
of  the  stomach,  uncontrollable  vomiting,  and  severe  pains.  This  disease  was  for  a 
long  time  considered  to  result  from  spasm  of  the  intestine.  Later  it  received  the 
name  of  intestinal  strangulation.  This  name  is  wrong,  since  it  only  states  a  part  of  the 
question,  and  therefore  the  name  intestinal  occlusion  (O.  Massan)  is  to  be  preferred, 
as  it  has  the  advantage  of  being  applicable  to  all  cases  of  obliteration  of  the  intestine. 


DISEASES  OF  THE  INTESTINE  815 

etiology. — The  various  causes  of  intestinal  occlusion  are  as  follows 
(Jaccoud) : 

1.  Occlusion  by  Constriction. — The  constriction  of  the  intestine  may 
be  due  to  compression  by  a  neighbouring  tumour,  such  as  a  cystic  or  can- 
cerous tumour  of  the  peritoneum,  ovaries,  or  mesenteric  glands,  uterine 
fibroids,  and  aneurism  of  the  abdominal  aorta.  The  constriction  may  be 
due  to  changes  in  the  intestinal  walls  (cancer  or  polypus),  or  to  cicatrices 
caused  by  the  ulcerations  of  dysentery  and  tuberculosis.  Syphilis  usually 
produces  stricture  of  the  rectum.  Cancerous  strictures  of  the  small  intestine 
are  very  rare.  In  72  out  of  108  cases  the  trouble  was  seated  in  the 
sigmoid  flexure  and  rectum  (Bulteau).  Occlusion  consequent  on  spasmodic 
stricture  of  the  intestine  has  become  rare  since  the  other  causes  of  occlusion 
have  been  better  known.  It  does,  however,  exist,  and  I  have  seen  two 
cases. 

2.  Occlusion  by  Strangulation. — This  form  is  frequent.  It  is  analogous 
to  the  strangulation  of  hernia.  The  intestine  becomes  engaged  in  an 
abnormal  orifice  of  the  mesentery  or  omentum,  or  in  the  foramen  of  Winslow. 
At  other  times  the  strangulation  of  the  intestine  is  brought  about  by  a  band 
stretching  from  one  intestinal  coil  to  another ;  from  the  bowel  to  the  abdo- 
minal wall,  the  mesentery,  or  the  uterus  ;  from  the  omentum  to  the  peri- 
toneum ;  from  the  appendix  to  an  intestinal  coil ;  or  from  an  intestinal 
diverticulum  to  the  wall  of  the  abdomen.  Meckel's  diverticulum,  which  is 
adjacent  to  the  termination  of  the  small  intestine,  and  is  considered  to  be 
the  remnant  of  the  omphalo-mesenteric  duct,  may  attain  such  a  length  that 
it  forms  knots  around  the  intestine.  In  these  different  varieties  the  strangu- 
lation almost  always  occurs  at  the  end  of  the  ileum.  In  151  cases  collected 
by  Bulteau  the  strangulation  was  seated  133  times  in  the  small  intestine, 
and  only  18  times  in  the  large  intestine. 

3.  Occlusion  by  Volvulus. — Volvulus  results  from  twisting  of  the  in- 
testine. The  laxity  of  the  mesentery  favours  twisting  of  the  cajcum  and  of 
the  sigmoid  flexure.  The  small  intestine  is  strangulated  round  the  mesen- 
tery, which  serves  as  an  axis.  Sometimes  there  is  simply  bending,  and  the 
intestinal  coil  forms  a  kink. 

•1.  Occlusion  by  Invagination.  —  By  invagination  is  understood  the 
entrance  of  one  portion  of  the  intestine  into  another  portion.  In  most  cases 
the  upper  portion  enters  the  lower  portion.  The  canal  of  the  invaginated 
segment  is  constricted,  and  the  new  wall  is  formed  of  the  tliree  layers  of 
intestine.  The  mesentery,  which  has  followed  the  invaginated  portion,  is 
found  Ijetween  the  middle  and  the  internal  layer.  If  the  invagination  is 
not  followed  by  strangulation,  it  may  persist  in  the  chronic  state,  and  the 
intestinal  occlusion  is  incomplete.  The  complications  of  strangulation  which 
accompany  invagination  are  due  to  the  action  of  the  invaginating  segment, 


816  TEXT-BOOK  OF  MEDICINE 

which  acts  Kke  a  ring  as  regards  the  invaginated  segment,  and  it  is  probable 
that  the  mesentery  which  pulls  on  the  invaginated  cylinder  has  some  share 
in  the  phenomenon  of  occlusion. 

The  invaginated  portion  is  compressed  by  the  ensheathing  portion,  and 
becomes  congested,  swollen,  and  inflamed.  The  serous  layers  become 
adherent,  and  the  inflammatory  process  causes  one  of  the  following  ter- 
minations :  (1)  The  inflammation  and  the  acute  symptoms  may  disappear, 
and  give  place  to  a  chronic  invagination,  which  narrows  the  lumen  of  the 
intestine,  and  gives  rise  to  further  troubles.  (2)  The  invaginated  cylinder 
becomes  gangrenous,  and  is  passed  per  rectum,  whilst  the  adhesions  of  the 
walls  prevent  perforation,  and  render  recovery  possible.  (3)  Partial  sub- 
acute peritonitis  may  occur  around  the  intestinal  segment  which  is  the  seat 
of  the  invagination  ;  perforation  may  cause  fatal  peritonitis. 

With  regard  to  the  seat  of  the  invagination,  out  of  a  total  of  763  cases 
392  have  been  found  to  be  ileo-csecal ;  220  were  invaginations  of  the 
small  intestine,  and  151  of  the  large  intestine.  In  children  in- 
vagination is  practically  the  sole  cause  of  intestinal  occlusion.  The 
length  of  the  invaginated  cyHnder  is  very  variable.  It  attains  large 
dimensions  in  the  large  intestine.  A  second  intestinal  segment  often  enters 
the  invaginated  cylinder,  and  a  third  segment  has  even  been  known  to  enter 
the  other  two, 

5.  Occlusion  by  Obstruction. — The  accumulation  of  faecal  matter 
in  the  caecum  or  large  intestine,  intestinal  concretions  (enterohths),  gall- 
stones, round  worms,  and  foreign  bodies  introduced  into  the  rectum  (Ver- 
neuil),  may  cause  intestinal  occlusion. 

6.  Occlusion  by  Pseudo-Strangulation. — The  stoppage  of  faecal  matter 
from  intestinal  paralysis  occurs  in  peritonitis  and  appendicitis.  In 
some  cases  the  patient  has  all  the  symptoms  of  intestinal  occlusion.  An 
operation  fails  to  reveal  the  obstruction.  Has  the  occlusion  its  origin  in  a 
paralysis  of  the  intestine  ?  Is  this  paralytic  condition  accompanied  by 
kinking  of  the  intestine  ?     These  facts  are  not  completely  elucidated. 

Symptoms. — The  onset  shows  many  variations.  In  some  cases  the 
occlusion  comes  on  suddenly,  in  the  absence  of  any  apparent  cause,  with 
sharp  pain,  which  spreads  over  the  abdomen.  Nausea,  hiccough,  and 
vomiting  of  food  and  bile  then  appear.  In  the  next  few  days  the  vomit 
becomes  faecal.  The  abdomen  is  at  first  retracted,  but  soon  becomes  dis- 
tended, and  the  intestinal  coils  stand  out  in  more  or  less  relief.  The  patient 
passes  neither  faeces  nor  gas.  The  loss  of  strength  is  rapid,  the  tempera- 
ture falls,  the  general  symptoms  grow  worse,  the  pulse  becomes  small  and 
irregular,  and  death  may  supervene  in  three  or  four  days.  This  variety, 
which  somewhat  resembles  strangulated  hernia  or  acute  peritonitis,  is  not 
the  most  frequent  one.     We  shall  study  it  later  under  Tubercular  Peri- 


DISEASES  OF  THE  INTESTINE  817 

tonitis.     It  is,  indeed,  often  the  first  index  of  a  tubercular  peritonitis  which 
has  previously  been  latent. 

In  the  great  majority  of  cases  the  symptoms  of  intestinal  occlusion  come 
on  more  slowly.  The  pain  is  neither  so  sudden  nor  so  intense  as  in  the  pre- 
ceding case.  It  is  sometimes  Hmited  to  the  diseased  region  ;  at  other  times 
it  radiates  in  various  directions.  Constipation  is  not  absolute  till  the 
second  or  third  day,  when  the  patient  has  emptied  the  lower  end  of  the 
intestine.  From  this  moment,  if  the  occlusion  is  complete,  the  patient 
passes  neither  fseces  nor  flatus,  though  he  may  void  a  little  mucus.  The 
passage  of  blood  or  shreds  (detritus  of  the  mucous  membrane)  indicates 
sloughing  in  the  case  of  invagination. 

The  vomit,  which  at  first  consists  of  food,  mucus,  and  bile,  becomes 
faecal  about  the  third  or  fourth  day,  or  later.  It  is  quite  liquid,  because  it 
is  mixed  with  the  fluid  swallowed  by  the  patient,  and  is  composed  of  the 
matter  which  is  contained  in  the  upper  part  of  the  intestine,  and  has  re- 
gurgitated into  the  stomach  by  the  antiperistalsis.  After  the  onset  of 
occlusion  the  stomach  becomes  distended,  the  meteorism  grows  excessive, 
and  in  some  cases,  especially  during  the  paroxysms  of  pain,  the  intestinal 
coils  stand  out  in  relief  around  the  umbihcus  or  in  the  flanks.  The  urine  is 
scanty,  especially  if  the  obstacle  is  seated  near  the  stomach  (Barlow),  while 
the  thirst  is  great,  and  the  ingestion  t)f  the  smallest  quantity  of  liquid  pro- 
vokes vomiting.  Prostration  and  loss  of  strength  are  early  symptoms.  The 
pulse  is  small  and  rapid  ;  the  face  is  pale,  thin,  and  drawn ;  the  skin  is  cold 
and  wrinkled  ;  the  voice  is  reduced  to  a  whisper. 

Several  terminations  are  possible.  In  the  happiest,  but  the  rarest,  cases 
the  faecal  vomiting  ceases,  and  the  patient  passes  flatus  and  faeces  fer 
rectum.  The  motions  are  passed  freely.  In  other  cases  the  acute  symptoms 
of  occlusion  disappear,  but  are  then  followed  by  symptoms  of  chronic 
invagination,  which  constitute  a  permanent  danger.  Perforation  and  acute 
peritonitis  in  the  course  of  intestinal  invagination  are  rapidly  fatal ;  but 
this  is  not  the  manner  in  which  death  usually  supervenes.  The  acute 
symptoms  of  the  onset  improve,  the  pain  in  the  abdomen  is  not  so  severe, 
and  we  are  almost  tempted  to  speak  of  improvement ;  but  the  patient  grows 
cold,  the  voice  sinks  to  a  whisper,  the  pulse  becomes  irregular  and 
imperceptible,  dyspnoea,  hiccough,  and  muscular  spasms  appear,  the 
extremities  become  Uvid,  and  death  occurs  on  the  tenth  or  twelfth  day — 
not  from  peritonitis,  but  from  the  auto-intOxication  which  Gubler 
has  called  peritonism.  Its  origin  lies  in  the  abdominal  sympathetic 
nerves. 

Diagnosis.  —  In  order  not  to  confound  intestinal  occlusion  with 
strangulated  hernia,  the  usual  sites  of  liernia  must  be  examined.  Intes- 
tinal occlusion  must  not  be  mistaken  for  peritonitis  from  perforation  of 

52 


818  TEXT-BOOK  OF  MEDICINE 

simple  ulcer  of  the  stomach  and  duodenum.  This  question  has  already 
been  discussed.  Appendicitis  is  sometimes  accompanied  by  marked 
tympanites  and  arrest  of  flatus.  The  reader  will  find  this  point  discussed 
under  Appendicitis.  Intestinal  occlusion  must  not  be  confounded  with 
lead  colic  or  with  acute  intoxication.  Obstruction  in  the  rectum  will  be 
recognized  by  digital  examination. 

The  cause  of  the  occlusion  is  often  obscure.  The  mode  of  onset  is  not 
enough.  It  has  been  said  that  acute  symptoms  occur,  especially  in  strangu- 
lation or  volvulus,  and  that  gradually  increasing  symptoms  are  due  to  the 
compression  of  the  intestine  or  to  the  growth  of  a  tumour  in  the  walls,  etc. 
These  assertions  are  not  always  true,  and  it  is  not  rare  to  see  symptoms 
appear  with  all  the  suddenness  of  strangulation  when  the  obstruction  is  really 
secondary  to  cancer  of  the  intestine. 

The  diagnosis  of  the  cause  is,  however,  possible,  in  certain  cases.  If  the 
occlusion  occurs  in  a  patient  who  has  been  suffering  from  alternate  diar- 
rhoea and  constipation,  melsena,  and  loss  of  flesh,  intestinal  cancer  will  be 
thought  of,  even  though  a  tumour  is  not  appreciable  on  digital  exammation 
of  the  rectum  or  on  abdominal  palpation.  If  the  occlusion  comes  on  sud- 
denly during  good  health,  with  sharp  pain,  vomiting,  which  rapidly  becomes 
faecal,  and  absolute  constipation  :  internal  strangulation  or  volvulus  may  be 
inferred.  If  the  onset  is  less  sudden,  the  pain  is  less  severe,  the  fsecal 
vomiting  occurs  later,  while  the  constipation  does  not  set  in  early,  and  a 
doughy  mass  can  be  felt  in  one  part  of  the  abdomen  ;  it  is  probable  that  the 
case  is  one  of  invagination.  If  the  symptoms  of  occlusion  have  been  pre- 
ceded by  obstinate  constipation,  and  if  palpation  reveals  a  painless,  soft, 
and  pasty  mass  in  the  region  of  the  caecum  or  the  sigmoid  flexure ;  a  faecal 
accumulation  is  present. 

Recognition  of  the  site  of  the  lesion  is  also  difficult.  Digital  examination 
'per  vaginam  and  per  rectum  must  always  be  carried  out,  the  finger  being 
pushed  up  as  high  as  possible  into  the  rectum,  for  we  may  thus  discover  a 
cicatricial  etenosis,  cancer,  faecal  accumulation,  or  invagination  in  this 
region.  The  initial  seat  of  the  pain  is  a  valuable  but  uncertain  sign.  The 
absence  of  faecal  vomiting  would  prove  that  the  intestine  is  obHterated  high 
up,  probably  in  the  duodenum.  Ballooning  of  the  belly,  more  pronounced 
at  the  centre  of  the  abdomen  than  at  the  sides,  would  indicate  that  the 
obstacle  is  in  the  small  intestine.  Early  meteorism  over  the  whole  of  the 
abdomen  is  in  favour  of  obstruction  in  the  large  intestine.  An  early  onset 
and  severity  of  the  general  symptoms  point  to  a  lesion  of  the  small  intestine, 
which  is  so  rich  in  nerve  plexuses. 

The  prognosis  of  intestinal  occlusion  is  always  formidable,  even  when 
the  symptoms  are  shght  and  the  obstructioii  is  incomplete.  In  faecal 
accumulation  the  prognosis  is  good,  because  it  generally  yields  to  treatment. 


DISEASES  OF  THE  INTESTINE  819 

The  other  varieties — invagination,  volvulus,  and  especially  strangulation — 
are  very  grave. 

Treatment. — The  means  employed  in  intestinal  occlusion  are  medical 
and  surgical.  Purgatives  give  good  results  when  the  occlusion  is  due  to  a 
mass  of  faeces  or  intestinal  paresis  ;  in  other  circumstances  they  are  more 
harmful  than  useful.  They  must,  therefore,  be  used  with  great  care  in 
occlusion,  and  their  use  must  not  be  unduly  prolonged. 

Purgative  enemata  of  sulphate  of  soda,  syrup  of  buckthorn,  infusion  of 
senna,  and  enemata  containing  60  grains  of  bicarbonate  of  soda  and  30  grains 
of  tartaric  acid  in  each  enema,  and  repeated  three  or  four  times  during 
the  day,  have  given  good  results.  Large  injections  (Cantani),  given  with  a 
douche-can  and  high  rectal-tube,  are  of  service. 

Electricity  (continuous  currents  are  employed  to-day)  has  several  times 
been  successful  (Lacaille),  when  employed  prior  to  any  inflammatory  com- 
plications. 

Valuable  time,  however,  is  often  lost  by  medical  treatment,  and  surgical 
intervention  is  needed  in  the  majority  of  cases. 

XII.  CANCER  OF  VATER'S  AMPULLA. 

Discussion. — Ou  account  of  its  topography  and  symptomj,  cancer  of  Vater's  ampulla 
deserves  special  mention.  In  1890  Busson  had  collected  a  dozen  cases.  New  cases 
have  since  been  published. 

As  the  name  implies,  the  growth  affects  the  ampulla  of  Vater,  where  the  ducts  of 
the  liver  and  pancreas  open  into  the  gut.  Does  the  cancer  arise  in  the  intestine, 
the  common  bile-duct,  or  the  pancreatic  duct  ?  In  other  words,  is  it  an  intestinal, 
biUary,  or  pancreatic  cancer  ?  According  to  Rendu,  it  is  intestinal ;  according  to  Hanot, 
pancreatico-biUary ;  according  to  Bard,  pancreatic ;  and  according  to  Durand-Fardel, 
biliary. 

In  a  recent  case  pubhshed  by  Dorainici  a  primary  epithehoraa  developed  at  the 
expense  of  the  biliary  and  pancreatic  ducts.  It  must  be  distinguished  from  cancer  of 
the  head  of  the  pancreas  (alveolar  cancer)  commencing  in  the  pancreatic  acini. 

Pathological  Anatomy. — Primary  cancer  of  Vater's  ampulla  may  form 
a  plaque,  or,  more  frequently,  a  mushroom-like  growth  of  the  size  of  a 
hazel-nut  or  a  walnut.  The  tumour  projects  into  the  cavity  of  the  duo- 
denum. It  is  whitish,  fairly  soft,  and  rarely  ulcerates.  The  orifices  of  the 
common  bile  and  pancreatic  ducts  terminate  in  the  tumour,  which  obliterates 
them  more  or  less  completely.  In  some  cases  the  orifice  of  the  pancreatic 
or  of  the  common  bile-duct  may  be  found  in  the  cancerous  vegetation.  The 
mass  may  absorb  the  orifice  of  the  bile-duct  and  grow  into  the  opening  of  this 
canal,  as  if  the  cancer  had  commenced  in  the  orifice  of  the  duct  and  had 
then  invaded  the  ampulla  (Durand-Fardel's  case).  When  the  o})oiiing  of 
the  common  duct  is  obUterated,  this  duct,  as  well  as  the  cystic  and  hepatic 
ducts  and  the  gall-bladder,  may  be  much  dilated. 

52- -2 


820  TEXT-BOOK  OF  MEDICINE 

Cancer  of  Vater's  ampulla  is  almost  always  a  cylindrical  epithelioma, 
It  is  limited  to  the  ampulla,  and  has  no  tendency  to  become  general.  It  does 
not  invade  the  pancreas  or  the  liver,  though  it  may  cause  adenitis  in  the 
pancreatic  and  mesenteric  glands. 

The  pancreas  shows  no  cancerous  lesion.  It  is  sometimes  normal, 
sometimes  enlarged. 

The  liver  is  not  invaded  by  the  growth.  It  is  enlarged,  infiltrated  with 
biliary  pigment,  and  often  the  seat  of  incipient  fibrosis  of  the  portal  system 
(Hanot).  The  gall-bladder  is  often  distended  and  full  of  bile,  but  the  re- 
markable fact  is  that  it  very  rarely  contains  gall-stones  (once  in  fifteen 
cases).  This  finding  may  well  be  compared  with  their  extreme  frequency  in 
primary  cancer  of  the  biliary  passages.     The  spleen  is  often  enlarged. 

Summary.  —  Whether  the  growth  begins  in  the  pancreatico-biliary 
orifice  (orificial  cancer)  or  in  the  intestinal  mucous  membrane  of  the  ampulla, 
it  is  none  the  less  true  that  it  behaves  "  like  the  patches  of  intestinal  epi- 
theHoma  met  with  at  the  ileo-ceecal  valve  or  in  the  sigmoid  flexure.  It  has 
the  same  superficial  disposition  and  the  same  slow  course,  with  but  little 
tendency  to  ulcerate,  to  become  general,  or  to  spread  to  the  adjacent 
glands  "  (Rendu). 

Symptoms. — The  small  cancer  of  Vater's  ampulla  betrays  [its  presence 
by  jaundice.  It  may,  indeed,  be  said  that  jaundice  is  the  first  apparent 
symptom.  The  jaundice  is  due  to  the  obstruction  of  the  common  duct  by 
the  tumour,  and  has  therefore  the  characteristics  of  jaundice  from  obstruc- 
tion— colour  changing  from  yellow  to  olive-green,  bile-pigment  in  the 
urine,  and  colourless  faeces.  As  the  jaundice  is  not  always  continuous,  the 
skin  resumes  its  natural  colour,  and  the  faeces  become  coloured.  The 
intermittent  character  of  the  jaundice  proves  that  the  orifice  of  the  common 
duct  regains  its  permeability — for  a  time,  at  least.  Itching,  which  troubles 
the  patient  day  and  night,  is  sometimes  present.  Pigmented  spots  and 
xanthelasma  have  been  noticed. 

Pain,  either  spontaneous  or  provoked,  is  a  rare  symptom,  but  it  has  been 
noticed  in  some  cases.  Rendu's  patient  had  sharp  pain  in  the  right  hypo- 
chondrium  and  epigastrium.  Palpation  was  very  painful  in  the  pit  of  the 
stomach  over  the  left  lobe  of  the  Hver,  so  that  it  was  a  question  whether  the 
patient  was  not  suffering  from  a  stone  in  the  common  duct. 

Vomiting  of  food  is  a  fairly  frequent  symptom.  Diarrhoea  usually 
appears  late.     It  may  alternate  with  constipation. 

On  examining  the  patient,  the  Hver  is  found  to  be  enlarged.  The  gall- 
bladder is  often  much  distended,  and  can  be  felt  through  the  abdominal 
wall. 

Some  months  after  the  onset  of  the  disease  general  symptoms  appear. 
The  appetite  disappears,  and  the  patient  becomes  cachectic.     In  one  case 


DISEASES  OF  THE  INTESTINE  821 

fever  supervenes ;  in  another  intestinal  haemorrhage  appears.  (Edema  sets 
in,  and  is  sometimes  confined  to  the  right  side.  Finally,  after  a  period  which 
varies  from  six  to  eighteen  months,  the  patient  succumbs  from  cachexia,  or 
is  carried  off  by  some  complication. 

Diagnosis. — The  diagnosis  of  cancer  of  Vater's  ampulla  sometimes 
presents  insurmountable  difficulties.  On  what  signs  are  we  to  rely  ? 
Jaundice,  which  is  the  first  and  principal  symptom,  is  also  present  in  a 
number  of  conditions.  It  matters  little  whether  the  common  bile-duct  is 
compressed  or  obUterated  by  a  cancer  of  the  head  of  the  pancreas,  of  the 
bihary  passages,  or  of  Vater's  ampulla,  by  one  or  several  calculi,  or  by  the 
swelling  of  the  wails  which  occurs  in  catarrhal  icterus.  In  all  these  cases 
jaundice  and  its  symptom-complex  (bile  in  the  urine,  colourless  stools, 
enlarged  liver,  etc.)  may  be  the  only  symptom  for  weeks  or  months.  It  will 
be  objected,  no  doubt,  that  in  a  case  of  cancer  of  Vater's  ampulla  the  jaun- 
dice and  the  decoloration  of  the  stools  are  at  times  intermittent ;  but 
intermission  is  likewise  seen  in  calculus  of  the  common  duct  and  in  pro- 
longed catarrhal  icterus.  Cases  have  been  seen,  and  I  myself  have  published 
some,  in  which  this  same  phenomenon — viz.,  reappearance  of  bile  in  the 
stools  and  momentary  suspension  of  jaundice — was  present  in  cancer  of  the 
head  of  the  pancreas.  This  feature,  therefore,  is  not  special  to  cancer  of 
Vater's  ampulla. 

On  the  other  hand,  it  will  be  said  that  spontaneous  or  provoked  pain  is 
particularly  the  result  of  stones  in  the  common  duct ;  but  I  would  point  out 
that  primary  cancer  of  the  biliary  passages  and  cancer  of  Vater's  ampulla  are 
also  accompanied  by  similar  pain,  as  in  Rendu' s  case.  Diarrhoea  is  said  to 
be  an  important  symptom,  but  in  reality  it  has  no  more  value  than  the 
preceding  ones  in  the  diagnosis  of  cancer  of  Vater's  ampulla,  and  most 
frequently,  it  must  be  admitted,  the  diagnosis  is  founded  on  conjectures. 
I  have  nothing  to  say  on  the  subject  of  treatment,  unless  it  be  to  suggest 
surgical  intervention. 


XIII.  DYSENTERY. 

etiology.  —  Dysentery  has  every  appearance  of  being  a  microbic 
disease.  Two  forms  are  seen — amoebic  dysentery,  due  to  a  protozoon, 
and  bacillary  dysentery,  due  to  a  bacillus. 

The  latter  occurs  in  temperate  zones,  and  is  common  in  France,  but  it 
is  also  found  in  tropical  countries  in  conjunction  with  the  amoebic  form. 
The  amoebic  form  is  scarcely  ever  seen  in  temperate  climates,  but  is  met  with 
in  tropical  lands.     It  may  or  may  not  l)e  associated  with  the  bacillary  form. 

Although  the  organisms  are  different  in  the  two  forms,  tiie  symptoms 
are  alike  in  both  cases. 


822  TEXT-BOOK  OF  MEDICINE 

Dysentery  is  sporadic,  endemic  or  epidemic,  and  acute  or  chronic,  and 
its  character  differs  according  to  the  variety. 

Sporadic  dysentery  breaks  out  during  the  great  heat  of  summer,  and 
disappears  towards  the  end  of  the  autumn.  It  has  been  asserted  that  bad 
water,  cold  drinks,  and  green  fruit  favour  its  development. 

Endemic  dysentery  occurs  in  Senegal,  Cochin-China,  Mexico,  the  West 
Indies,  India,  Algeria,  etc.  Are  the  climatic  conditions  and  the  excessive 
heat  of  these  countries  setiological  factors  ?  They  are,  doubtless,  important, 
but  they  are  not  the  sole  factor.  Are  the  conditions  of  the  soil  and  malaria 
causative  ?  And  are  we  to  say,  with  Cambay  and  Dutrouleau,  that  dysentery, 
hke  hepatitis  and  swamp  fever,  is  a  manifestation  of  paludal  intoxication  ? 
The  answer  is  that  in  certain  countries  where  malaria  is  endemic,  dysentery 
is  unknown  or  exceptional.  Thus,  Guadeloupe  and  Pointe-a-Pitre  are  deci- 
mated with  marsh  fever,  while  dysentery  is  fairly  rare  ;  and  the  same  may 
be  said  of  the  Departements  of  Aunis  and  of  Saintonge.  The  final  argument 
is  that  each  of  these  diseases  possesses  its  specific  microbe. 

Epidemic  dysentery  is  favoured  by  the  eetiological  conditions  of  the  two 
preceding  varieties,  but  as  special  causes  of  the  epidemic,  writers  have 
cited  overcrowding,  famine,  bad  water,  and  defective  hygienic  conditions, 
such  as  are  observed  with  armies  in  the  field  or  in  besieged  towns,  etc. 
"  But,"  says  Trousseau,  "  these  are  only  occasional  causes.  Something  else 
is  required  independent  of  them,  and^is  something,  which  we  know  only 
through  its  effects,  we  call  the  epidemic  constitution."  The  discovery  of 
the  micro-organisms  of  dysentery  has  confirmed  the  far-seeing  observations  of 
Trousseau. 

Dysentery  is  contagious.  This  fact  is  well  proved,  and  the  contagion 
is  probably  due  to  the  dejecta.  Water  seems  to  play  a  considerable  part  in 
the  dissemination  of  dysentery.  This  fact  has  been  clearly  proved  by  the 
medical  officers  with  our  troops  in  Cochin-China. 

Pathological  Anatomy. — The  chief  lesion  is  an  ulcerative  inflammation 
of  the  large  intestine.  The  ulcers  are  found  in  the  rectum  and  sigmoid 
flexure.  They  present  different  degrees,  according  as  the  dysentery  is 
shght  or  severe,  but  in  the  main  they  are  quite  analogous.  We  must  first 
consider  briefly  the  structure  of  the  large  intestine. 

The  large  intestine  is  composed  of  several  coats,  which  are,  from  within  outwards, 
serous  coat,  formed  of  fiat  cells  and  connective  tissue  ;  next  two  layers  of  smooth 
muscles,  the  one  longitudinal  and  the  other  circular  ;  and,  lastly,  an  internal  or  mucous 
coat.  The  two  last-named  coats  present  the  following  pecuharities  :  The  superficial 
portion  of  the  mucous  membrane  is  composed  of  tubular  glands,  analogous  to  Lieber- 
iiiihn's  glands  in  the  small  intestine,  but  somewhat  longer.  These  glands  are  united 
by  a  veiy  fine  fibro-vascular  framework,  and  their  cyUnch-ical  epitliehum  is  continuous 
with  that  of  the  mucosa.  Next  to  this  glandular  layer  we  find  smooth  muscular  fibres 
and  connective  tissue,  which  is  more  hke  ordinary  connective  tissue  than  the  reticu- 


DISEASES  OF  THE  INTESTINE  823 

lated  tissue  of  the  small  intestine.  The  closed  follicles  in  this  cellular  coat  are  less 
numerous  but  larger  than  those  of  the  small  intestine.  The  cellular  coat  is  traversed 
by  large  vascular  branches,  which  form  a  compact  plexus  (Doellinger's  vascular  mem- 
brane) at  the  inner  limit  of  the  cellular  coat,  whence  the  perpendicular  branches  arise, 
and  ramify  between  the  tubular  glands.  The  lymphatics  are  much  less  abundant  than 
in  the  small  intestine. 

1.  Benign  Dysentery.— The  lesions  attack  the  rectam  and  the  sig- 
moid flexure.  At  the  onset  the  mucous  membrane  is  red,  thickened,  ecchy- 
mosed,  and  granulating.  It  is  covered  with  a  yellowish,  puriform  mucous 
exudation,  streaked  with  blood,  and  analogous  to  the  stools  characteristic 
of  this  period.  The  hypertrophied  lymphatic  follicles  stand  out  in  relief. 
A  few  days  later  punched-out  ulcers,  a^  well  as  larger  and  more  irregular 
ones,  are  found  on  the  mucoiLs  membrane.  On  microscopic  examination, 
the  vessels  of  the  glandular  layer  appear  swollen  and  surrounded  with  con- 
nective tissue  that  is  infiltrated  with  embryonic  cells.  The  tubular  glands 
are  compressed  and  elongated.  The  subjacent  vascular  network  is  likewise 
surrounded  with  fibrinous  exudate  and  connective  tissue,  infiltrated  with 
embryonic  cells.  The  swollen  follicles,  which  are  also  infiltrated  with  lym- 
phatic cells,  stand  out  on  the  surface  of  the  mucous  membrane.  The 
rounded  follicular  ulcers  are  due  to  softening  and  suppuration  in  the  centre 
of  the  follicles.  The  more  extensive  ulcers  arise  from  gangrene  of  the 
mucous  membrane,  which  lacks  proper  blood-supply,  because  it  is  infiltrated 
and  compressed  by  new  elements.  The  ulcers  extend  and  suppurate.  In 
slight  cases,  however,  the  process  rapidly  ends  in  recovery. 

2.  Grave  Dysentery. — The  lesions  are  similar  to  those  just  described, 
though  they  are  much  more  severe.  They  are  spread  over  the  large 
intestine,  and  may  be  found  in  the  small  bowel.  The  ulcers  are  extensive, 
deep,  and  distributed  over  the  whole  of  the  large  intestine.  In  places  the 
mucous  membrane  resembles  a  piece  of  wood  eaten  by  worms  (Kelsch). 
In  other  cases  the  mucous  membrane  is  removed  in  patches  over  a  large 
extent,  and  we  find  on  the  cellular  coat  only  a  few  tubular  glands,  which 
are  the  remnants  of  the  exfoliated  mucous  membrane.  The  ulcerated 
surfaces  are  reddish,  granular,  and  covered  with  purulent  debris ;  the  edges 
of  the  ulcers  are  clean-cut.  The  vascular  network  subjacent  to  the 
glandular  layer  is  infiltrated  with  embryonic  cells  and  coagulated  fibrin. 
The  vessels  are  dilated  and  congested  with  blood,  and  their  walls  have 
returned  to  the  embryonic  condition,  while  the  submucous  cellular  tissue 
resembles  a  phlegmon  spread  like  a  sheet  over  the  glandular  layer.  These 
vascular  changes  sum  up  the  chief  lesion  in  dysentery.  The  morl)id  process 
is  centred  in  the  vascular  zone  of  the  cellular  coat  and  in  its  peripheral 
expansion  in  the  mucous  membrane  (Kelsch).  As  the  nuicous  membrane  is 
deprived  of  its  blood-supply,  it  necroses  en  masse,  and  is  cast  off  in  the  form 
of  sloufflis. 


824  TEXT-BOOK  OF  MEDICINE 

The  parts  underlying  the  glandular  layer  (cellular  coat)  are  twice  or 
thrice  as  thick  as  in  the  normal  state.  This  swelKng  is  due  to  the  fullness 
of  the  bloodvessels,  the  congestion  of  the  lymphatics,  and  the  infiltration  of 
the  connective  tissue.  Perforation  of  the  intestine  is  very  rare.  The 
ulceration  may  lead  to  scar  tissue,  which  causes  stenosis  of  the  gut.  The 
ileum  often  shows  catarrhal  changes  in  the  grave  forms  of  dysentery. 
Lieberkiihn's  glands  are  in  part  replaced  by  embryonic  tissue,  and  the 
vascular  walls  are  likewise  converted  into  new  tissue  ;  but  the  changes  do 
not  attack  the  cellular  layer,  the  follicles,  or  Peyer's  glands. 

In  acute  dysentery  we  find  suppurative  adenitis  of  the  mesenteric 
glands  and  softening  and  hypertrophy  of  the  spleen.  Hepatitis  and 
abscesses  of  the  liver  will  be  described  later  (see  Liver). 

3.  Chronic  Dysentery. — Chronic  dysentery  and  the  chronic  diarrhoeas 
of  hot  countries  present  analogous  changes.  The  divergence  between  these 
two  morbid  states  is  chiefly  in  the  symptoms.  In  chronic  dysentery  the 
mucous  membrane  of  the  large  intestine  is  congested  in  places,  and  at 
certain  spots  there  are  small  rounded  ulcerations,  which  are  not  very  deep, 
and  have  a  brown  or  slaty  surface.  The  ulcers  arise  in  the  closed  follicles, 
and  are  the  end  of  the  orifices  which  lead  into  small  cavities.  These 
cavities  or  follicular  depressions  are  elliptical  or  rounded.  They  are 
formed  of  one  or  three  pockets,  and  contain  a  gelatiniform  mucus,  which 
may  be  extracted  by  pressure.  It  is  probable  that  the  follicular  diverticulum 
occupies  the  place  of  the  destroyed  follicle. 

The  submucous  connective  tissue  which  separates  the  muscular  layers 
of  the  intestine  and  the  subserous  tissue  are  thickened  and  fibrous,  so  that 
the  intestine  tends  to  become  converted  into  a  canal  with  rigid  walls.  In 
the  chronic  diarrhoea  of  hot  countries  this  change  also  affects  the  small 
intestine. 

Bacteriology. — The  bacillus  of  dysentery,  discovered  by  Chantemesse 
and  Widal,  is  a  short,  slightly  mobile  rod,  which  neither  stains  with  Gram 
nor  liquefies  gelatine.  It  does  not  coagulate  milk.  It  does  not  cause  sugar 
to  ferment,  and  it  never  produces  indol,  so  that  it  somewhat  resembles  the 
typhoid  bacillus.  Shiga  has  proved  that  it  is  a  specific  bacillus  by  obtaining 
the  agglutination  of  cultures  only  with  the  blood-serum  of  patients  suffering 
from  dysentery.  Krase  in  Germany,  Flexner  in  the  Philippines,  Strong  and 
Murgrave  in  Manilla,  Rosenthal  in  Moscow,  and  Vaillard  and  Doepter,  have 
all  found  the  same  bacillus,  with  some  slight  modification.  It  is  exceedingly 
abundant  in  the  stools,  but  not  in  a  pure  state. 

Vaillard  and  Doepter,  by  the  subcutaneous  inoculation  of  the  bacillub 
or  its  toxine,  have  produced  in  certain  animals  the  symptoms  and  the 
lesions  characteristic  of  epidemic  dysentery,  and  have  thus  furnished  a 
fresh  proof  of  its  specific  nature.     Amoebic  dysentery  is  only  seen  in  hot 


DISEASES  OF  THE  INTESTINE  825 

countries,  and  is  noteworthy  because  it  gives  rise  to  abscess  of  the  liver. 
The  blood  of  patients  suffering  from  amoebic  dysentery  does  not  agglutinate 
the  bacillus  of  Chantemesse  and  Widal. 

Symptoms. — The  description  of  dysentery  varies  in  benign  or  grave 
cases  as  well  as  in  different  epidemics,  and  I  shall  select,  therefore,  a  case  of 
average  severity  as  my  type,  indicating  subsequently  the  different  forms  of 
the  disease. 

At  the  onset  the  patient  is  taken  ill  with  diarrhoea  and  abdominal 
pains.  At  the  end  of  twenty-four  or  forty-eight  hours  the  stools  become 
dysenteric,  and  contain  whitish  mucus  analogous  to  partially  coagulated 
albumin.  The  mucus  is  sometimes  transparent  and  mixed  with  shreds 
of  blood  ;  at  other  times  it  has  the  rusty  appearance  of  pneumonic  sputum. 
Intestinal  ulcers  have  not  yet  formed.  The  evacuations  are  preceded  by  a 
painful  feeling  of  tension  and  constriction  at  the  anus  (spasms  and  tenesmus), 
and  by  an  incessant  desire  to  stool,  but  the  patient  is  unable  to  pass  more 
than  a  teaspoonful  of  matter.  The  tenesmus  sometimes  spreads  from  the 
rectum  to  the  bladder  (dysuria).  The  tenesmus,  which  is  so  painful,  is  not 
due,  as  was  believed,  to  the  convulsive  contraction  of  the  sphincter,  because 
the  anus  is  gaping,  but  to  the  acute  inflammation  of  the  passage. 

In  addition,  colic  is  felt  around  the  umbilicus  and  along  the  course  of 
the  large  intestine.  The  pain  is  increased  by  pressure,  especially  in  the  left 
iliac  fossa. 

When  ulcers  are  present,  the  stools  change,  and  contain,  in  addition  to 
mucus,  pure  blood  and  shreds  of  ulcerated  mucous  membrane.  It  is  not 
uncommon  to  find  moulded  faecal  matter  in  the  stools.  At  this  period  the 
effort  of  defalcation  is  repeated  several  times  an  hour,  and  in  very  grave 
epidemic  cases  the  patients  have  as  many  as  100  to  200  stools  in  the  twenty- 
four  hours,  and  the  total  quantity  of  matter  voided  may  amount  to  7  or 
8  pints. 

During  the  second  week  the  stools,  which  are  horribly  foetid,  contain 
practically  no  mucus,  because  the  mucous  glands  are  partially  destroyed, 
but  consist  of  a  serous  and  reddish  licjuid  in  which  shreds  of  membrane 
float.  They  may  also  contain  pus  in  considerable  quantity  at  this 
time. 

I  shall  next  describe  the  general  symptoms,  which  vary  in  different 
epidemics  and  in  different  countries. 

1.  In  the  benign  form  the  temperature  does  not  rise  above  100°  F.,  and 
the  stools  do  not  exceed  twelve  to  fifteen  a  day.  The  patient,  however, 
wastes  rapidly,  and  his  appearance  changes  quickly.  These  cases  recover 
in  about  a  week. 

In  the  grave  forms  the  general  .symptoms  ra})idly  become  alarming. 
There  is  great  thir.st,  the  skin  is  dry,  and  the  pulse  variable.     The  evacua- 


826  TEXT-BOOK  OF  MEDICINE 

tions  are  incessant,  and  the  intolerable  pain  wears  out  the  patient.  His 
strength  declines  suddenly,  and  the  loss  of  flesh  is  considerable.  Prostra- 
tion, somnolence,  and  chilling  often  complete  this  picture,  and  death  may 
supervene  from  the  fourth  to  the  twentieth  day  of  the  disease. 

2.  The  inflammatory  form  is  characterized  by  marked  febrile  reaction, 
with  quickening  and  hardness  of  the  pulse.  The  tongue,  instead  of  being 
coated,  is  red  and  dry.  The  stools  are  scanty,  and  when  they  become  more 
frequent,  the  fever  speedily  falls. 

3.  In  the  bilious  form,  contrary  to  what  is  observed  in  dysentery, 
there  is  conjointly  diarrhoea,  and  the  dysenteric  stools  are  mixed  with 
yellow  and  greenish  bilious  matter.  The  patients  complain  of  nausea  and 
vomiting,  and  the  tongue  is  covered  with  a  thick  fur,  but  the  fever  is  not 
high. 

4.  The  rheumatic  form,  says  Stoll,  is  remarkable  for  metastases  in  the 
joints.  In  the  medical  parlance  of  to-day  we  say  :  dysenteric  infection 
produces  an  arthropathy  which  belongs  to  the  class  of  pseudo-rheumatism. 
This  variety  of  arthropathy  is  observed  in  the  slight  forms  of  dysentery 
more  often  than  in  the  graver  cases.  It  appears  chiefly  about  the  period 
of  convalescence.  It  commences  generally  in  the  knee,  and  then  affects 
several  joints,  such  as  the  ankle,  the  shoulder,  and  the  small  joints  of  the 
fingers.  Dysenteric  arthropathy  supervenes  suddenly,  causing  neither  fever 
nor  acute  pain.  In  some  cases  its  appearance  coincides  with  the  arrest  of 
the  dysenteric  flux.  Alternation  of  the  intestinal  and  articular  localizations 
have  been  recorded  twice  or  thrice  in  the  same  individual.  These  cases 
of  arthropathy  are  obstinate,  and  may  last  for  weeks  or  months,  but  they 
are  not  accompanied  by  any  of  the  visceral  complications  of  true  rheu- 
matism. During  an  epidemic  observed  at  Montargis  (Huette)  the  rheumatic 
complications  took  the  form  of  arthritis  analogous  to  blennorrhagic 
arthritis. 

5.  The  intermittent  form  is  characterized  by  remissions,  followed  by 
exacerbations,  and  must  not  be  confounded  with  dysenteric  pernicious 
fever. 

6.  The  adynamic  and  ataxic  forms  are  characterized,  on  the  one 
hand,  by  prostration  and  depression,  leading  rapidly  to  coma,  and,  on  the 
other,  by  delirium,  restlessness,  carphology,  and  subsultus  tendinum. 
These  terrible  forms  occur  in  association  or  in  succession,  and  constitute 
malignant  dysentery, 

7.  Chronic  dysentery  is  frequently  seen  in  hot  countries,  and  generally 
follows  after  several  acute  attacks.  It  is  characterized  by  the  symptoms 
of  acute  dysentery,  though  greatly  modified.  Thus  the  evacuations  are 
serous  or  puriform,  and  rarely  bloody.  The  anus  is  gaping,  and  the  tenesmus 
is  replaced  by  a  painful  feeling  of  weight.     The  abdomen  is  retracted  and 


DISEASES  OF  THE  INTESTINE  827 

painful  on  pressure.  Apvrexia  is  complete,  and  the  appetite  is  normal  or 
increased.  In  spite  of  this,  the  loss  of  flesh  proceeds,  and  the  patient 
generally  becomes  cachectic.  The  disease  lasts  for  months  and  years,  and 
its  progress  is  sometimes  interrupted  by  acute  attacks.  Cure  is  possible, 
but  death  is  the  most  frequent  termination. 

Complications.  —  The  complications  of  dysentery  are  as  follows : 
(1)  Perforation  of  the  intestmes,  which  may  cause  local  or  general  peri- 
tonitis, phlegmon  localized  to  the  rectum  or  to  the  cgecum,  and  intestinal 
haemorrhage,  which  may  be  copious  enough  to  cause  death.  (2)  Parotitis, 
characterized  by  inflammation  and  suppuration  in  the  parotid  glands  and 
the  surrounding  cellular  tissue.  The  pus  may  invade  the  cellular  tissue  of 
the  neck  and  dissect  out  the  muscles.  (3)  Partial  and  temporary  paralyses, 
such  as  follow  acute  diseases.  (4)  Cicatrices  of  the  intestine,  a  late  com- 
plication, which  may  cause  stenosis  and  symptoms  of  intestinal  occlusion, 
(o)  Abscess  of  the  liver,  which  is  the  most  typical  complication  of 
dysentery. 

Diagnosis. — The  diagnosis  of  acute  dysentery  presents  no  difficulties. 
The  finding  of  the  microbe  in  the  stools  and  especially  the  sero-diagnosis 
are  specific.  In  difficult  cases  they  clear  up  the  diagnosis.  The  chronic 
diarrhoea  of  Cochin-China  must  not  be  confounded  with  chronic  dysentery. 
In  chronic  diarrhoea  bloody  stools  &,nd  tenesmus  do  not  occur.  The  dejec- 
tions are  mucous  or  bilious,  and  the  course  of  the  disease  is  not  interrupted 
by  acute  phases,  as  in  dysentery. 

The  prognosis  is  generally  benign  in  sporadic  dysentery,  but  it 
is  much  graver  in  the  endemic  form,  and  becomes  alarmmg  in  certain 
epidemics. 

Treatment.  —  Trousseau  advocates  the  following  measures  :  At  the 
onset  ipecacuanha  in  emetic  doses  should  be  prescribed — 45  grains,  divided 
into  four  powders  to  be  taken  at  intervals  of  ten  minutes,  until  vomiting 
occurs.  On  the  next  day  a  neutral  salt,  such  as  sulphate  of  soda  or  Seignette 
salt,  in  doses  of  3  to  5  drachms,  should  be  given,  and  purgation  continued 
every  day,  or  twice  a  day,  until  the  stools  become  fsecal.  At  the  same  time 
the  disease  should  be  attacked  by  means  of  enemata,  containing  3  to  10  grains 
of  nitrate  of  silver  in  10  ounces  of  water.  The  patient  must  be  fed  with 
soups,  thick  panadas,  or  eggs  beaten  up  in  broth.  Rice-water,  albumin- 
water,  or  the  white  decoction  of  Sydenham,  may  be  given  to  drink. 
Enemata  of  1  quart  of  water,  with  a  few  drops  of  laudanum  added,  may  help 
to  relieve  the  spasms  and  the  tenesmus. 

The  treatment  of  chronic  dysentery  is  different.  Enemata  of  nitrate 
of  silver  and  saUne  purgatives  in  small  doses  are  recommended,  and  we  may 
also  employ  subnitrate  of  bismuth  in  large  doses.  Milk  diet  and  the  use 
of  raw  meat  constitute  the  most  essential  part  of  the  regimen. 


828  TEXT-BOOK  OF  MEDICINE 

As  precautionary  measures  we  should  filter  and  boil  water,  avoid  sudden 
changes  of  temperature,  and  destroy  putrid  foci  as  far  as  possible.  The 
patient  must  be  isolated.  Contagion  must  be  avoided,  and  soiled  linen  and 
faecal  matter  must  be  disinfected. 

Vaillard  and  Doepter  have  immunized  horses  against  the  bacillus,  and 
have  obtained  a  serum  that  has  given  good  results  in  bacillary  dysentery. 

Their  conclusions  are  as  follows  :  In  an  adult  20  c.c.  of  serum  usually 
causes  rapid  relief  of  the  symptoms,  and  recovery  in  cases  of  moderate 
severity.  If  the  symptoms  are  not  better  at  the  end  of  twenty-four  hours, 
the  injections  are  repeated,  but  in  diminished  doses. 

In  grave  cases  40  to  60  c.c.  are  at  once  injected.  A  similar  dose  is  given 
next  day  if  need  be.     The  serum  is  then  given  in  diminishing  doses. 

In  the  worst  cases  it  is  necessary  to  give  80,  90,  and  even  100  c.c.  This 
quantity  is  given  in  divided  doses  twice  daily  until  the  intestinal  symptoms 
improve.  The  serum  must  then  be  continued  in  decreasing  doses.  In 
children  the  amount  is  reduced  to  one-half  of  the  adult  dose.  Very  satis- 
factory results  have  been  obtained  by  this  treatment. 

Prophylactic  injections  of  10  c.c.  give  immunity  which  lasts  for  ten  or 
twelve  days. 

XIV.  INTESTINAL  WORMS. 

Of  the  worms  (helminthes)  which  live  in  the  intestine  of  man,  some  are 
ribbon-like  (Cestodes,  from  Kear6<i,  festooned),  and  others  are  cylindrical 
(Nematodes,  from  t-f/yu-a,  thread).  The  former  are  the  taeniae  (from  raivta, 
ribbon),  and  the  cylindrical  worms  are  the  Ascaris  lumbricoides,  the 
Oxyuris  vermicularis,  and  the  Trichocephalus. 

Ascaris  Lumbricoides. — This  worm,  which  is  white  or  reddish,  cylindrical, 
and  tapered  at  both  ends,  attains  a  length  of  6  to  10  inches.  The  ascarides 
live  in  the  small  intestine,  and  several  hundred  may  be  present.  They  often 
pass  unnoticed,  until  their  presence  is  revealed  by  the  escape  of  a  worm  from 
the  anus  or  the  mouth.  At  other  times  they  cause  vomiting,  ballooning  of 
the  abdomen,  colic,  diarrhoea,  and  reflex  nervous  complications,  such  as 
convulsions,  mental  troubles,  or  paralysis.  It  is  j)robable  that  the  ascarides 
enter  the  digestive  passages  in  the  form  of  eggs  contained  in  non-filtered 
water  (Davaine).  The  anthelmintics  most  used  against  ascarides  are 
semen-contra  (10  to  30  grains),  santonin  (1  to  4  grains),  and  Corsican  moss 
(30  to  60  grains). 

Oxyuris  Vermicularis.— The  oxyuris  is  a  small  white  worm,  which  is 
^  inch  in  length.  It  is  very  common  in  children,  and  is  usually  found  in 
the  rectum  and  around  the  anus,  where  it  causes  severe  itching.  The 
oxyuris  may,  however,  invade  the  vulva  and  the  vagina  or  the  prepuce  and 


DISEASES  OF  THE  INTESTINE  829 

the  urethra.  It  may  also  pass  up  the  digestive  tube  and  be  vomited  by  the 
mouth.  The  chief  symptom  is  pruritus,  which  may  become  intolerable  just 
after  the  patient  has  retired  to  bed.  Saline  enemata  generally  suffice  to 
destroy  or  drive  away  the  worms.  If  this  treatment  is  not  efficacious, 
enemata  composed  of  mucilage  of  gum,  holding  in  suspension  1  to  4  grains 
of  calomel,  should  be  given. 

Trichocephalus. — This  is  a  httle  worm  1  to  2  inches  in  length.  Its 
posterior  extremity  is  swollen.  It  is  generally  found  in  the  caecum,  but  it 
does  not  give  rise  to  special  symptoms.  Metchnikoff  thought  it  played 
some  part  in  appendicitis. 

Bothriocephalus — Cachexia. — The  bothriocephalus,  so  called  because 
it  has  two  dimples  {^oOpiov,  a  dimple)  on  the  lateral  parts  of  the  head, 
is  very  common  in  Switzerland,  Finland,  Livonia,  etc.,  but  is  somewhat 
rare  in  France.  This  fact  is  not  sufficiently  borne  in  mind  when  rapid 
cachexia  occurs,  and  the  signs  recall  those  of  cancer  of  the  stomach  and  of 
pernicious  anaemia.  The  diagnosis,  however,  is  important,  because  we  can 
effect  a  rapid  cure  in  a  patient  who  appears  doomed  to  an  early  grave.  The 
following  case  at  the  Hotel-Dieu  has  been  published  by  Nattan-Larrier  : 

A  patient  was  admitted  for  acute  epigastric  pain.  He  vomited  after  every  meal, 
had  lost  16  pounds  in  weight,  and  was  extremely  weak.  His  colour  was  waxy,  his  eyes 
were  dark,  his  conjunctivse  and  his  hpg  were  colourless,  and  he  had  shght  oedema  of 
the  legs.     The  diagnosis  of  cancer  had  been  made. 

The  illness  had  commenced  five  months  before  with  epigastric  pain,  followed  by 
diarrhoea,  anorexia,  pallor,  vertigo,  daily  vomiting,  and  wasting.  No  haematemesis,  no 
melaena,  and  no  induration  of  the  stomach,  which  would  have  pointed  to  cancer.  The 
blood-count  differed  from  that  of  cancerous  anaemia,  the  figures  being :  red  corpuscles, 
1,400,000  ;  white  corpuscles,  2,500  ;  percentage  of  white  corpuscles  :  polynuclears,  48  ; 
mononuclears,  52  ;  no  eosinophiles,  no  myelocytes,  no  nucleated  red  corpuscles  ;  a  few 
deformed  red  corpuscles  ;  haemoglobin  coefficient,  1-2.  The  number  of  red  corpuscles, 
though  small,  did  not  put  cancer  out  of  count ;  the  other  features  of  the  count,  however, 
did  so.  In  cancerous  ana?mia  the  haemoglobin  coefficient  is  always  below  normal ;  in 
this  case  it  was  above  normal.  In  one-third  of  the  cases  of  aniemia  due  to  new  growths 
we  find  nucleated  red  corpuscles  ;  in  this  case  both  normoblasts  and  megaloblasts  were 
absent.  In  cancerous  anaemia  the  number  of  leucocytes  is  increased ;  in  this  case  it 
was  diminished. 

Was  the  blood-count  compatible  with  pernicious  anaemia  ?  In  this  disease  we  find 
similar  anaemia  to  that  of  our  patient,  but  the  characters  of  the  anaemia  are  more  marked. 
The  red  corpuscles  fall  below  a  million  ;  the  haemoglobin  coefficient  is  above  the  normal ; 
the  blood  contains  myelocytes  and  nucleated  red  cells,  which  were  absent  in  this  case  ; 
lastly,  in  pernicious  ana-mia  the  morphology  of  the  red  corpuscles  is  more  profoundly' 
modified. 

Could  the  affection  be  a  severe  secondary  anaemia  due  to  lead,  malaria,  or  syphilis  ? 
These  factors  could  all  be  eliminated.  We  had  to  find  out  whether  the  antemia  was 
due  to  an  animal  parasite,  the  ankylostoma,  or  the  botiiriocephahis. 

Neither  his  trade  nor  his  home  was  in  favour  of  ankylostomiasis.  Was  he,  then, 
Buftering  from  anamia  due  to  the  bothriocephalus  ?  On  inquiry,  he  said  that  he  had 
Had  ■'  a  solitary  worm  "  for  many  years.  A  dose  of  castor-oil  led  to  the  expulsion  of 
an  intestinal  worm  10  inches  long  and  ^  inch  broad,  of  a  greyish  colour.     It  had  broad, 


830  TEXT-BOOK  OF  MEDICINE 

short  segments,  which  were  all  similar.  The  genital  pores  were  situated  in  the  middle 
line.  The  head  was  almond-shaped  ;  it  had  no  hooklets,  but  possessed  two  lateral  slits. 
The  shts  contained  innumerable  eggs,  70  yu.  in  length,  and  45  /x  in  breadth.  Each  had 
a  double  wall,  and  a  valve  at  one  pole.     The  worm  was  a  bothriocephalus. 

Oil  of  male-fern  was  given,  and  some  hours  later  he  passed  eight  worms,  varying  in 
length  from  4  to  12  inches.  Next  day  he  was  much  better,  and  had  a  good  appetite. 
In  a  week  he  gained  3  pounds  in  weight.  The  red  corpuscles  rose  to  3,000,000,  while  the 
white  corpuscles  were  4,000.  Shdes  showed  nucleated  red  corpuscles  and  myelocytes, 
indicating  regeneration  of  the  blood.     He  left  the  hospital  in  excellent  health. 

General  Description. — In  many  persons  the  bothriocephalus  may  be 
present  for  many  years,  and  only  cause  intestinal  troubles  and  moderate 
anaemia.  The  scene  at  times  changes  suddenly,  and  cachexia  is  established 
within  two  weeks.  Careful  examination,  however,  shows  that  for  two  or 
three  years  the  patient  has  suffered  from  general  weakness,  headache, 
vertigo,  and  buzzing  in  the  ears,  before  the  slight  anaemia  changed  into 
marked  cachexia. 

The  gastro-intestinal  symptoms  of  cachexia  due  to  the  bothriocephalus 
simulate  those  of  malignant  cachexia,  and  thus  render  the  diagnosis 
obscure.  The  rapid  anaemia  leads  to  a  diagnosis  of  an  essential  pernicious 
anaemia.  The  colour  of  the  patient  is  an  ivory-white,  and  the  mucous 
membranes  are  colourless.  Anaemic  murmurs  are  heard  over  the  precordial 
region  and  the  vessels  of  the  neck.  Retinal  haemorrhages  ofcen  occur.  In 
a  few  months,  or  even  in  a  few  weeks,  the  wasting  is  considerable.  In 
about  half  of  the  cases  slight  oedema  is  present  over  the  malleoli.  At  the 
same  time  the  dyspeptic  symptoms  grow  worse  :  the  anorexia  is  constant, 
vomiting  is  frequent,  and  diarrhoea  is  commonly  present. 

The  red  corpuscles  may  fall  below  a  million.  The  haemoglobin  is  rarely 
diminished,  and  is  never  much  increased.  The  corpuscles  are  not  much 
deformed ;  microcytes  are  numerous,  while  the  macrocytes  are  said  by 
Schaumann  to  be  scanty.  Normoblasts  and  megaloblasts  have  often  been 
found,  but  they  were  not  present  in  my  case.  At  times  the  myelocytes 
show  the  participation  of  the  bone-marrow  in  the  blood  regeneration.  An 
increase  of  the  eosinophiles  has  never  been  found  during  the  stationary 
stage  of  the  disease. 

Certain  differences  in  the  blood-counts  distinguish  this  disease  from 
pernicious  anaemia.  Examination  of  the  stools  yields  the  eggs  of  the  taenia, 
provided  it  has  not  been  expelled.  They  are  so  numerous  that  their  dis- 
covery is  easy.  Their  appearance  is  so  characteristic  that  doubt  cannot 
exist.  If  the  patient  has  just  passed  fragments  of  the  worm,  examination 
will  give  the  diagnosis. 

The  pathogenesis  of  anaemia  and  cachexia  due  to  the  bothriocephalus 
is  a  matter  of  theory.  It  is  evidently  an  intoxication,  but  the  mechanism 
is  imperfectly  understood,  and  in  spite  of  many  experiments  it  is  not  easy 


DISEASES  OF  THE  INTESTINE  831 

to  say  why  the  worm  may  be  harmless  for  many  years  and  then  suddenly 
give  rise  to  rapid  cachexia. 

We  cannot  explain,  moreover,  why  in  certain  comitries  (Livonia,  Finland) 
the  bothriocephalus  often  tends  to  cause  anaemia  and  cachexia,  and  why 
these  troubles  are  rare  in  other  countries. 

Trichina. — The  trichina  is  a  parasite  of  the  muscles,  and  only  attains 
its  perfect  state  in  the  aHmentary  canal.  Trichinosis  is  common  in  pigs.  In 
man  the  trichina  ingested  with  the  food  is  set  free  in  the  aHmentary  canal, 
gives  birth  to  rectilinear  trichinae,  which  perforate  the  intestine,  and  lodge 
in  the  muscles. 

Taeniae. — The  taeniae  which  are  met  with  in  the  intestine  of  man  are 
the  T(Bnia  inermis  and  the  T.  armis,  or  T.  solium.  The  following  descrip- 
tion is  taken  from  Laboulbene's  monograph  :  The  patient  brings  in  a  bottle 
the  fragments  of  a  worm  which  he  has  passed.  We  can  tell  at  once  whether 
it  is  a  case  of  T.  inermis  or  T.  solium.  If  the  segments  of  the  worm  are 
separated  or  isolated,  and  if  they  are  voided  involuntarily  and  without  the 
patient's  knowledge,  it  is  a  case  of  T.  inermis.  If,  on  the  contrary,  the 
fragments  consist  of  five  or  six  to  ten  rings,  and  if  they  have  not  been 
passed  without  the  patient's  knowledge,  but  have  been  expelled  in  the 
stools,  then  it  is  a  case  of  T.  solium.  The  following  are  the  distinguish- 
ing characteristics  : 

The  T.  inermis  {mediocanellata),  which  is  twenty  times  as  frequent  as 
the  T.  armis,  looks  like  a  ribbon  of  12  or  15  feet  in  length.  One  of  its 
extremities  is  pointed,  and  terminates  in  a  slight  swelhng,  which  is  the 
head.  The  head,  or  scolex,  is  provided  with  four  suckers,  by  which  the 
animal  adheres  to  the  intestine  ;  the  body  is  formed  of  segments,  of  which 
the  last  ones  are  longer  than  they  are  broad,  and  are  called  cuciirbitins, 
on  account  of  their  resemblance  to  a  pumpkin-seed.  They  are  filled  with 
eggs.  Each  segment  contains  both  male  and  female  organs  of  generatioii, 
except  the  posterior  segments  or  cucurbitins,  in  which  the  male  organ  is 
atrophied.  The  genital  pores  are  found  on  the  sides  of  the  segments. 
The  unarmed  taenia  of  man  comes  from  the  cysticercus  of  the  ox,  or 
from  measly  veal.  The  T.  solium,  or  armed  taenia,  is  thinner  than 
the  unarmed  taenia.  Its  head  is  provided  with  four  suckers  and  booklets, 
arranged  in  a  double  crown.  Each  of  the  segments  forming  the  body  of  the 
animal  contains  both  male  and  female  organs  of  generation,  and  the  genital 
pores  are  most  frequently  alternate,  whilst  they  are  placed  in  series  on  the 
same  side  in  the  unarmed  taenia.  T.  solium  comes  from  the  cysticercus  of 
the  pig,  in  whi<'h  it  constitutes  measles. 

The  symptoms  occasioned  by  taenia  are  multiple.  Amongst  the 
digestive  troubles  I  may  mention  salivation,  vomiting,  attacks  of  nausea, 
and  gastro-intestiual  troubles.     Amongst  the  nervous  troubles  of  a  reflex 


832  TEXT-BOOK  OF  MEDICINE 

kind  we  see  vertigo,  laryngeal  spasms,  nasal  pruritus,  spasm,  hiccough,  and 
epileptiform  convulsions.  Eosinophilia  has  not  the  diagnostic  importance 
which  has  been  attributed  to  it. 

The  vermifuges  generally  employed  are  ethereal  oil  of  male-fern,  the 
root  of  the  wild  pomegranate-tree,  kousso,  and  pelletierine.  I  obtain  almost 
constant  success  with  the  male-fern,  which  I  administer  according  to 
Trousseau's  prescription.     The  method  of  administration  is  as  follows  : 

The  patient  is  placed  on  a  milk  diet  for  twenty-four  hours.  Next  morn- 
ing he  takes  fasting  12  to  15  capsules,  each  containing  5  drops  of  ethereal 
oil  of  male-fern.  One  capsule  is  taken  every  three  minutes.  A  quarter  of 
an  hour  after  the  last  capsule  he  takes  ^  ounce  of  castor-oil,  and  half  an 
hour  later  he  again  takes  |  ounce.  This  is  the  method  which  I  had  inaugu- 
rated at  the  Necker  Hospital,  where  I  used  to  see  every  year  more  than 
a  hmidred  patients  suffering  from  taenia.  It  has  succeeded  in  cases  where 
other  remedies  have  failed.  The  doses  which  I  have  given  are  for  an  adult, 
and  must  be  modified  in  the  case  of  a  child. 


CHAPTER  VI 
DISEASES  OF  THE  PERITONEUM 

I.  INTRODUCTION  TO  THE  STUDY  OF  PERITONITIS. 

During  the  past  few  years  a  radical  change  has  been  brought  about  in  the  study  of 
peritonitis.  From  the  peritoneal  chaos  we  have  estabhshed  clearly-defined  types, 
which  have  taken  their  place  in  the  nosological  list,  and  have  been  substituted  for  the 
mistaiies  of  the  past.  The  old  classification  of  peritonitis  admitted  two  groups  :  on 
the  one  hand,  secondary  peritonitis,  and  on  the  other,  so-called  primary  or  idiopathic 
peritonitis.  The  causes  of  secondary  peritonitis  were  perforations  of  the  stomacli, 
intestines,  or  bihary  passages  ;  lesions  of  the  uterus  and  its  adnexa,  puerperal  infection, 
tuberculosis,  cancer,  etc.,  were  described.  The  commonest  variety  of  secondary  peri- 
tonitis— I  mean  appendicular  peritonitis^was  unknown.  Grisolles  wrote  on  typhhtis, 
perityphhtis,  and  ihac  phlegmon,  but  appendicitis  and  appendicular  peritonitis  were 
passed  over  in  silence.  A  few  hues  on  perforation  of  the  appendix  by  foreign  bodies 
were  inserted  in  tlie  descrij^tion  of  intestinal  perforations. 

In  direct  opposition  to  the  incongruous  group  of  secondary  peritonitis,  writers 
described  the  so-called  primary  or  idiopathic  peritonitis,  which  was  behevcd  to  come 
a  frigore,  and  which  Grisolles  had  called  "  simple  acute  peritonitis."  This  peritonitis 
served  as  the  model  for  the  classical  description  of  peritonitis,  and  was  called  "  acute 
peritonitis,"  without  any  other  designation. 

This  so-called  simple  or  idiopathic  peritonitis  does  not  exist.  Many  of  these  cases 
are  in  reality  appendicular  peritonitis.  We  know  how  the  toxi-infection  elaborated  in 
the  closed  cavity  traverses  the  walls  of  the  appendix,  and  causes  acute  peritonitis 
without  obvious  perforation.  These  facts  were  formerly  unlaiown.  The  peritonitis 
was  called  simple  or  idiopathic,  because  the  original  focus  in  the  appendix  had  remained 
unnoticed. 

Writers  also  placed  to  the  credit  of  simple  acute  peritonitis  the  peritoneal  infections 
which  are  known  to  be  caused  by  the  pneumococcus  and  the  streptococcus,  the  epithet 
"  primary  "  being  applied  to  cases  in  which  the  entrance-gate  of  the  infective  agent 
remained  unknowTi. 

It  follows,  therefore,  that  we  cannot  to-day  give  the  general  description  of  acute 
peritonitis.  The  description  must  be  spUt  up  according  to  the  origin  of  the  peritonitis, 
because  each  variety  may  present  a  clinical  picture  which  difTers  according  to  the 
cause. 

Puerperal  Peritoneal  Infection. — The  uterine  cavity  in  the  normal  condition  or 
after  accouchement  docs  not  contain  microbes  ;  consequently,  tlie  usual  agents  of 
puerperal  peritonitis — strej)tococcuH,  coli  bacillus,  or  otlier  microbes — must  have  been 
carri(;d  to  tlie  woman  by  the  accoucheur,  the  midwife,  the  instruments,  the  linen,  and 
the  dressings,  by  attempts  to  procure  abortion,  or  by  erysipelas.  Tlie  microbes  pass 
through  the  lymphatic  vessels  eleven  times  out  of  twelve  (Widal),  and  in  some  cases 
along  t  lie  mucosa  of  the  Fallopian  tube.  This  variety  of  puerperal  infection  has  become 
exceedingly  rare. 

833  53 


834  TEXT-BOOK  OF  MEDICINE 

Amongst  the  varieties  of  peritonitis  peculiar  to  women  and  girls  I  may  mention 
inflammation  consecutive  to  pyosalpinx.  Blennorrhagic  peritonitis  has  been  well 
described  by  Charrier,  It  usually  begins  with  acute  pain  in  the  lower  abdomen  (Bernutz's 
cry  of  alarm).  The  onset  often  coincides  with  the  end  of  the  first  menstruation  which 
follows  infection  of  the  uterus  by  the  gonococcus.  In  addition  to  the  usual  symptoms 
of  peritonitis,  local  examination  reveals  induration  in  the  culs-de-sac  and  fixation  of 
the  pelvic  organs  by  adhesions.  This  perimetro -salpingitis,  which  is  benign  as  far  as 
life  is  concerned,  is  a  jjossible  cause  of  sterihty  (Charrier).  Blennorrhagic  vulvo- 
vaginitis in  young  girls  is  also  a  cause  of  peritonitis.  The  detailed  description  of 
blennorrhagic  peritonitis  -will  be  given  under  Blennorrhagia. 

Appendicular  Peritonitis. — As  I  have  described  this  form  in  detail  under  Appen- 
dicitis, I  shall  simply  mention  it  here.  General  or  local  peritonitis  and  remote  peri- 
toneal abscesses  are  seen  in  the  course  of  appendicitis.  The  appendix  may  or  may  not 
be  perforated.     I  have  explained  the  process  when  describing  the  closed  cavity. 

Peritoneal  Infection  due  to  Perforation  of  Organs. — This  group  contains  cases  of 
peritonitis  resulting  from  trauma,  perforation  of  the  stomach  (simple  ulcer)  and  of  the 
intestine  (ulcer  of  the  duodenum,  typhoid  and  tubercular  ulcerations).  I  shall  here 
merely  mention  these  varieties  of  peritonitis.  They  are  discussed  in  detail  in  the 
sections  on  Ulcer  of  the  Stomach,  Ulcer  of  the  Duodenum,  Typhoid  Fever,  etc. 

This  group  contains  the  varieties  of  peritonitis  due  to  perforation  of  the  bile-ducts. 
The  bile  itself  is  harmless  and  sterile,  and  the  passage  of  aseptic  bile  into  the  peritoneum 
does  not  cause  peritonitis.  Acute  peritonitis,  however,  develops  if  the  bile  is  con- 
taminated \rith  pathogenic  microbes  (rupture  of  the  gall-bladder  or  of  the  bile-duct, 
calculous  obstruction). 

The  same  remark  appHes  to  the  urine.  Physiological  urine  is  inoffensive  to  the 
peritoneum,  as  to  all  other  tissues,  because  it  does  not  contain  microbes.  If  the  urinary 
tract  is  infected  by  the  streptococcus  or  the  coli  bacillus,  perforation  of  the  bladder  or 
of  the  peh^s  of  the  kidney  wiU  be  followed  by  peritonitis. 

Peritoneal  Infection  due  to  Purulent  Collections. — To  ^  this  category  belong  the 
various  kinds  of  peritonitis  due  to  contact  with  or  to  rupture  of  perirenal  suppurations 
(Albarran),  abscesses  of  the  liver,  iliac  phlegmons,  inflammation  of  the  abdominal  wall, 
jDui'ulent  pleurisy,  etc. 

Primary  Peritonitis. — Primary,  pneumococcal,  and  streptococcal  peritonitis  will 
be  described  later. 

Anatomy  of  the  Peritoneum. — It  will  be  useful  to  note  a  few  anatomical  facts 
which  are  indispensable  in  studying  diseases  of  the  peritoneum. 

The  peritoneum,  like  every  serous  membrane,  presents  a  parietal  and  a  visceral 
layer.  The  parietal  layer  is  more  resistant  and  thicker.  It  is  hned  with  cellular  tissue, 
which  plays  an  important  part  in  certain  regions.  This  cellular  tissue  is  loose  over  the 
anterior  wall,  where  it  forms  the  fascia  propria,  and  is  abundant  in  the  iHac  fossae  and 
the  pelvis,  where  it  readily  becomes  inflamed.  It  is  still  more  abundant  around  the 
kidneys,  where  its  inflammation  constitutes  perinephritis.  The  parietal  layer  is  easily 
separated  from  the  diaphragm,  and  still  more  easily  from  the  other  regions  which  I 
have  just  enumerated. 

The  visceral  peritoneum  is  thin  and  transparent,  being  so  intimately  united  with 
certain  viscera  (spleen,  Hver,  ovary)  that  it  forms,  as  it  were,  part  of  their  structure ; 
but  elsewhere  it  is  separable  as  a  thin  sheet  (stomach  and  intestines). 

The  peritoneum  forms  three  varieties  of  folds  in  the  abdominal  cavity :  (1)  Folds 
which  pass  from  the  posterior  walls  of  the  abdomen  to  the  digestive  organs.  The 
name  of  the  organ  into  which  they  have  been  inserted,  with  the  prefix  meso,  has  been 
given  to  them,  and  in  this  way  the  names  mesocolon,  mesorectum,  mesentery  have 
originated.  (2)  Folds  which  proceed  from  the  walls  of  the  abdomen  to  organs  other 
than  those  of  the  digestive  tube.     To  these  the  name  of  ligaments  has  been  given — 


DISEASES  OF  THE  PERITONEUM  835 

coronary  ligament ;  right  and  left  triangular  Ugaments,  which  pass  to  the  liver ;  and 
broad  ligaments,  which  pass  to  the  uterus.  (3)  Folds  which  extend  from  one  viscus  to 
another  one.  They  are  three  in  number,  and  are  called  omenta.  They  are  the 
small  omentum,  or  gastro-heijatic  omentum,  which  unites  the  stomach  to  the 
liver ;  the  great  omentum,  or  gastro-coUc  omentum,  which  unites  the  stomach  to 
the  transverse  colon  ;  and  the  gastro -splenic  omentum,  which  passes  from  the  liver 
to  the  spleen. 

All  these  folds  of  the  peritoneimi  are  formed  by  the  two  layers  of  the  serous  mem- 
brane. Between  the  layers  there  is  ceUulo-fatty  tissue  in  which  the  vessels  and  the 
nerves  ramify. 

In  the  normal  condition  the  peritoneal  cavity  does  not  contain  any  micro-organisms. 

Description. — As  the  symptoms  of  peritonitis  vary  according  to  the 
exciting  cause,  I  shall  sketch  three  principal  types  which  answer  fairly  to  the 
clinical  pictures  of  acute  peritonitis. 

In  the  first  type  the  peritonitis  arises  suddenly,  and  is  acute  or  super- 
acute.  It  follows  trauma,  perforation  of  an  organ  (ulcer  of  the  stomach 
or  duodenum),  opening  of  an  abscess,  ruptiu:e  of  the  pelvis  of  the  kidney  or 
of  the  bladder,  and  perforating  appendicitis.  Violent  pain,  with  or  without 
rigors,  opens  the  scene.  The  pain,  which  is  at  first  local,  extends  rapidly 
to  the  whole  of  the  abdomen.  It  is  acute  and  at  times  agonizing,  being 
increased  by  the  least  movement,  contact  with  the  bedclothes,  cough, 
hiccough,  vomiting,  or  intestinal  peristalsis. 

The  abdomen  soon  becomes  distended,  and  the  meteorism  is  excessive. 
At  the  onset,  however,  the  abdomen  is  flat,  hard,  and  tense,  and  the  muscles 
are  contracted.  Hiccough  is  frequent,  and  vomiting  occurs  at  more  or 
less  close  intervals.  The  vomited  matter  at  first  consists  of  mucus,  and 
later  of  bile,  and  the  patient,  after  much  straining,  vomits  streams  of  bitter, 
greenish  fiuid  (porraceous  vomiting).  Constipation  is  the  rule.  Dysuria 
is  frequent,  and  the  urine  is  scanty. 

The  fever  is  sometimes  high,  but  the  temperatm-e  may  fall  below 
normal.  Fluid,  in  variable  quantity,  accumulates  in  the  peritoneum.  The 
general  symptoms  rapidly  become  more  marked.  On  the  second  or  third 
day  the  pulse  becomes  quick  and  thready ;  the  tongue  is  dry  and  cracked, 
and  there  is  great  thirst.  The  face  is  thin  and  pinched,  the  nose  is  cold, 
the  eyes  are  hollow,  the  weakness  is  excessive,  the  extremities  grow  cold,  the 
respiration  Ls  short  and  jerky,  the  voice  is  thin  and  husky,  and  collapse  is 
imminent.  All  these  symptoms  become  accentuated,  except  the  pain, 
which  diminishes  or  disappears.  The  patient,  not  having  lost  conscioiLs- 
ness,  congratulates  himself  on  the  disappearance  of  the  pain ;  but  this  calm 
is  generally  the  prelude  of  death,  and  the  sufEerer  dies  speaking,  as  Grisolles 
said.  In  tliLs  variety  of  peritonitis  recovery  is  the  exception  (except  in 
the  case  of  early  surgical  intervention).  Death  may  supervene  on  the  first, 
second,  or  third  day  (peritonitis  due  to  perforation),  though  it  rarely  takes 
place^  before  the  sixth  or  seventh  day.     in  some  cases,  especially  in  children, 

53— li 


836  TEXT-BOOK  OF  MEDICINE 

a  slow  phase  follows  the  sudden  onset  (pneumococcal  peritonitis),  and  the 
pus  often  finds  its  way  through  the  umbilicus.     Recovery  may  then  occur. 

In  the  second  type  we  have  still  to  deal  with  acute  diffuse  peritonitis, 
but  the  complication  appears  in  subjects  who  are  already  sick,  and  suffering, 
for  example,  from  typhoid  fever.  In  such  a  case  the  symptoms  of  peritonitis 
are  not  very  marked,  and  the  reaction  is  less  acute.  The  pain,  hiccough, 
and  vomiting  are  not  as  severe  as  in  the  former  type.  A  sudden  fall  in  the 
temperature  is  frequent,  and  the  abdominal  meteorism  is  very  marked. 

In  the  third  type  the  different  symptoms  of  acute  peritonitis  are  less 
pronounced,  and  the  chief  feature  is  the  general  condition  of  the  patient, 
when  a  rapid  tendency  to  collapse  (primary  streptococcal  peritonitis)  is  seen. 

Partial  Peritonitis. — Partial  peritonitis  has  its  seat  of  election  in  the 
iliac  fossae,  the  subphrenic  region,  and  the  peri-uterine  region.  It  is  neither 
so  acute  nor  so  grave  as  general  peritonitis,  and  often  causes  an  abscess  in 
one  of  the  regions  just  mentioned.  Abdominal  palpation  and  vaginal  and 
rectal  examination  will  aid  in  the  diagnosis  of  partial  peritonitis.  The 
description  of  these  varieties  of  encysted  peritonitis  will  be  found  under 
Appendicitis  and  Simple  Ulcer  of  the  Stomach. 

Chronic  Peritonitis. — General  peritonitis  does  not  pass  into  the 
chronic  state.  The  chronic  form  is  seen  in  ]5artial  peritonitis  and  in 
tubercular  or  cancerous  peritonitis. 

Pathological  Anatomy. — In  acute  peritonitis  the  peritoneum  is  found 
to  be  injected,  thickened,  and  infiltrated  with  pus.^  The  fibrino-purulent 
infiltration  exists  in  the  folds  of  the  great  omentum  and  of  the  mesentery, 
in  the  connective  tissue  of  the  serous  membrane,  and  upon  its  surface. 
Fibrinous  adhesions  rapidly  form  between  the  intestinal  coils,  as  well  as 
between  the  various  organs  of  the  abdomen  and  the  parietal  and  visceral 
layers.  The  great  omentum  is  thickened,  vascular,  and  adherent  to  the 
intestines  and  to  the  abdominal  wall.  The  false  membrane  is  covered  with 
puriform  mucus.  A  quantity  of  fibrino-purulent  hquid  is  found  in  the 
peritoneal  cavity,  and  varies  in  amount  from  a  few  ounces  to  several  pints. 
This  hquid  is  sometimes  very  foetid.  To  these  lesions  must  be  added  the 
changes  in  the  organs  which  have  caused  peritonitis. 

Treatment. — There  is  no  medical  treatment  for  acute  peritonitis. 
The  pain  is  treated  with  injections  of  morphia.  Ice-compresses  are  applied 
to  the  abdomen,  and  ice  is  given  to  the  patient  to  suck.  Surgical  interven- 
tion is  the  only  real  treatment.  We  must  act,  however,  without  delay, 
and  if  too  much  precious  time  has  not  been  lost  in  medical  treatment,  the 
greater  are  the  chances  of  saving  the  patient.  This  question  of  surgical 
treatment  is  given  in  detail  mider  Appendicitis,  Ulcer  of  the  Stomach  and 
of  the  Duodenum,  Primary  Pneumococcal  and  Streptococcal  Peritonitis, 
Peritonitis  in  Typhoid  Fever,  etc. 


DISEASES  OF  THE  PERITONEIBI  837 


11.  ACUTE  AND  SUBACUTE  TUBERCULAR  PERITONITIS. 

Tubercular  peritonitis  may  be  partial  or  general  and  acute  or  chronic. 
[  shall  first  consider  acute  and  subacute  peritonitis. 

Peritonitis  due  to  Perforation. — A  patient  is  suffering  from  tuber- 
cular ulceration  of  the  intestine.  The  sufferer  is  seized  with  symptoms  of 
acute  peritonitis  from  perforation  ;  he  has  terrible  pain  in  the  abdomen, 
vomiting,  hiccough,  etc.,  and  succumbs  in  a  few  days.  Post  mortem, 
general  peritonitis  due  to  perforation  of  a  tubercular  ulcer  of  the  ileum  is 
found.  Although  the  peritonitis  is  not  tubercular  in  the  true  sense  of  the 
word,  because  it  is  not  due  to  the  tubercle  bacillus,  but  to  virulent  microbes 
which  have  passed  from  the  intestine  into  the  peritoneum,  it  is  none  the 
less  true  that  a  tubercular  lesion  of  the  intestine  has  caused  the  perfora- 
tion, so  that  we  may  clinically  place  this  variety  under  Tubercular  Peri- 
tonitis. 

It  must  not,  however,  be  supposed  that  these  cases  are  common. 
As  far  as  I  am  concerned,  I  have  never  seen  one.  Tubercular  ulcerations  of 
the  intestine,  though  common,  very  rarely  cause  perforation  and  peri- 
tonitis. Barbe,  in  his  thesis  on  perforation  of  the  small  intestine,  only 
mentions  two  cases,  and  adds  that  the  average  of  these  perforations  in 
tubercular  patients  amounts,  according  to  Potain,  to  2  per  cent. 

Miliary  Peritonitis. — The  tubercular  process  does  not  affect  the 
peritoneum  alone,  but  forms  part  of  a  more  or  less  general  miliary  tuber- 
culosis. An  acute  febrile  disease  which  often  simulates  typhoid  fever  in 
adults  and  meningitis  in  children  declares  itself.  The  typhoid  symptoms 
in  the  one  case  and  the  meningeal  .symptoms  in  the  other  are  so  marked 
that  the  peritoneal  symptoms  pass  almost  unnoticed.  They  may,  however, 
be  fairly  severe,  and  the  abdominal  pain,  porraceous  vomiting,  meteorism, 
and  ascites  prove  the  presence  of  peritonitis.  The  patient  succumbs,  and 
at  the  autopsy  we  find  a  small  quantity  of  sero-fibrinous  or  sero-purulent 
liquid,  which  is  rarely  hsemorrhagic,  in  the  peritoneum.  The  peritoneal 
cavity  is  not  partitioned  off  by  false  membranes,  and  we  find  on  the  layers 
of  the  peritoneum  (especially  on  the  parietal  one)  small,  discrete,  or  con- 
fluent tubercles,  which  resemble  grains  of  semolina,  and  are  often  surrounded 
by  ecchymotic  patches.  The  intestinal  coils  are  more  or  less  congested 
and  matted  together  by  fibrinous  exudate.  Miliary  tubercles  are  likewise 
found  in  the  lungs,  pleura,  meninges,  ])ericardium,  etc.  The  jieritonitis  is, 
therefore,  merely  a  local  manifestation  of  general  tuberculosis  (tuberculosis 
by  blood  infection).  As  Marfan  says,  when  miliary  tii])erculosis  attacks 
young  ])eo])lp,  "  the  bacillus  seems  to  have  a  certain  affinity  for  the  peri- 
toneum, pleura,  meninges,  and  pericardium." 


838  TEXT-BOOK  OF  MEDICINE 

Subacute  Pleuro-Peritoneal  Tuberculosis. — In  the  adult  the  course 
of  events  is  somewhat  different,  and  we  often  see  a  subacute  variety,  which 
takes  its  origin  in  tuberculosis  of  the  lung,  and  invades  successively  the 
pleura  and  the  peritoneum.  This  variety,  described  by  Fernet  under  the 
name  of  "  Subacute  Pleuro-Peritoneal  Tuberculosis,"  is  much  less  common 
in  children  than  in  adults.  It  is  much  less  severe  than  general  tuberculosis, 
the  fever  being  less  marked,  the  symptoms  more  moderate,  and  the  course 
less  rapid.  Even  the  origin  is  different :  general  tuberculosis  is  the  result 
of  infection  through  the  bloodvessels,  but  in  pleuro-peritoneal  tuberculosis 
the  bacilli  seem  to  follow  the  lymphatic  passages,  and  pass  from  the  pleura 
to  the  peritoneum  through  the  diaphragm. 

In  one  case  of  pleuro-peritoneal  tuberculosis  we  were  able  to  trace  the 
extension  of  the  tuberculosis  from  the  pleura  to  the  peritoneum  through 
the  lymphatic  tracts  in  the  diaphragm. 

Reference  to  the  published  cases  shows  that  the  patient  usually  had 
well-marked  disease  in  the  pleura  when  the  peritonitis  appeared.  The 
symptoms  of  pleurisy  are  at  times  quite  evident ;  in  other  cases  the  pleural 
stage  is  latent,  and  it  is  only  discovered  when  the  alarm  has  been  given  by 
the  peritoneal  symptoms. 

In  this  variety,  as  in  the  other  varieties  of  tubercular  pleurisy,  we  j&nd 
more  or  less  abundant  fluid,  which  may  be  hfemorrhagic,  but  very  rarely 
purulent,  except  in  recurrence  of  the  effusion  after  thoracentesis,  etc. 

The  peritoneal  stage  is  rather  insidious  than  acute.  In  the  latter  event 
we  find  pain,  fever,  vomiting,  distension  of  the  abdomen,  and  ascites ;  in 
the  former  the  peritonitis  is  not  very  painful,  and  betrays  itself  only  by 
digestive  troubles  and  enlargement  of  the  abdomen.  The  liquid  is  generally 
free  in  the  peritoneal  cavity.  It  is  usually  yellow  in  colour,  and  may 
amount  to  8  or  10  pints. 

We  find  post  mortem  not  only  the  lesions  of  pleuro-peritoneal  tuber- 
culosis, but  also  tubercular  lesions  in  the  lungs  and  liver,  perihepatitis, 
perisplenitis,  etc. 

The  diagnosis  of  pleuro-peritoneal  tuberculosis  is  often  very  difficult, 
because  hepatic  cirrhosis  may  produce  peritoneal  and  pleural  effusion.  In 
cirrhosis,  however,  pleural  or  peritoneal  pain  is  absolutely  wanting,  a  col- 
lateral circulation  is  established,  and  the  patient  has  signs  of  cirrhosis  or  of 
precirrhosis. 

The  laboratory  measures  described  under  Tubercular  Pleurisy  may  be 
employed  in  the  diagnosis  of  peritoneal  effusions.  Although  the  peritoneal 
fluid  does  not  lend  itself  as  well  to  investigation  as  the  pleural  effusion,  it 
nevertheless  supplies  valuable  information.  I  have  several  times  made 
use  of  cyto-diagnosis,  sero-diagnosis,  and  of  injections  of  the  liquid  into  the 
mamma  of  a  nursing  guinea-pig. 


DISEASES  OF  THE  PERITONEUM  839 

Summary. — I  have  just  reviewed  three  varieties  of  tubercular  peri- 
tonitis. The  first  is  superacute,  and  very  rare.  It  results  from  perforation 
of  a  tubercular  ulcer.  The  second  is  acute,  and  fairly  frequent  in  children. 
It  is  characterized  by  peritonitis,  which  forms  part  of  a  general  infection. 
The  third  or  subacute  variety  is  often  curable.  It  is  usually  found  in 
adults,  and  is  characterized  by  the  pleuro-peritoneal  syndrome. 


III.  CHRONIC  TUBERCULAR  PERITONITIS. 

Chronic  tubercular  peritonitis  comprises  three  varieties  of  lesions :  (1)  more 
or  less  abundant  peritoneal  effusion  ;  (2)  caseous,  ulcero-caseous,  or  fibro- 
caseous  lesions  ;  and  (3)  fibro-adhesive  lesions.  This  cicatricial  process 
has  a  curative  tendency,  although  it  sometimes  oversteps  its  object,  and 
creates  vicious  adhesions.  These  three  kinds  of  lesions  are  found  in  every 
case  of  chronic  tubercular  peritonitis.  'Sometimes,  however,  one  of  them 
is  so  marked  that  it  gives  a  special  character  to  the  chronic  peritonitis,  and 
I  shall  therefore  describe  an  ascitic  and  a  fibro-caseous  form. 

A.  Ascitic  Form. 

In  some  cases  the  effusion  is  so  Jarge  that  the  condition  at  first  sight 
appears  to  be  ordinary  ascites.  These  cases  of  chronic  peritonitis,  in  which 
the  peritoneal  effusion  is  the  dominant  symptom,  may  be  compared  with 
those  cases  of  tubercular  pleurisy  in  which  a  large  effusion  is  the  only  sign. 
The  ascitic  form  is  far  more  common  in  children  than  in  adults  ;  it  is, 
indeed,  the  most  common  form  of  tubercular  peritonitis  in  youth. 

Pathological  Anatomy. — Abdominal  surgery  has  revealed  the  follow- 
ing lesions  :  Abundant  fluid,  which  is  citron-coloured,  transparent,  and 
hardly  ever  sero-purulent  or  sero-sanguineous.  The  quantity  of  liquid 
is  rarely  as  large  as  in  hepatic  ascites,  and  rarely  calls  for  tapping.  The 
liquid  is  free  in  the  peritoneal  cavity,  which  presents  no  septa.  The  peri- 
toneum is  injected,  dull,  and  covered  in  places  with  fibrinous  exudate. 
Tubercles  of  every  size  and  age  are  found  on  the  peritoneum,  which  is  more 
or  less  vascular.  These  greyish  or  yellowish  granulations  are  superficial, 
or  inserted  into  the  wall.  Caseous  and  fibrous  lesions  are  absent  in  most 
cases. 

Description. — The  on.sct  is  often  febrile  in  infants,  the  temperature 
rising  to  101°  or  10.3°  F.  The  child  complains  of  colic,  nausea,  and 
vomiting,  and  the  abdomen  is  distended  and  painful.  Examination  reveals 
ascites  without  dilatation  of  the  abdominal  veins,  and  sometimes  a  little 
liquid  in  the  j)leura.  After  this  acute  onset  the  disease  enters  on  a  more 
silent  stage,  in  which  the  pains  and  the  fever  disappear,  and  the  ascites  alone 


840  TEXT-BOOK  OF  MEDICINE 

persists,  sometimes  increasing,  sometimes  diminishing,  but  without  reaching 
— in  the  child,  at  least — such  proportions  as  to  necessitate  tapping.  During 
this  stationary  stage,  which  may  last  several  months,  the  child  grows  pale 
and  thin,  the  appetite  is  poor,  and  yet  the  condition  does  not  grow  worse, 
because  the  other  organs  generally  remain  healthy.  The  ascitic  fluid  is 
often  absorbed  spontaneously,  and  cure  occurs  in  more  than  half  the  cases. 
The  disease,  therefore,  well  deserves  its  name  of  benign  chronic  tubercular 
ascites  of  youth  (Marfan).  In  some  cases,  however,  which  are  rarer  in 
children  than  in  adults,  fibro-caseous  peritonitis  may  be  associated  with  the 
ascitic  form,  and  when  the  peritoneum  is  tapped,  thickening  of  the  omentum 
and  of  the  peritoneum  is  found. 

The  diagnosis  of  chronic  tubercular  ascites  is  often  very  difficult, 
because  ascites  due  to  cirrhosis  and  cardiac  or  renal  disease  may  present 
much  analogy  to  it.  In  these  different  varieties,  however,  fever  and  pain 
are  absent  at  first.  Furthermore,  in  cirrhotic  ascites  the  Hver  is  small,  and 
the  collateral  circulation  is  well  developed.  In  cardio -hepatic  ascites  the 
causative  lesion  is  found  in  the  heart,  and,  finally,  in  the  ascites  of  Bright's 
disease  we  can  discover  symptoms  of  Brightism  and  albuminuria.  The 
diagnosis  of  tubercular  ascites  may  be  confirmed  by  cyto-diagnosis,  sero- 
diagnosis,  and  injection  of  the  ascitic  fluid  into  the  mammae  of  guinea- 
pigs. 

B.  Chronic  Peritonitis — Fibro-Caseous  Form. 

This  is  the  usual  form  in  adults,  and  is  chronic  tubercular  peritonitis, 
without  other  designation. 

Pathological  Anatomy. — On  opening  the  belly,  the  viscera  may  be 
hidden  by  thick,  greyish  false  membranes,  forming  tumours  or  nodules 
that  may  have  given  rise  to  errors  m  diagnosis.  The  peritoneum,  the  meso- 
colon, the  mesentery,  and  the  great  omentum  are  much  thickened.  The 
thickening  is  due  to  sero-purulent  infiltration,  tubercular  granulations,  and 
embryonic  tissue  between  the  layers  of  these  membranes.  In  some  cases 
the  thickened  and  indurated  omentum  forms,  as  it  were,  a  transverse  band, 
which  is  clearly  felt  during  life. 

The  anterior  abdominal  wall  is  often  adherent  to  the  omentum  and  the 
intestines.  Adhesions  are  formed  between  the  layers  of  the  peritoneum, 
between  the  omentum  and  the  intestines,  and  between  the  intestinal  coils, 
which  are  matted  together,  and  cannot  always  be  separated  without  tearing. 
After  separation  of  these  adhesions,  little  cavities,  filled  with  serous  fluid 
and  altered  blood,  or  with  pus  mixed  with  fsecal  matter,  are  sometimes 
met  with.  Cavities  filled  with  caseous  matter,  forming  cold  abscesses  in 
the  peritoneum,  may  also  be  found.  The  diameter  of  the  intestine  is  con- 
tracted, and  its  walls  are  sodden,  friable,  and  atrophied.     The  intestina 


DISEASES  OF  THE  PERITONEUM  841 

canal  may  be  only  one-third  of  its  normal  length  (Grisolles).  Tubercular 
ulcerations  are  found  on  its  surface.  The  omentum  becomes  retracted,  and 
the  mesentery  draws  the  small  intestine  towards  itself.  This  matting  of 
the  intestinal  coils  may  simulate  a  tumour  situated  above  the  umbihcus. 
The  false  membranes  may  compress  the  portal  vein,  and  cause  thrombosis. 

Perforations  and  communications  between  two  adherent  coils  of  bowel 
are  sometimes  met  with.  In  exceptional  cases,  when  the  adhesions  have 
not  had  time  to  establish  themselves,  the  rupture  of  an  ulcer  may  cause 
acute  peritonitis. 

The  peritoneal  effusion  is  not,  as  a  rule,  abundant ;  sometimes  it  is 
absent.  The  effusion  is  serous,  sero-purulent,  and  flaky.  It  encysts  itself 
in  the  dependent  parts,  and  becomes  caseous.  The  fluid  may  in  some  cases 
have  a  hoemorrhagic  tint.  There  are  at  times  true  haemorrhages  into  the 
peritoneum,  Baumgarten  reports  a  case  in  which  the  haemorrhage  was  so 
copious  as  to  form  large  clots  in  the  abdominal  cavity. 

The  vessels  and  the  lymphatic  glands  always  take  part  in  the  tubercular 
process.  The  glands  are  sometimes  so  large  (mesenteric  phthisis)  that  they 
may  cause  oedema  of  the  lower  limbs  from  compression  of  the  vena  cava. 
Tubercles  are  often  found  in  the  other  organs  of  the  abdomen  (liver,  spleen, 
female  genital  organs,  bladder  and  ureters  in  children).  The  lungs  often 
contain  tubercles,  which  are  few  in  number  and  of  recent  growth.  When 
the  tubercular  lesions  end  in  a  fibro-adhesive  process,  almost  complete 
adhesion  is  found  between  the  intestines  and  the  abdominal  wall.  The 
omentum  retracts  the  transverse  colon  and  the  stomach,  while  the  mesen- 
tery draws  the  small  intestine  backward,  thus  favouring  intestinal  occlusion. 

Description. — Tubercular  peritonitis  is  almost  always  chronic  from  the 
fijst,  and  we  may  say  that,  with  the  exception  of  a  few  cases  and  cancer 
excluded,  it  sums  up  the  history  of  chronic  general  peritonitis.  In  twelve 
cases  of  chronic  peritonitis,  says  Grisolles,  eleven  were  tubercular.  The 
disease  chiefly  affects  young  people  and  adults,  and  not  patients  with 
advanced  phthisis,  but  those  who  are  in  the  early  stage.  As  a  consequence, 
the  abdominal  lesions  assume  a  predominant  importance,  and  the  peri- 
tonitis seems  to  represent  the  entire  disease,  whereas  it  is  sometimes  only 
an  episode  in  phthisis. 

In  some  cases  chronic  tubercular  peritonitis  is  preceded  ])y  an  acute 
or  subacute  phase,  but  generally  it  is  chronic  from  the  outset.  The 
jjatients  complain  of  abdominal  pains,  with  alternate  diarrhoea  and  (u)n- 
stipation.  The  abdomen  is  sensitive  to  pressure  ;  meteorism  and  ascites 
are  present.  The  peritoneal  effusion  is  not  abundant,  and  exploration  of 
the  abdomen  reveals  a  feeling  of  induration,  especially  in  the  umbilical 
and  hyi)ogastric  regions.  The  induration  is  due  to  matting  of  the  intestinal 
coils.     The  fibroid  thickening  of  the  omentum  gives  rise  to  an  omental 


842  TEXT-BOOK  OF  MEDICINE 

band,  stretcliing  transversely  from  one  hypochondrium  to  the  other.  The 
Hquid  in  the  peritoneal  cavity  does  not  vary  in  position,  and  is  often  encysted 
by  the  false  membranes.  At  the  points  where  the  membranes  glide  over  one 
another  a  kind  of  rustling  is  perceptible  both  on  palpation  and  auscultation. 

The  digestive  functions  are  impaired  from  the  first  (vomiting,  diarrhoea, 
and  Hentery) ;  the  appetite  fails,  and  progressive  wasting  follows.  The 
general  symptoms  of  fever,  sweating,  oedema,  and  cachexia  are  especially 
marked  when  phthisis  is  also  present.  The  course  and  duration  of  the 
disease  depend  greatly  on  the  state  of  the  lungs.  Chronic  tubercular 
peritonitis  runs  a  slow  course,  that  is  sometimes  interrupted  by  subacute 
attacks.  It  lasts  from  one  to  two  years,  and  often  has  a  fatal  ending,  but 
recovery  is  possible  when  the  disease  is  limited  to  the  abdomen,  and  the 
lung  remains  healthy. 

Peritoneal  Abscesses  and  Fsecal  Fistulae.  —  During  the  course  of 
chronic  peritonitis  fistulse  and  peritoneal  abscesses  may  form  in  the  neigh- 
bourhood of  the  liver,  of  the  spleen,  of  the  caecum,  in  the  pelvis,  in  the 
omentum,  or  between  two  intestinal  coils.  These  encysted  abscesses  contain 
pus  and  caseous  matter.  Fever  and  other  symptoms  may  be  absent,  as 
in  a  cold  abscess.  The  fever  often  declares  itself  with  rigors,  evening  rise 
of  temperature,  pain,  and  vomiting.  These  infectious  attacks  may  ter- 
minate in  resolution,  but  they  more  often  end  in  the  perforation  of  a  neigh- 
bouring organ,  and  the  evacuation  of  the  focus  by  the  ileum,  colon,  caecum, 
or  bronchi. 

In  some  cases  the  intestinal  matter  enters  the  open  fistula,  and  makes 
its  exit  in  the  umbilical  region,  or  elsewhere.  Cutaneous  fistulae,  dis- 
charging faecal  and  purulent  matter,  are  thus  formed. 

Intestinal  Occlusion. — Lejars,  in  speaking  of  the  causes  of  faecal  obstruc- 
tion in  the  course  of  tubercular  peritonitis,  describes  four  kinds.  In  the 
first  variety  the  intestinal  occlusion  is  due  to  a  band  which  strangles  the 
intestine.  These  fibrous  bands  are  very  common  in  tubercular  peritonitis. 
The  strangulation  may  affect  the  small  or  the  large  intestine.  Occlusion  by 
a  band  may  supervene  at  any  stage  of  tubercular  peritonitis  ;  it  may  be  the 
first  indication  of  tubercular  peritonitis  which  has  been  previously  latent. 
Occlusion  may  also  occur  when  the  tubercular  peritonitis  is  cured,  the 
fibrous  band  being  a  relic  of  the  peritonitis,  as  in  the  following  case  : 

A  young  woman  had  been  operated  on  by  Marchant  and  cured.  Four  years  later 
slie  came  to  me  at  the  Necker  Hospital  for  intestinal  occlusion.  An  operation  was 
performed  by  Routier,  who  found  strangulation  due  to  a  band,  and  the  patient  recovered. 

In  the  second  variety  we  have  intestinal  occlusion  by  kinking  of  the 
intestine.  Lejars  has  figured  a  very  good  illustration  of  this,  in  which  the 
intestine  is  astride  a  band,  occlusion  being  the  result.  Here  also  the  symp- 
toms of  occlusion  were  the  first  sign  of  latent  tubercular  peritonitis. 


DISEASES  OF  THE  PERITONEUM  843 

In  the  third  variety  the  occlusion  is  due  to  matting  of  the  intestinal 
coils.  In  this  matted  lump  we  find  adhesions,  bands,  kinks,  and  com- 
pression by  tubercular  masses  or  by  an  encysted  collection.  Surgical 
intervention,  which  is  so  favourable  in  the  preceding  varieties,  is  here 
rarely  successful. 

In  the  last  variety  intestinal  paralysis  is  present.  The  faecal  matter 
no  longer  passes,  owing  to  the  absence  of  peristalsis,  and  we  have  a  pseudo- 
strangulation — frequent,  by  the  way,  in  all  varieties  of  peritonitis. 

The  symptoms  of  intestinal  occlusion  in  tubercular  peritonitis  may  be 
sudden  or  slow  in  their  appearance  (Lejars).  When  this  occlusion  takes 
place  suddenly,  it  is  almost  always  the  first  signal  of  latent  tuberculosis 
of  the  peritoneum.  "  The  patient  is  seized  suddenly  with  intestinal  occlu- 
sion, and  there  is  no  suspicion  of  tubercular  peritonitis.  The  abdomen  is 
opened,  and  we  fuid  a  band,  a  kink,  paralysis  of  the  intestine,  or  a  crop  of 
tubercular  granulations,  especially  in  the  parietal  layer  of  the  peritoneum." 
This  proves  once  more  that  tubercular  peritonitis  is  often  latent  during  the 
first  phase  of  its  evolution.  The  symptoms  of  sudden  occlusion  are  com- 
plete arrest  of  faeces  and  gas,  ballooning  of  the  abdomen,  vomit  of  varying 
composition  including  faecal  matter,  abdominal  pains,  and  subnormal  tem- 
perature. Nevertheless,  tympanites  and  faecal  vomiting  may  be  absent  if 
the  intestinal  occlusion  is  very  high  up,  as  in  the  duodenum,  for  example. 

Intestinal  occlusion  of  the  slow  type  is  chiefly  seen  in  confirmed  tuber- 
cular peritonitis.  It  commences  with  constipation,  and  tympanites  then 
sets  in.  Temporary  improvement  occurs  after  each  fresh  attack.  The 
situation  becomes  worse,  and  the  occlusion  complete.  This  slow  form  is 
almost  always  due  to  matting  of  the  intestines,  and  offers,  therefore,  less 
chance  to  the  operator  than  the  preceding  variety. 

Diagnosis. — While  the  diagnosis  of  chronic  tubercular  peritonitis  is 
very  difficult  at  first,  it  is  far  more  difficult  later,  when  the  abdominal  walls 
become  deformed,  and  indurations  appear,  with  or  without  ascites.  Tuber- 
cular peritonitis  is  sometimes  so  insidious  that  it  is  hard  to  define  its 
existence,  because  the  patient's  health  is  excellent,  and  the  lungs  appear  to 
be  healthy. 

We  shall  see  later  that  the  distinction  between  hydatid  cysts  of  the 
peritoneum  and  tubercular  peritonitis  is  sometimes  very  difficult. 

Chronic  tubercular  peritonitis  is  not  to  be  confounded  with  the  peri- 
tonitis of  alcoholics,  and  with  the  rare  cases  of  peritonitis  in  Bright's  disease. 

When  the  effusion  is  great,  symptomatic  ascites  from  atrophic  cir- 
rhosis may  be  thought  of.  In  cirrhosis  the  ascites  is  not  encysttMl,  the 
fluctuation  is  not  limited,  and  the  collateral  circulation  is  well  marked  ; 
the  liver  is  small,  and  the  sj)lcen  is  hypertrophied.  On  the  other  hand,  in 
the   ascitic  form   of   tubercular  peritonitis   the   indurated   and  retracted 


844  TEXT-BOOK  OF  MEDICINE 

omentum  sometimes  gives  the  feeling  of  a  tense  band  in  the  umbilical 
region  (Aran),  Finally,  it  must  be  remembered  that  tubercular  peritonitis 
and  cirrhotic  tuberculosis  of  the  liver  may  coincide,  and  the  diagnosis  is 
then  particularly  difficult  (Hanot). 

In  the  dry  form  of  the  disease  the  masses  of  false  membranes  or  the 
matted  intestinal  coils  may  simulate  a  sohd  tumour  or  an  ovarian  cyst. 
The  diagnosis  from  ovarian  cyst,  though  generally  easy,  is  in  certain  cases 
a  matter  of  great  difficulty.  It  will  be  sufficient  to  recall  the  celebrated 
case  of  Spencer  Wells,  who  performed  laparotomy  for  an  ovarian  cyst,  and 
found  tubercular  peritonitis.  The  fluid  was  evacuated,  the  wound  sutured, 
and  the  patient  recovered. 

We  must  also  exclude  cancer  of  the  peritoneum.  In  this  case  the  yellow, 
straw  tint  is  characteristic,  the  inguinal  glands  are  often  enlarged,  the 
abdominal  pains  are  very  sharp,  and  if  elusion  supervenes,  it  is  generally 
hsemorrhagic. 

etiology. — Tubercular  peritonitis  generally  attacks  children  between 
six  and  twelve  years  of  age.  It  is  not  uncommon  in  adults,  and  especially 
amongst  young  soldiers,  but  it  is  exceptional  in  old  people.  Privation, 
overwork,  insufficient  food,  traumatism  of  the  abdominal  region,  chills, 
and  alcoholism  favour  the  onset  of  the  disease. 

Tubercular  peritonitis  is  due  to  Koch's  bacillus.  How  does  the  tubercle 
bacillus  reach  the  peritoneum  ? 

When  I  undertook  the  discussion  of  this  subject  at  the  Faculte,  I  had 
arrived  at  the  same  conclusion  as  Marfan  :  It  seems  at  first  sight  that  the 
tubercular  ulcers  in  the  intestine  would  be  the  most  likely  point  of  origin 
for  peritonitis.  This  opinion  has  been  upheld  by  many  authors  (Grancher, 
Koenig),  and  yet  I  cannot  accept  it.  However  paradoxical  the  assertion  may 
seem,  I  do  not  think  that  the  peritonitis  arises  from  the  lesions  in  the  intestine. 
Clinical  medicine  teaches  us  that  many  patients  suffer  from  tubercular 
peritonitis,  and  yet  they  present  none  of  the  symptoms  of  tubercular  enteritis. 
On  the  other  hand,  we  find  tubercular  enteritis  in  phthisical  patients  who 
do  not  suffer  from  peritonitis. 

Pathological  anatomy  teaches  us  that  most  phthisical  patients  who  die 
with  ulcers  in  the  gut  have  neither  general  nor  local  peritonitis.  We  cer- 
tainly find  infected  lymphatics  proceeding  from  the  intestinal  ulcers,  as 
well  as  chains  of  caseating  mesenteric  glands,  but  no  peritonitis — or, 
at  least,  only  slight  traces  of  peritonitis — are  met  with.  In  favour  of  this 
assertion,  I  know  of  no  more  convincing  argument  than  the  work  of  Tchisto- 
vitch.  In  his  monograph  on  "  Intestinal  Tuberculosis  in  Man,"  Tchistovitch, 
although  he  is  not  dealing  with  peritoneal  tuberculosis,  discusses  the  way  in 
which  intestinal  infection  is  brought  about,  and  the  migration  of  the  tubercle 
bacilli  through  the  intestinal  walls  is  effected  by  way  of  the  lymphatics. 


DISEASES  OF  THE  PERITONEUM  845 

I  have  studied  the  account  of  the  autopsies  on  which  this  work  is  based, 
and  I  find  that  the  intestine  (ileum,  caecum,  large  intestine)  was  the  seat 
of  deep,  extensive,  and  serpiginous  tubercular  ulcers  in  seven  cases ;  but 
though  they  were  in  appearance  so  favourable  to  the  development  of  tuber- 
cular peritonitis,  no  trace  of  it  was  present.  In  the  three  other  cases,  in 
which  no  tubercular  lesion  of  the  intestine  was  found,  tubercular  peritonitis 
was  present.  It  is  true  that  in  these  three  last  cases  tubercular  pleurisy 
(pleuro-peritoneal  tuberculosis)  was  also  present. 

From  a  careful  study  of  these  ten  autopsies  I  draw  the  following  con- 
clusions :  chronic  tubercular  peritonitis  is  not  brought  on  by  intestinal 
tuberculosis,  and  the  infection  travels  from  the  pleura  to  the  peritoneum 
by  the  lymphatics  which  pass  through  the  diaphragm. 

Treatment. — We  must  remember  that  chronic  tubercular  peritonitis, 
when  primary,  is  often  cured  without  surgical  intervention  by  hygienic 
and  medicinal  measures  (superaUmentation,  injections  of  cacodylate  of 
soda,  etc.).  When  I  say  that  chronic  tubercular  peritonitis  is  often  curable 
by  medical  and  hygienic  means,  I  include  both  the  ascitic  form  seen  in 
young  subjects,  and  also  tubercular  peritonitis  in  adults,  in  whom  we  find 
peritoneal  effusion,  fibro-caseous  lesions  in  the  omentum  and  mesentery, 
peritoneal  thickening,  and  intestinal  matting. 

I  remember  a  cavalry  officer  who  suffered  from  chronic  peritonitis,  with  peritoneal 
abscess  and  a  peri-umbilical  fistula.  He  was  completely  cured.  A  few  years  ago,  in 
company  with  Berger  and  Barth,  I  saw  a  young  girl  suffering  from  chronic  peritonitis, 
with  peritoneal  matting  and  false  fluctuation  in  the  right  iUac  fossa,  and  all  these  lesions 
ended  in  a  cure  without  any  surgical  intervention.  For  some  two  years  I  attended  a 
young  woman  suffering  from  chronic  tubercular  peritonitis.  In  this  case  hygienic 
measures,  cod-liver  oil  in  large  doses,  salt  baths,  and  superalimentation  brought  about 
marked  improvement.  In  consultation  with  Hammonic,  I  saw  a  young  girl  with 
chronic  tubercular  peritonitis  of  a  febrile  type  and  grave  prognosis,  but  she  is  now 
convalescent. 

In  other  circumstances,  however,  surgical  intervention  is  indicated. 
The  question  has  been  ably  discussed  by  Legueu,  whose  conclusions  are  : 
The  ascitic  type  of  chronic  and  subacute  peritonitis  is  naturally  the  one  in 
which  the  best  results  are  obtained.  In  children  below  fifteen  years  of  age, 
40  operations  resulted  in  35  cures,  4  of  which  remained  so  after  one  year, 
1  after  two  years,  and  2  after  fourteen  years.  In  adults,  out  of  131  cases, 
99  cures  were  obtained,  56  of  which  remained  so  after  one  year  and  25  after 
two  years.  Out  of  the  total  cures  (children  and  adults),  recurrences  have 
been  observed  seventeen  times. 

The  fibro-caseous  type  is  less  suited  to  surgical  intervention.  Out  of 
twenty-two  patients  operated  upon,  thirteen  were  cured,  and  in  several  in- 
stances the  cure  has  been  perfect,  except  for  a  faecal  fistula.  The  sclero- 
adhesive  type  gave,  on  an  average,  a  cure  in  a  third  of  the  cases. 


846  TEXT-BOOK  OF  MEDICINE 

Summary. — In  well-selected  cases,  when  the  indications  are  well- 
defined,  surgical  intervention  has  given  most  encouraging  successes,  and 
saves  patients  from  certam  death.  There  are,  however,  cases  in  which 
laparotomy  is  not  indispensable,  and  tapping  of  the  peritoneum,  followed 
by  injections  of  various  kinds,  has  given  good  results. 

In  1890  Debove  reported  a  case  of  tubercular  peritonitis  cured  by  tap- 
ping and  the  injection  of  3  pints  of  a  warm  saturated  solution  of  boric  acid. 
In  1893  Rendu  reported  a  case  of  peritoneal  tuberculosis  cured  by  injections 
of  camphorated  naphthol.  In  1895  Caubert  obtained  a  cure  by  means  of 
lavage  with  steriHzed  water  at  a  temperature  of  115°  F.  I  would  add,  how- 
ever, that  medicated  injections  into  the  peritoneum  are  to  be  avoided  as 
a  routine  practice. 

IV.  PRIMARY  PNEUMOCOCCAL  PERITONITIS— ASSOCIATION 
OF  THE  COLI  BACILLUS. 

Pneumococcal  peritonitis  is  almost  always  primary,  especially  in 
children.  It  breaks  out  in  healthy  subjects  who  have  had  no  other  pneumo- 
coccal infection.  The  secondary  form,  which  is  far  less  common,  is  most 
often  met  with  in  adults.  A  moment's  thought  will  show  how  exceptional 
is  the  appearance  of  pneumococcal  peritonitis  in  pleurisy  or  pneumonia. 
I  have  seen  it  twice  in  patients  suffering  from  general  pneumococcia.  In 
one  of  the  patients  we  were  able  to  prove  that  the  peritonitis  was  on  the 
road  to  recovery,  thus  showing  that  the  secondary  form  may  terminate  by 
resolution.  Secondary  peritonitis  figures  only  in  five  out  of  twenty-seven 
cases  which  I  have  collected,  the  peritonitis  being  primary  in  twenty-two. 

This  is  not  because  the  pneumococcus  does  not  reach  the  peritoneum. 
In  many  fatal  cases  of  pneumonia  the  pneumococcus  has  been  found  in  the 
peritoneum.  But  it  seems,  says  Boulay,  that  this  serous  membrane  opposes 
the  development  of  the  pneumococcus,  or,  at  least,  that  the  microbe  does 
not  flourish  on  it.  Thus,  in  a  man  already  infected  with  a  pneumococcal 
lesion,  the  pneumococcus  may  emigrate  to  the  peritoneum,  but  it  does  not 
cause  peritonitis.  A  similar  thing  occurs  in  experiments.  An  animal  dies 
after  inoculation,  and  though  pneumococci  are  found  in  its  peritoneum, 
no  peritonitis  is  present.  When  pneumococci  are  injected  into  the  peri- 
toneum of  a  guinea-pig  or  of  a  rabbit,  the  animal  dies  of  general  infection, 
but  peritonitis  is  usually  absent. 

The  following  case  *  is  one  of  primary  pneumococcal  peritonitis  : 

A  little  girl  eight  years  of  age  was  in  perfect  health  on  November  25,  1896.     She 
ate  her  supper  and  went  to  bed  at  nine  o'clock.     About  two  o'clock  in  the  morning 

*  This  case  is  taken  from  my  lecture  on  "  Pneumococcal  Peritonitis  "  {Clinique 
Medicale  de  V Hotd-Dieu,  p.  396). 


DISEASES  OF  THE  PERITONEUM  847 

she  was  awakened  by  sharp  pain  in  the  belly,  and  commenced  to  vomit.  The  vomiting 
was  incessant.  At  first  food  and  then  bile  were  rejected,  but  later  the  vomit  became 
greenish.  Profuse  diarrhcea  soon  appeared,  the  motions  being  very  frequent.  Dr. 
Schmidt  saw  the  patient,  whose  symptoms  led  him  to  think  of  appendicitis.  The 
presence  of  the  diarrhcea  and  the  absence  of  well-defined  local  symptoms  in  the  appen- 
dicular region  induced  him  to  reserve  his  diagnosis.  Next  day  the  child  was  able  to 
get  a  few  hours'  sleep  ;  the  vomiting  ceased,  but  the  diarrhcea  persisted.  On  the  morning 
of  the  27th  the  child's  temperature  stood  at  100-5°  F.  Renon,  who  saw  her  at  six  in 
the  evening,  foimd  the  belly  sUghtly  distended,  with  general  tenderness  on  pressure. 
The  diarrhcea  persisted.  In  spite  of  the  absence  of  spots,  the  possibiHty  of  tyjjhoid 
fever  was  thought  of,  and  cold  compresses  were  appUed  to  the  abdomen.  On  the  28th 
the  diarrhoea  still  persisted.  The  general  condition  was  satisfactory,  and  the  tempera- 
ture morning  and  evening  was  101°  F.  On  the  29th  rectal  tenesmus,  which  came  on 
two  evenings  previously,  became  so  painful  that  it  provoked  a  desire  to  stool  five  or 
six  times  every  hour.  The  pains  in  the  abdomen  were  stationary,  and  the  urine  did 
not  contain  albumin.  Typhoid  fever  was  feared  more  and  more,  and  to  decide  the 
point  sero-diagnosis  was  performed,  with  a  negative  result. 

What  was  the  matter  with  the  child  ?  The  disease  continued  its  course.  During 
the  early  days  of  December,  the  abdomen  being  more  distended  and  indurated,  espe- 
cially in  the  right  iliac  fossa,  the  diagnosis  was  appendicitis  complicated  with  a  csecal 
abscess.  I  was  oalled  in  consultation  with  Routier,  and  on  December  13  we  went  to 
see  the  little  patient,  \dth  Schmidt  and  Renon.  "When  I  saAv  the  child  I  was  surprised 
to  find  her  looking  so  well.  She  certainly  had  no  peritoneal  facies,  and  gave  accurate 
information  concerning  her  condition.  The  abdomen  was  more  distended  on  the  right 
side  than  on  the  left.  The  impaired  resonance  was  extensive,  but  it  was  difficult  to 
define.  Palpation  gave  the  sensation  of  a  huge  liquid  collection,  which  bulged  under 
pressure.  From  the  onset  and  the  course  of  the  disease  I  suggested  pneumococcal 
peritonitis,  basing  my  diagnosis  on  the  age  of  the  child,  the  sudden  onset  of  the  disease, 
the  diarrhoea,  and  the  presence  of  a  peritoneal  collection,  which,  though  extensive, 
seemed  to  have  a  tendency  to  become  locahzed.  I  suggested  an  exploratory  puncture 
in  order  to  ascertain  the  virulence  of  tlie  pneumococcus.  The  puncture  was  made  on 
the  following  day,  December  14,  at  eight  o'clock  in  the  morning  by  Routier,  who  drew 
off  2  pints  of  creamy  pus.  It  was  homogeneous,  greenish,  odourless,  and  contained  a 
number  of  fibrinous  flakes.  The  bacteriological  examination,  which  was  carried  out 
an  hour  later,  revealed  the  presence  of  the  pneumococcus  in  a  pure  state.  A  mouse 
inoculated  -nath  two  drops  of  pus  died  in  forty-eight  hours,  and  its  blood  contained 
pneumococci.  The  diagnosis  of  pneumococcal  peritonitis  having  been  verified,  we 
decided  to  perform  immediate  laparotomy,  and  Routier  did  so.  A  few  weeks  later  I 
saw  the  child,  who  had  completely  recovered. 

Description. — Pneumococcal  peritonitis  is  rare  in  the  adult,  and  I  find 
it  noted  only  five  times  in  twenty-seven  cases.  It  is  especially  frequent 
between  the  ages  of  three  and  twelve  years,  and  is  far  more  common  in 
girls  than  boys.  This  difference  may  perhaps  be  due  to  vulvitis  (Marfan), 
which  has  been  noticed  in  several  cases.  On  the  other  hand,  as  the  pneumo- 
coccus has  been  found  in  the  uterine  cavity  (Boulay),  "  it  is  permissible  to 
ask,"  says  Brun,  "  whether  pneumococcal  peritonitis  does  not  have  the  same 
pathogenesis  as  other  kinds  of  peritonitis — passage  of  the  micro-organisms 
from  the  uterus  into  the  peritoneal  cavity  by  the  lymphatics  or  by  the 
tubes.  However  hypothetical  tliis  opinion  may  be,  it  may  rest  on  this 
fact — that  in  all  cases  where  the  locahzation  of  the  le-sions  has  been  clearly 


848  TEXT-BOOK  OF  MEDICINE 

defined,  it  is  always  in  tlie  lower  portion  of  the  serous  membrane,  the  iliac 
fossa,  and  the  true  pelvis,  that  they  are  met  with."  However  seductive 
this  theory  may  be,  it  takes  no  account  of  pneumococcal  peritonitis  in 
boys. 

The  present  description  refers  to  primary  pneumococcal  j)eritonitis  in 
children,  for  the  disease  behaves  somewhat  differently  in  adults,  being  more 
frequently  secondary,  and  more  subject  to  extra-peritoneal  complications ; 
it  may  be  accompanied  by  multiple  thromboses  (Sylvian,  radial,  and  popUteal 
arteries). 

The  first  point  to  mention  is  the  sudden  onset,  in  the  midst  of  excellent 
health,  with  sharp  pain  in  the  belly,  comparable  to  the  pain  in  the  side 
of  pneumonia.  The  cases  collected  in  my  clinical  lecture  show  in  almost 
every  instance  this  sudden  onset,  with  pain  and  fever.  The  little  patient 
to  whom  I  have  referred  had  eaten  a  good  supper,  and  had  gone  to  sleep 
quietly  about  nine  o'clock.  About  two  o'clock  in  the  morning  she  was 
awakened  by  sharp  abdominal  pain,  followed  by  vomiting. 

Let  the  pain  be  situated  in  the  right  iliac  fossa,  as  it  often  is,  and  it  is 
clear  that  at  first  sight  pneumococcal  peritonitis,  with  its  pain  and  vomiting, 
closely  simulates  appendicitis.  We  shall  see  later  how  to  differentiate  them. 
The  onset  of  the  disease  is  generally  accompanied  by  fever.  The  sudden 
rise  in  temperature  (102°  or  103°  F.)  has  even  been  compared  with  the 
similar  rise  of  temperature  in  pneumonia.  The  comparison  is  not  absolutely 
justified,  for  though  there  are  cases  of  peritonitis  in, which  the  temperature 
is  raised  from  the  outset,  there  are  others  in  which  during  the  first  two  days 
the  temperature  is  not  above  99°  F. 

The  onset  of  pneumococcal  peritonitis  is  further  characterized  by 
vomiting  of  food  and  bile,  which  is  never  absent,  and  which  may  be  incessant. 
I  do  not  find  hiccough  mentioned  in  any  of  these  cases — a  strange  fact, 
because  it  is  a  common  symptom  in  other  kinds  of  peritonitis.  On  the 
other  hand,  in  almost  every  case  there  is  special  mention  of  diarrhoea, 
which  is  a  very  exceptional  symptom  in  other  forms  of  peritonitis.  Though 
I  am  unable  to  explain  the  cause  of  this  diarrhoea,  it  is  certain  that  its 
constancy  and  its  characteristics  are  important  in  pneumococcal  peritonitis. 
It  has  an  especial  value  from  a  diagnostic  point  of  view. 

It  may,  consequently,  be  said  that  pain  in  the  belly,  vomiting,  and 
diarrhoea,  with  more  or  less  high  fever,  form  the  characteristic  syndrome 
01  pneumococcal  peritonitis,  and  the  recognition  of  this  syndrome  simpUfies 
the  diagnosis  considerably.  The  early  diagnosis  of  pneumococcal  peritonitis 
is  not  free  from  difficulties,  chiefly  because  we  are  liable  to  forget  it.  The 
onset  is  much  like  that  of  appendicitis,  and  in  most  cases  appendicitis  is  at 
first  thought  of.  This  is  the  more  easily  understood  as  the  early  age  at 
which  pneumococcal  peritonitis  is  see.n  is  the  usual  age  for  appendicitis, 


DISEASES  OF  THE  PERITONEUxM  849 

Nevertheless,  close  inspection  shows  that  there  is  a  difference  between 
the  two  affections.  Though  the  pain  of  pneumococcal  peritonitis  may 
commence  in  the  ihac  region,  it  is  not,  as  a  rule,  clearly  marked  at  McBurney's 
point.  Furthermore,  diarrhoea,  which  is  hardly  ever  absent  at  the  onset 
of  pneumococcal  peritonitis,  is  very  rare  in  appendicitis. 

Evolution  of  Pneumococcal  Peritonitis. — For  some  days  the  symp- 
toms show  but  Httle  change.  The  temperature  is  about  102°  F.,  the  ab- 
dominal pain  may  persist  or  grow  less,  and  the  fits  of  vomiting  may  cease  ; 
but  the  diarrhoea,  as  a  rule,  continues.  On  the  fourth,  fifth,  or  sixth  day 
of  the  disease  we  find  fever,  diarrhoea,  abdominal  pains,  and  ballooning 
of  the  belly ;  but  if  we  take  care  to  find  out  our  position  by  considering  the 
syndrome  of  the  onset,  the  idea  of  typhoid  fever  may  be  dismissed.  It 
must  be  admitted  that  this  diagnosis  might  be  somewhat  embarrassing 
— at  least,  for  a  few  days — did  not  Widal's  sero- diagnosis  remove  all  doubt. 

As  the  disease  goes  on  new  symptoms  appear.  In  this  phase  the  fever 
has  sometimes  disappeared  ;  it  may,  indeed,  have  ceased  as  suddenly  as  in 
pnemnonia.  This  sudden  defervescence,  considered  by  some  authors  as  a 
sign  of  pneumococcal  peritonitis,  is  wanting  in  many  cases.  In  proportion 
as  the  abdomen  becomes  swollen,  the  dullness  generally  limits  itself  to  the 
hypogastric  region  and  to  the  flank^.  Palpation  reveals  induration  and 
resistance  in  the  same  region,  and  fluid  is  noticed.  The  diagnosis  of  peri- 
tonitis is  then  obvious,  and  if  the  peritonitis  is  limited  to  the  right  iho- 
inguinal  region,  the  diagnosis  of  appendicitis  with  peritoneal  abscess  is 
naturally  made.  One  sign  at  this  period  of  the  disease  is,  however,  of  great 
value — viz.,  the  unfolding  of  the  umbilicus,  which  becomes  red  and  prom- 
inent.    The  abscess  bursts,  giving  exit  to  a  variable  quantity  of  pus. 

In  many  cases  pneumococcal  peritonitis  causes  an  umbilical  fistula. 
Three,  four,  or  five  weeks  after  the  onset,  a  reddish,  shi-ny,  fluctuating  swell- 
ing of  the  size  of  a  nut  appears  in  the  umbilical  region.  If  intervention  is 
delayed,  the  abscess  opens,  and  the  pus  in  the  peritoneum  is  evacuated,  so 
to  say,  by  a  "  peritoneal  vomica."  The  pus  is  generally  greenish,  creamy, 
inodorous,  and  mixed  with  false  membranes.  Spontaneous  opening  at 
the  umbilicus  is  found  in  half  the  cases,  but  it  might  be  avoided  by  timely 
operation.  In  some  cases  spontaneous  opening  has  occurred  not  only  at 
the  umbilicus,  but  also  in  the  vagina  (Brun,  Pochon).  The  fluid  is  some- 
times very  abundant,  and  as  much  as  5  pints  have  been  found  in  the  abdomen 
of  a  child  eight  years  of  age.  The  fluid  has  not,  however,  the  mobility  of 
ascitic  fluid,  and  collects  in  foci,  limited  by  thick  false  membranes. 

Primary  pneumococcal  j^eritonitis  may  be  cured  by  spontaneous  evacua 
tion  of  the  pus,  just  as  some  cases  of  purlent  pleurisy  recover  by  vomical 
In  loss  favourable  cases  it  causes  pneumonia,  pleurisy,  endopericarditis,  or 
otitis,  and  death  is  the  result.     Hence  the  rule  of  operating  in  pneumococca. 

54 


850  TEXT-BOOK  OF  MEDICINE 

peritonitis  before  the  infection  has  had  time  to  become  general.  In  some 
cases  the  disease,  if  left  to  itself,  drags  on :  the  pus  does  not  make  its  exit, 
the  abdomen  remains  large,  and  the  fever  returns  every  evening,  while  the 
child  grows  thin  and  cachectic,  as  in  phthisis  (Brun).  Tubercular  peri- 
tonitis is  incorrectly  diagnosed,  and,  for  want  of  proper  information  or  of 
timely  operation,  the  patient  is  allowed  to  die. 

Such  is  the  course  of  pneumococcal  peritonitis.  I  have  already*  indi- 
cated the  diagnosis  in  each  stage  of  the  disease,  but  I  return  to  this  subject 
in  order  to  add  a  few  words.  Sudden  onset,  very  sharp  pain  in  the  belly, 
vomiting  of  food  and  bile,  abundant  and  foetid  diarrhcsa,  and  rise  of  tem- 
perature, form  the  syndrome  characterizing  the  onset  of  pneumococcal  peri- 
tonitis. This  syndrome  is  not  found  in  other  peritoneal  diseases,  and  must, 
therefore,  be  our  guide  at  every  stage  of  the  malady.  As  SOOn  as  the 
peritoneal  fluid  is  appreciable,  we  must  employ  an  exploratory  aspiration, 
and  look  for  the  pneumococcus. 

Pneumococcal  peritonitis  is  often  encysted,  the  purulent  collection 
occupying  one  large  or  several  pockets.  The  surgeon  must  not  forget 
this  fact  at  the  time  of  the  operation.  In  one  of  Brun's  cases  the  abdominal 
viscera  were  covered  on  their  anterior  surface  with  an  extensive  false  mem- 
brane, thicker  in  the  lateral  than  in  the  middle  portions,  and  circumscribing 
a  large  suppurating  cavity  that  extended  upwards  and  to  the  left  as  far  as 
the  diaphragm,  upwards  and  to  the  right  as  far  as  the  anterior  edge  of  the 
liver,  and  descended  into  the  pelvis  as  far  as  the  lowest  part  of  Douglas's 
pouch.  In  Brault's  case  the  peritonitis  occupied  the  right  lower  half  of 
the  abdomen.  In  Sevestre's  case  the  peritonitis  was  encysted  below  the 
umbilicus.  In  Gaillard's  case  the  peritonitis  was  encysted,  and  Jalaguier 
had  to  open  several  pockets. 

The  peritoneal  fluid  is  greenish,  thick,  creamy,  and  fibrino-purulent, 
and  has  all  the  characteristics  of  pneumococcal  pus.  In  one  case,  however, 
it  was  not  purulent,  but  sero-fibrinous  (Weichselbaum's  case),  an  exception 
also  found  in  pneumococcal  pleurisy  which  may  not  be  purulent.  Numerous 
flakes  and  thick  membranes  float  in  the  fluid. 

Very  Grave  Forms. — Although  pneumococcal  peritonitis  is  not  grave 
as  a  rule,  it  may  be  formidable,  as  in  two  cases  reported  by  Brun  : 

A  little  girl  awoke  at  six  o'clock  in  the  morning  with  pain  in  the  abdomen,  vomiting 
and  diarrhoea.  Next  day  the  vomiting  persisted,  and  the  child  was  sent  to  the  hospital. 
The  general  condition  was  bad :  the  facies  was  peritoneal,  the  eyes  were  hollowed,  the 
pulse  was  160,  and  the  temperature  100°  F.  The  belly  was  slightly  ballooned,  but 
tense  and  painful,  especially  on  the  right  side.  Immediate  intervention  was  decided 
upon.  The  disease  was  of  three  days'  duration,  and  Brun  found  in  the  peritoneum  a 
small  quantity  of  odourless,  turbid  fluid,  and  some  false  membranes  over  the  intestinal 
coils.  The  appendix,  which  was  apparently  healthy,  was  resected.  After  the  opera- 
tion an  injection  of  serum  was  given.     The  little  patient  passed  a  very  restless  night, 


i 


DISEASES  OF  THE  PERITONEUM  851 

and  died  the  next  morning  at  five  o'clock,  on  the  fourth  day  of  the  disease,  the  clinical 
picture  being  that  of  primary  streptococcal  peritonitis. 

At  the  autopsy  hardly  any  fluid  was  found  in  the  peritoneum,  excepting  at  the 
posterior  surface  of  the  stomach  and  on  a  level  with  the  spleen,  where  greenish  pus  was 
discovered.  False  membranes  were  scattered  over  part  of  the  abdomen,  the  mesentery 
was  packed  wi£h  glands,  and  the  right  tube  was  congested.  False  membranes  covered 
the  right  pleura,  but  were,  however,  less  abundant  than  in  the  peritoneum.  The  lungs 
were  healthy.  The  histological  examination  of  the  appendix  proved  its  healthy  con- 
dition. 

The  bacteriological  examination  of  the  pus  was  made  by  Zuber,  and  on  the  sUdes 
he  found  only  encapsuled,  lanceolated  diplococci,  which  stained  by  Gram.  The  pus. 
sown  on  the  surface  of  agar-tubes,  after  successive  dilutions,  produced  colonies  of  the 
same  diplococci.  This  pus,  sown  in  the  deeper  parts  of  the  agar-tubes  for  the  purpose 
of  demonstrating  anaerobic  microbes,  gave  colonies  of  this  same  diplococcus.  The 
inoculation  of  the  pus  under  the  skin  of  the  thigh  in  a  mouse  caused  death  in  twenty- 
four  hours,  and  the  pneumococcus  was  found  in  a  state  of  purity  in  blood  from  the 
heart.  The  little  girl  succumbed,  then,  to  an  attack  of  primary  pneumococcal  peri- 
tonitis. 

A  little  girl  of  four  years  and  a  half  was  taken  ill  with  sore  throat,  fever,  dysphagia, 
and  headache  on  April  9,  and  a  whitish  exudate  was  also  noticed  on  the  tonsils.  On 
April  14  the  sore  throat  was  better,  but  she  was  then  seized  with  pains  in  the  abdomen 
and  frequent  vomiting.  The  belly  was  ballooned,  and  as  the  symptoms  became  worse, 
she  was  admitted  into  hospital  on  April  16.  Her  condition  was  very  bad  indeed  : 
dyspncea ;  pulse  uncountable  ;  the  eyes  were  surrounded  by  black  circles ;  the  look  was 
dull ;  and  the  belly  was  distended  and  painful,  but  there  were  no  areas  of  dullness.  Half 
an  hour  after  admission  into  hospital  the  child  vomited  copiously,  and  as  she  was  on  the 
point  of  death,  an  injection  of  serum  was  administered.  At  ten  o'clock  Brun  operated. 
On  opening  the  peritoneum  a  small  quantity  of  greenish  odourless  pus  flowed  forth.  This 
small  collection  was  not  seated  around  the  appendix.  The  intestinal  coils  were  covered 
with  thin  false  membranes.  Immediately  after  the  operation  injections  of  serum, 
ether,  and  caffeine  were  administered.  The  patient  died  on  the  afternoon  of  the  third 
day  from  superacute  peritonitis.  The  clinical  picture  in  this  case  was  that  of  primary 
streptococcal  infection  of  the  peritoneum. 

At  the  post-mortem  examination  a  few  spoonfuls  of  pus  were  found  in  the  pelvia, 
and  false  membranes  were  adherent  over  the  whole  of  the  intestine.  The  appendix  was 
normal,  and  all  the  viscera  were  healthy.  Bacteriological  examination  of  the  pus 
removed  during  the  operation  was  made  by  Bernheim,  who  found  only  the  pneumo- 
coccus. 

These  two  cases  of  superacute  peritonitis  differ  in  a  singular  manner 
from  the  ordinary  pneumococcal  peritonitis.  Clinically,  the  early  intensity 
of  the  symptoms,  the  rapidity  of  the  infection,  and  the  extreme  gravity  of 
the  prognosis,  bring  them  into  close  relation  with  streptococcal  peritonitis. 
I  see  only  one  way  of  making  a  rapid  diagnosis,  and  that  is  to  employ  sero- 
diagnosis  at  once  by  Bezan9on  and  Griffon's  method,  as  described  under 
Pneumonia, 

Association  with  the  Bacillus  Coli.— The  pneumococcus  is  the  only 
microbe  in  pneumococcal  peritonitis,  but  at  the  autopsy  the  Bacillus  coli 
which  has  invaded  the  peritoneum  post  mortem  is  often  found.  In  cases 
of  umbilical  fistula  other  microbes  may  also  invade  the  peritoneal  cavity 
(secondary  infection). 

51—2 


852  TEXT-BOOK  OF  MEDICINE 

I  am  not  sure  that  the  Bacillus  coli  may  not  be  associated  with  the 
pneumococcus  during  hfe,  as  the  following  cases  seem  to  show  : 

On  March  16,  1898,  in  consultation  -nath  Blache,  I  saw  a  child  of  nine  years  of  age 
who  had  suffered  for  the  past  few  days  from  abdominal  symptoms.  Several  children  in 
the  same  family  had  been  laid  up  with  influenza,  and  our  patient  had  had  a  slight  attack. 
During  the  night  of  March  14  the  child  awoke  with  pains  in  the  stomach.  Next  day 
the  pains  persisted,  but  had  no  definite  localization.  The  child  vomited,  and  the  tem- 
perature rose  to  102°  F.  On  March  16  I  saw  the  patient  with  Blache.  In  a  child  with 
sharp  pain  in  the  stomach,  fever,  and  vomiting  the  first  thought  is  of  appendicitis. 
In  this  case  local  pain  and  muscular  resistance  were  not  present  at  McBurney's  point. 
The  pain  was  diffused  over  the  lower  abdomen.  The  subumbilical  region  was  prom- 
inent, painful,  and  tympanitic,  but  not  uniformly  resonant.  The  pulse  was  quick,  and 
the  vomiting  continued.  The  child  had  passed  a  bad  night,  and  the  facies  was  changed. 
We  were  face  to  face  with  peritoneal  infection,  but  of  what  kind  ?  The  diagnosis  of 
appendicitis  was  eliminated,  because  the  signs  of  appendicitis  were  absent.  Still,  the 
child  was  suffering  from  peritonitis,  as  shown  by  the  sharp  pain,  vomiting,  fever,  dis- 
tension of  the  abdomen,'  and  subumbilical  tympanites. 

When  a  child  is  suddenly  taken  ill  with  abdominal  pain,  vomiting,  tympanites,  and 
fever,  and  when  he  has  not  appendicitis,  we  must  think  of  primary  pneumococcal  peri- 
tonitis. The  age  of  the  child,  the  sudden  onset,  the  fever,  the  intense  pain,  the  vomit- 
ing, and  the  limitation  of  the  peritonitis  to  the  lower  abdomen,  were  all  in  favour  of 
pneumococcal  peritonitis. 

Diarrhoea  alone  was  lacking  in  the  clinical  picture.  As  a  matter  of  fact,  diarrhoea 
is  usually  present  from  the  onset.  I  said  to  Blache  :  "  If  the  child  had  diarrhoea,  there 
would  not  be  any  hesitation  as  to  the  diagnosis  of  pneumococcal  peritonitis."  Though 
this  peritonitis  is  not  dangerous  in  the  early  stage,  the  idea  of  surgical  intervention 
came  to  my  mind.  We  agreed  to  see  the  child  on  the  following  day.  As  soon  as  I 
arrived,  I  was  told  of  the  appearance  of  the  expected  symptom,  diarrhoea.  During  the 
night  the  child  passed  about  fifteen  yellowish  loose  stools. 

The  malady  was  undoubtedly  primary  pneumococcal  peritonitis.  We  had  then  to 
think  of  operation,  which,  however,  was  not  urgent,  since  pneumococcal  peritonitis  is 
not  as  grave  as  appendicular  and  primary  streptococcal  peritonitis.  The  latter,  even 
from  the  first,  causes  alarming  symptoms  :  drawn  look,  acceleration  of  the  pulse, 
delirium,  and  prostration,  which  rapidly  end  in  collapse.  Moreover;  the  operation 
must  be  performed  early.  As  regards  appendicular  j^eritonitis,  the  danger  does  not 
come  solely  from  the  peritonitis  :  it  comes  from  the  toxi-infection,  which  demands  early 
intervention. 

Pneumococcal  peritonitis  is  quite  different.  We  have  just  seen  that  this  kind  of 
peritonitis  runs  a  somewhat  slow  course,  and  that  patients  operated  upon  on  the  eighth, 
tenth,  or  fifteenth  day  recover.  I  therefore  saw  no  harm  in  postponing  the  operation 
till  the  follo^dng  day  (sixth  day  of  the  disease),  and  I  believe,  too,  that  there  is  no  case 
in  which  the  operation  for  pneumococcal  peritonitis  has  been  performed  before  the 
tenth  or  twelfth  day.  The  operation  was  therefore  fixed  for  the  next  day.  When  I 
arrived  I  was  quite  surprised  to  note  the  change  in  the  patient.  The  child  had  passed  a 
bad  night,  with  insomnia,  restlessness,  and  much  crjdng.  The  facies  was  peritoneal,  the 
pulse  was  much  accelerated,  the  pain  and  tympanites  were  general.  The  condition 
did  not  in  the  slightest  way  resemble  the  first  phase  of  pneumococcal  peritonitis.  Had 
we  made  an  error  in  diagnosis,  and  was  this  peritonitis  not  due  to  the  pneumococcus  ?  A 
doubt  arose  in  my  mind.  As  the  operation  was  urgent,  Routier  performed  it  that  day. 
As  soon  as  the  peritoneal  cavaty  was  opened  we  noticed  the  tainted  odour  indicative 
of  the  Bacillus  coli.  A  large  quantity  of  sero-purulent,  foetid  fluid  flowed  out  from 
the  peritoneal  cavity,  together  with  thick  greenish  fluid  and  fibrinous  membranes. 


DISEASES  OF  THE  PERITONEUM  853 

Routier  asked  himself  whether  the  appendix  was  not  the  origin  of  this  peritonitis. 
It  was,  however,  found  to  be  healthy. 

At  first  sight  the  fibrinous  membranes  and  the  homogeneous  pus  gave  the  idea  of 
pneumococcal  peritonitis.  On  the  other  hand,  the  fcetid  sero-purulent  fluid  bore 
witness  to  peritonitis  caused  by  Bacillus  colt.  Bacteriological  examination  showed  the 
presence  of  both  microbes— pneumococcus  and  Bacillus  coli.  There  were  no  other 
varieties.     The  patient  was  very  ill  for  some  days,  and  then  slowly  recovered. 

We  have  here,  then,  a  case  of  peritonitis  with  mixed  infection  which  occurred  in 
two  stages.  During  the  first  stage  the  peritonitis  was  pneumococcal,  and  was  charac- 
terized by  its  sudden  onset,  pain  and  vomiting,  subumbilical  pain,  and  diarrhoea.  The 
general  condition  was  not  bad,  and  to  look  at  the  child  no  one  would  have  said  that 
he  was  suffering  from  peritonitis.  On  the  fifth  day  the  scene  changed.  The  fades 
grew  peritoneal,  the  general  condition  became  alarming,  and  the  Bacillus  coli  entered 
upon  the  scene. 

What  do  we  actually  know  of  primary  peritonitis  due  to  the  coli  bacillus  ?  Nothing. 
I  do  not  know  of  a  single  published  case.  Of  all  kinds  of  secondary  peritonitis,  peri- 
tonitis due  to  the  Bacillus  coli  is  the  most  frequent.  It  is  the  peritonitis  caused  by 
perforation  of  the  intestine,  and  especially  the  peritonitis  of  appendicitis,  whether 
there  is  perforation  of  the  appendix  or  migration  of  the  microbes  through  the  unper- 
forated  walls  of  the  appendix. 

Such,  however,  was  not  the  case  here.  How,  then,  was  the  poly-infection  to  be 
explained  ?  I  do  not  know.  It  may  be  said  that,  thanks  to  the  pneumococcus,  the 
Bacillus  coli  penetrated  into  the  peritoneal  cavity. 

Charrin  and  Veillon  have  pubhshed  a  case  of  pure  pneumococcal  peritonitis  which 
was  invaded  after  death  by  the  Bacillus  coli,  but  this  microbic  association  did  not 
take  place  during  life,  as  it  did  in  our  patient. 

Treatment. — Pneumococcal  peritonitis  is  often  fatal  if  left  to  itself. 
The  patient  succumbs  from  cachexia  or  from  general  intoxication,  with 
secondary  troubles  in  the  pleura,  lungs,  heart,  etc.,  and  death  is  sometimes 
very  rapid  (Brun's  case).  It  is  therefore  right  to  intervene  at  an  early  date, 
and  not  to  wait  for  secondary  infections.  Numerous  recoveries  have  been 
obtained  by  opportune  surgical  intervention.  The  failures,  on  the  contrary, 
must  be  placed  to  the  debit  of  late  operation.  The  patient  operated  on 
late  succumbs  to  infection  of  the  lungs,  the  pericardium,  or  the  pleura. 
As  soon  as  peritonitis  is  recognized,  we  must  operate. 

It  may  be  asked  if  laparotomy  is  necessary  in  the  case  of  spontaneous 
opening.  Cases  of  cure  are  cited,  but  the  spontaneous  evacuation  of  the 
pus  cannot,  in  my  opinion,  be  relied  upon.  In  this  event  two  complications 
are  to  be  feared — viz.,  the  penetration  of  a  new  and  formidable  microbe, 
such  as  the  streptococcus  or  the  staphylococcus,  into  the  focus,  or  fresh 
infection  in  one  of  the  peritoneal  fistulae  which  have  been  incompletely 
empti('(l.  Early  suff^Mcal  interventiou  is  therefore  the  only  rational  treat- 
ment I'or  imcuuiucoccal  peritonitis. 


854  TEXT-BOOK  OF  MEDICINE 


V.  PRIMARY  STREPTOCOCCAL  PERITONITIS. 

The  following  case  is  taken  from  a  clinical  lecture  on  the  subject  at  the 
Hotel-Dieu  :* 

On  January  9,  1900,  a  young  girl  was  taken  ill  with  "  sore  tlircTat,  accompanied 
by  fever  and  lassitude.  She  kept  her  bed  for  three  days  without  sending  for  a  doctor. 
On  the  12th  she  fancied  she  was  better,  and  got  up,  but  remained  in  her  room.  On 
the  13th  she  drove  out  to  see  a  friend,  but  became  so  ill  that  she  had  to  be  brought 
home.  A  doctor  was  called  in  on  the  14th.  He  thought  it  was  a  case  of  influenza, 
and  advised  the  patient  to  go  into  hospital.  She  passed  a  bad  day  on  the  15th,  and 
came  into  my  ward  the  same  evening.  The  temperature  reached  105°  F.  During  the 
night  she  vomited  porraceous  matter.  The  scene  changed  rapidly,  and  on  the  morning 
of  the  16th,  when  I  came  to  the  hospital,  I  foimd  her  suffering  from  peritonitis.  She 
was  prostrated,  and  incapable  of  giving  any  information,  with  sunken  eyes  and  peri- 
toneal facies.  Tlie  stools  were  liquid,  and  were  passed  unconsciously  ;  the  temperature 
was  103°  F.,  and  the  pulse  uncountable ;  the  extremities  were  cyanosed  and  cold,  and 
collapse  was  imminent. 

The  abdomen  was  slightly  distended,  not  hard  and  retracted,  as  in  peritonitis  due 
to  perforation  of  a  gastric  or  duodenal  ulcer.  It  was  painful  on  exploration,  as  far  as 
could  be  judged  from  the  complaints  of  the  patient.  Arrest  of  faeces  and  flatus  :  blood- 
stained fluid  flowed  from  the  vulva. 

I  diagnosed  superacute  general  peritonitis.  The  uterus  and  its  adnexa  seemed 
healthy.  I  eliminated  the  hypothesis  of  peritonitis  due  to  appendicitis  or  to  perfora- 
tion of  an  ulcer  of  the  stomach  or  duodenum,  and  I  likewise  put  on  one  side  the  idea 
of  pneumococcal  peritonitis,  because  of  the  rapidity  and  severity  of  the  symptoms. 
I  ordered  an  injection  of  artificial  serum,  and  requested  Marion  to  perform  laparotomy. 
The  abdomen  being  opened,  the  great  omentum  was  found  to  be  adlierent,  and  beneath 
it  a  layer  of  non-foetid,  homogeneous,  but  not  very  thick,  pus.  The  coils  of  the  small 
intestine  did  not  form  masses  covered  with  thick  membranes,  as  in  pneumococcal 
peritonitis.  The  appendix  was  healthy.  In  the  pelvis  pus  was  found  around  the 
right  tube,  but  no  salpingitis.  The  adnexa  were  healthy,  the  uterus  was  normal,  and 
Douglas's  pouch  was  blocked  up  by  soft  purulent  adhesions. 

During  the  evening  the  temperature  fell  to  98°  F.,  the  pulse  was  bad,  and  the 
patient  became  collapsed.  She  was  very  restless  during  the  night,  the  temperature 
rose  to  103°  F.,  and  she  died  next  day. 

At  the  post-mortem  examination  we  foimd  general  peritonitis,  but  no  lesion  to 
explain  this  peritonitis.  The  stomach,  uterus,  tubes,  and  ovaries  were  healthy.  The 
gall-bladder  and  the  liver  were  normal.  The  kidneys,  heart,  pleura,  and  the  lungs 
showed  not  the  slightest  lesion — in  short,  as  there  was  not  a  lesion  anywhere, 
primary  peritonitis  was  the  verdict. 

Griffon  made  a  bacteriological  examination  of  the  pus  removed  during  the  opera- 
tion, and  found  only  a  streptococcus  (long  flexuous  chains  without  capsules),  but  not  a 
trace  of  the  pneumococcus. 

The  pus  was  sown  on  agar  broth  and  rabbit  serum.  The  surface  of  the  agar  showed 
a  growth  of  very  fine  colonies,  less  transparent  than  those  of  the  pneumococcus.  There 
were  no  other  foreign  colonies.  The  microscope  showed  that  these  colonies  were 
formed  of  streptococci.  In  the  broth  culture  the  clots  characteristic  of  the  strepto- 
coccus were  seen.  In  the  rabbit's  serum  streptococci  in  long,  flexuous  chains,  without 
capsules,  and  no  pneumococci,  were  found.  The  absence  of  any  other  microbe  during 
the  examination  made  anaerobic  cultures  unnecessary. 

*  Clinique  Medicale  de  l' Hotel-Dieu,  1903,  ll"^  le9on. 


DISEASES  OF  THE  PERITONEUM  855 

Summary. — The  girl  succumbed  in  a  few  days  to  peritonitis,  the  streptococcus 
being  present  alone,  without  other  microbes.  The  intensity  of  the  symptoms  and  the 
superacute  course  of  the  disease  show  how  great  the  virulence  of  the  infection  must 
have  been. 

In  tliis  case,  how  had  the  pathogenic  agents  entered  ?  Can  we  blame  the  angina 
from  which  the  patient  was  suffering  a  few  days  before  ?  As  I  did  not  see  her  before 
the  onset  of  peritonitis,  and  did  not  verify  the  angina,  I  do  not  dare  to  express  an 
opinion  as  to  the  pathogenesis  of  the  peritoneal  infection.  This  hypothesis,  however, 
cannot  be  rejected. 

I  have  collected  a  few  cases  of  primary  streptococcal  peritonitis,  which 
closely  resemble  my  case.  They  will  serve  to  show  the  details  of  this  terrible 
infection. 

The  following  case  was  piibhshed  by  MiUan  and  Herrenschmidt : 

On  June  13,  1899,  at  11  a.m.,  a  young  woman  of  nineteen  years  of  age  was  brought 
to  the  Lariboisiere  Hospital,  and  placed  under  the  charge  of  Landrieux.  She  had  been 
ill  for  a  few  days.  She  was  examined  at  2  p.m.  She  was  lying  on  her  back,  prostrated ; 
the  lips  and  cheeks  were  cyanosed,  the  skin  was  clammy,  the  extremities  were  cold, 
the  pulse  was  uncountable,  the  tongue  was  parched,  the  respiration  was  quick,  and  the 
temperature  was  97°  F. 

The  patient  passed  her  motions  under  her.  The  belly  was  hyperaesthetic  and 
moderately  tympanitic.  No  hiccough,  no  vomiting.  She  was  collapsed,  and  could 
hardly  answer  questions.  We  found  out,  however,  that  she  had  been  ill  for  about  a 
week,  and  that  the  disease  had  commenced  with  a  sore  throat.  As  adynamia  accom- 
panied by  diarrhoea,  distension,  and  abdominal  pain  were  present,  we  thought  of 
typhoid  fever  with  cardiac  failure.  The  'parents  told  us  later  of  the  existence  of  por- 
raceous  vomiting,  with  obstinate  constipation.     The  patient  died  during  the  night. 

At  the  post-mortem  examination  we  found  peritonitis  and  pus  which  was  turbid 
and  not  homogeneous.  A  very  thin  layer  of  fibrin  covered  the  intestinal  coils.  In 
spite  of  a  minute  search,  it  was  impossible  to  discover  any  lesion  to  explain  the  peri- 
tonitis. All  the  organs  were  healthy.  It  was,  therefore,  a  case  of  primary  peritonitis. 
The  bacteriological  examination  proved  that  the  peritonitis  was  streptococcal.  Had 
the  angina  been  the  entrance-gate  of  the  microbe  ?     It  is  possible. 

The  following  case  has  been  pubHshed  by  Meunier  : 

A  young  girl  came  under  the  care  of  Millard.  Two  evenings  prior  to  her  admission 
into  hospital  she  had  suddenly  been  seized  with  a  sharp  rigor,  followed  by  headache, 
prostration,  repeated  vomiting,  and  severe  diarrhoea.  During  the  night  she  became 
deUrious ;  the  restlessness  was  extreme,  and  the  menses,  which  had  appeared  two  days 
previously,  stopped  suddenly.  Next  day  the  vomiting,  diarrhoea,  and  abdominal  pain 
continued.  On  the  third  day  the  .symptoms  became  worse,  and  she  was  admitted  to 
hospital.  The  patient  was  so  weak  that  it  was  impossible  to  take  her  liistory  or  locate 
the  nature  of  the  infection.  Her  lips  were  covered  with  sordcs,  her  face  was  drawn, 
and  her  speech  was  short  and  halting.  The  pulse  was  156  and  tlie  temperature  102°  F. 
The  abdomen  was  nlightly  distended  and  tender  on  pressure  in  the  left  iUac  fossa. 
The  motions  were  liquid  and  passed  under  her.  Nothing  found  on  auscultation  of 
the  heart  and  the  lungs.  The  condition  did  not  alter  tlirough  the  night,  and  on  her 
admission  (fourth  day  of  the  disease)  she  was  completely  prostrated,  with  cold  sweats 
and  cyanosis  of  the  face.     She  died  on  the  fifth  day. 

The  autopsy  revealed  acute  sero-purulont  peritonitis,  ^vith  false  membranes  ;  no 
adhesions,  and  no  matting  of  the  coils.  The  pelvis  contained  some  ounces  of  turbid 
but  uon-fcetid  fluid.     The  case  was,  therefore,  apparently  one  of  primary  peritonitis 


856  TEXT-BOOK  OF  MEDICINE 

Bacteriological  examination  of  the  peritoneal  fluid  taken  away  one  hour  after  death 
showed,  after  staining  with  gentian  violet,  innumerable  little  chains  of  streptococci, 
which  did  not  stain  with  Gram.  Agar  cultures  gave  a  rich  growth,  having  all  the 
characteristics  of  colonies  of  streptococci.  The  peritonitis  was  therefore  primary,  and 
due  to  the  streptococcus. 

The  epithet  "  primary  "  is,  perhaps,  not  strictly  appUcable  to  this  case,  for,  as  Meunier 
says,  the  cause  and  the  origin  of  the  peritoneal  infection  may  be  as  follows  :  The  patient 
was  a  servant,  and  was  tending  a  lady  suffering  from  severe  facial  erysipelas,  with  high 
fever,  invasion  of  the  face  and  of  the  scalp,  suppuration,  and  eye  comphcations,  which 
called  for  surgical  intervention.  The  servant,  whose  menses  had  just  appeared,  had, 
to  keep  herself  clean,  used  a  towel  upon  which  she  had  wiped  her  hands  after  dressing 
her  mistress.  While  out  for  a  walk  she  was  suddenly  taken  ill  with  a  violent  rigor, 
headache,  and  vomiting.  She  was  brought  home  and  put  to  bed.  Fever,  diarrhoea, 
restlessness,  and  delirium  appeared,  and  the  menses  suddenly  stopped.  In  this  case 
the  virulent  streptococcus  of  erysipelas  may  have  caused  the  peritonitis,  being  conveyed 
by  the  contaminated  towel  used  as  a  napkin  by  the  servant. 

This  pathogenesis  is  quite  acceptable,  because  we  know  that,  on  the  one  hand,  the 
streptococcus  can  cause  erysipelas  and  abscess  (Widal),  and,  on  the  other  hand,  we 
know  that  immediate  contagion  through  the  uterine  mucous  membrane  may  be  brought 
about  by  virtue  of  the  menstrual  loss  of  tissue  (Doleris).  Furthermore,  this  case  of 
streptococcal  infection  following  erysipelas  may  be  reconciled  with  the  views  put 
forward  by  Trousseau,*  who  wrote  an  admirable  chapter  on  the  relations  between  the 
puerperal  condition,  erysipelas,  and  peritonitis.  He  noticed  that  a  new-born  child 
suffering  from  facial  erysipelas  might  die  of  peritonitis. 

It  is  interesting  to  compare  with  this  case  two  of  Tarnier's  cases,  which  also  prove 
that  the  menstrual  loss  of  tissue  (the  uterus  being  perfectly  healthy)  may  be  the  entrance- 
gate  of  peritoneal  infection  or  of  septicaemia.  Tarnier  reports  in  his  thesis,  that  during 
an  epidemic  of  puerperal  fever  two  pupil  mid^^^ves  who  were  menstruating  were 
attacked  by  septicaemia,  with  rigors,  fever,  and  nervous  symptoms.  One  of  them  died 
of  peritonitis,  and  the  diagnosis  was  verified  at  the  post-mortem. 

I  have  still  to  quote  two  other  cases  of  primary  peritonitis.  Tlie  first  is  a  case  of 
Cornil.  On  January  26,  1901,  a  woman  fifty-six  years  of  age  was  admitted  into  the 
Hotel-Dieu  at  ten  o'clock  at  night.  She  walked  doubled  up,  and  was  suffering  from 
her  stomach.  The  pain  had  been  present  for  the  past  three  days.  In  the  surgical 
wards,  where  she  was  first  admitted,  appendicitis  or  ileus  was  at  first  thought  of.  The 
patient  had  a  di'awn  look  and  a  thready  pulse.  The  extremities  were  covered  with  a 
cold  sweat,  and  the  temperature  stood  at  99°  F.  The  stomach  was  distended  and  very 
painful  on  palpation,  but  without  any  appreciable  effusion.  The  pain  was  not  Umited 
to  McBurney's  point.  There  was  no  lesion  in  the  genital  organs.  The  evening  before, 
the  patient  had  had  nausea,  vomiting,  and  two  liquid  stools.  The  diagnosis  of  peri- 
tonitis was  made,  but  it  was  not  possible  to  determine  the  cause.  The  patient  was  so 
weak  that  an  operation  was  out  of  the  question.  On  the  following  day  at  6  a.m.  Celos 
was  called  to  the  patient,  who  had  just  had  a  copious  hsematemesis.  The  bedclothes 
and  the  floor  were  soiled  with  a  blackish  fluid  Uke  coffee-grounds.  Death  supervened 
a  few  moments  afterwards. 

At  the  autopsy  we  found  acute  peritonitis,  with  diffuse  redness  of  the  parietal  peri- 
toneum :  the  coils  of  the  small  intestine  were  congested,  and  covered  in  places  with  thin 
fibrinous  membranes  infiltrated  with  pus.  There  was  no  gas,  and  the  fluid  was  in  an 
unappreciable  quantity.  The  apr)  idix  was  normal,  and  the  genital  organs  were 
healthy.  The  stomach  contained  no  blood,  but  a  few  small  ecchymoses  were  present 
on  the  mucous  membrane.     The  bacteriological  examination  revealed  the  presence  of 

*  Trousseau,  Clinique  Medicale  de  I' Hotel-Dieu,  t.  i.,  p.  187. 


DISEASES  OF  THE  PERITONEUM  857 

streptococci  in  small  chains.  A  mouse  inoculated  with  the  culture-broth  died  in  twelve 
hours,  and  its  blood  contained  diplococci  without  capsules.  "  In  this  case  we  therefore 
had  to  do  with  primary  streptococcal  purulent  peritonitis,  or  at  least  with  infectious 
peritonitis  accompanied  by  copious  haematemesis,  without  being  able  to  discover  the 
cause." 

I  will  close  this  account  with  Leyden's  case,  which  occurred  in  1884,  and  is  the  first 
case  of  primary  streptococcal  peritonitis  verified  by  bacteriology  :  On  January  28  a 
young  woman  was  taken  ill  with  rigors,  repeated  vomiting  of  green  fluid,  and  sharp  pains 
in  different  parts  of  the  abdomen.  The  patient  could  give  no  cause  for  her  condition. 
Three  days  later,  on  January  31,  she  was  taken  to  hospital.  The  fever  was  not  high ; 
the  greenish  vomit  persisted ;  the  prostration  was  great ;  the  voice  was  feeble ;  the 
breathing  was  shallow  and  quick  ;  the  abdomen  was  distended,  and  the  pains  were 
sharp,  particularly  in  the  hypochondria  ;  the  stools  were  loose,  and  the  urine  was 
albuminous  ;  the  temperature  was  101°  F.,  and  the  pulse  116.  During  the  night  of 
January  31  the  vomiting  recurred  several  times,  and  was  copious. 

On  February  1  the  patient's  eyes  were  hollow  and  the  pulse  was  small ;  the 
stomach  was  very  painful.  The  ingestion  of  the  smallest  quantity  of  fluid  was  fol- 
lowed by  vomiting.  The  respiration  was  44  and  the  pulse  144.  The  following  night 
the  patient  was  delirious.  In  the  morning  the  collapse  was  complete :  the  pulse  was 
hardly  perceptible,  the  extremities  were  cold,  and  the  facies  was  hippocratic.  Death 
took  place  at  seven  o'clock  in  the  evening.  Tiie  diagnosis  had  been :  Diffuse  peritonitis. 
The  persistence  of  the  diarrhoea,  however,  had  given  rise  to  the  idea  of  typhoid  fever, 
with  perforation  of  the  intestine. 

The  autopsy  proved  that  it  was  not  a  case  of  typhoid  fever,  but  of  general  peri- 
tonitis. The  peritoneal  fluid  was  abundant,  purulent,  odourless,  and  contained  some 
fibrinous  flakes.  The  intestines  and  the  omentum  were  covered  with  fibrino- purulent 
deposits.  The  stomach,  intestine,  and  appendix  showed  no  lesions.  All  the  organs 
were  healthy.  The  peritonitis  was  held  to  be  primary.  Bacteriological  examination 
revealed  the  presence  of  streptococci  in  straight  and  curved  chains. 

All  these  cases  were  streptococcal  peritonitis  of  very  rapid  course  and  fatal  prog- 
nosis. I  have  reserved  a  special  place  for  the  exceptional  case  of  Lorrain,  which  differs 
from  the  others  in  the  relative  benignity,  the  slow  course  of  the  disease,  and  the  success 
which  followed  a  double  operation. 

The  case  is  as  follows  : 

On  November  21,  1896,  a  little  girl  of  eight  years  of  age  was  admitted  into  D'Heilly's 
ward.  She  had  had  no  previous  illness.  Her  mother  had  died  in  childbed  a  fortnight 
pre\nou8ly.  The  little  girl  had  been  ill  for  three  weeks.  No  precise  information  was 
available.  It  was  kno'wn  that  she  was  suffering  from  her  stomach,  and  a  doctor  who 
saw  her  several  times  diagnosed  typhoid  fever.  The  child  was  always  complaining  of 
her  stomach.  She  was  thin,  her  skin  was  dry,  her  nose  was  slightly  pinched,  and  her 
eyes  were  hollow.  The  stomach  was  distended  and  hard.  Pressure  caused  pain  and 
muscular  resistance.  Neither  tumour  nor  induration  could  be  felt.  The  right  iliac 
fossa  was  free.  The  spleen  was  not  enlarged,  and  no  lenticular  rose-spots  were  found. 
The  patient  had  alternate  diarrhtea  and  constipation,  with  some  vomiting.  On  auscul- 
tation the  heart  and  the  lungs  were  normal.  The  urine  was  albuminous;  the  tempera- 
ture oscillated  between  99°  and  101°  F.  The  general  condition  was  bad.  During  tho 
next  few  days  there  was  no  change.  The  vomiting  ceased,  but  the  diarrhooa  j)ersisted. 
The  stomach  was  still  distended  and  painful  on  pressure.  The  symptoms  of  loss  of 
flesh,  fever  at  night,  diarrha-a,  and  ballooning  of  the  sfoihach  led  to  tlio  idea  of  enteritis, 
with  probable  extension  to  the  peritoneum. 

On  December  2  a  hard  mass,  which  increased  rapidly  in  size  and  reached  the  surface, 
was  found  in  tho  left  ihac;  fossa.  On  December  6  tho  tumour  was  clearly  localized  in  the 
left  iliac  f()s.sa,  but  was  not  painful.    On  December  7  an  operation  was  performed  by  Brun. 


858  TEXT-BOOK  OF  MEDICINE 

An  encysted  coUection  of  pus  was  found.  The  pus  was  yellowish,  odourless,  and 
homogeneous.  No  false  membranes  were  seen.  The  quantity  of  pus  evacuated  was 
estimated  at  2  pints.  During  the  next  few  days  the  temperature  fluctuated  greatly— 
103°  F.  in  the  evening,  and  99°  F.  in  the  morning.  On  January  1  an  mduration  was 
felt  in  the  right  iUac  fossa,  and  a  second  operation  was  therefore  performed.  The 
appendix  was  found  to  be  healthy,  but  the  csecum  was  adherent  to  the  small  intestme. 
The  child  was  finally  discharged  cured. 

The  case  appeared  to  be  one  of  pneumococcal  peritonitis.  The  encysted  abscess, 
the  homogeneous  pus,  the  slowness  of  the  peritoneal  infection,  the  relative  benignity 
of  the  peritonitis,  and  the  recovery  in  no  way  correspond  to  streptococcal  peritonitis. 
Bacteriology,  however,  proved  that  it  was  a  case  of  streptococcal  peritonitis.  Direct 
examination  of  the  pus  on  sUdes  showed  the  presence  of  diplococci  in  chains,  staimng 
with  Gram,  and  the  absence  of  other  microbes.  The  pus,  sown  on  broth  and  agar, 
gave  pure  cultures  of  streptococci  at  the  end  of  twenty-four  hours.  Inoculation  of 
the  cultures  in  a  rabbit  caused  streptococcal  infection.  In  this  case,  therefore, 
we  must  admit  as  an  exception  primary  streptococcal  peritonitis  of  a  bemgu 
nature. 

Description.— Let  us  now  study  primary  streptococcal  peritonitis  as 

a  whole.  It  is  far  less  common  than  primary  pneumococcal  peritonitis. 
Furthermore,  streptococcal  peritonitis  deserves  the  name  of  primary  much 
less  than  pneumococcal  peritonitis.  If  the  reader  will  refer  to  the  section 
on  Primary  Pneumococcal  Peritonitis,  he  will  see  that  in  almost  every  case 
it  is  impossible  to  find  the  entrance-gate  of  the  pneumococcus.  The  disease 
breaks  out  in  the  midst  of  good  health,  and  we  are  unable  to  find  the  small 
lesion  which  has  opened  the  door  to  the  infection. 

It  is  not  always  the  same  in  so-called  primary  streptococcal  peritonitis. 
It  is  true  that  in  many  cases  the  term  "  primary ''  is  perfectly  applicable 
in  the  sense  that  the  peritonitis  occurs  in  a  healthy  subject,  and  that  the 
most  minute  examination  may  not  reveal  the  starting-point  of  the  infection. 
In  the  cases  of  Cornil  and  Leyden  the  name  "  primary  "  holds  good.  In 
my  case,  as  well  as  in  that  of  Milian  and  Herrenschmidt,  the  peritonitis  was 
likewise  primary.  The  tonsil  may,  perhaps,  be  the  origin  of  the  infection, 
but  this  is  pure  hypothesis.  In  Meunier's  case  the  peritonitis  was  primary 
in  the  sense  that  it  was  not  possible  to  find  the  causative  lesion,  but  it  is 
likely  that  the  streptococcus  of  erysipelas  was  carried  by  the  contaminated 
towel.  In  Lorrain's  case  the  peritonitis  may  be  considered  primary, 
because  it  was  not  caused  by  any  lesion.  The  child,  however,  lived  in  the 
midst  of  surroundings  infected  by  her  mother,  who  died  later  in  childbed, 
and  here,  too,  it  is  permissible  to  think  of  contagion. 

Primary  streptococcal  peritonitis,  like  primary  pneumococcal  peri- 
tonitis, is  chiefly  found  in  the  female  sex  ;  but  the  former  has  a  predilection 
for  adults,  whereas  the  latter  is  much  more  frequent  in  children.  The 
peritoneal  lesions  vary  in  the  two  cases.  Pneumococcal  peritonitis  tends  to 
form  encysted  pockets,  and  is  rarely  general.  It  gives  rise  to  thick,  fibrinous 
membranes,  which  cause  adhesions  of  the  intestinal  coils  and  of  the  organs. 


i 


DISEASES  OF  THE  PERITONEUM  S59 

The  pus  is  greenish,  thick,  homogeneous,  and  laudable.  Streptococcal 
peritonitis,  on  the  contrary,  has  no  tendency  to  become  encysted,  but  is 
prone  to  become  general.  It  gives  rise  to  thin  membranes,  which  cause 
but  slight  adhesions.  The  pus  is  neither  thick  nor  homogeneous,  but  a  sero- 
purulent  Hquid,  comparable  to  tainted  broth.  The  onset  of  both  varieties 
may  be  sudden  and  violent.  In  each  case  the  patient  is  attacked  in  the 
midst  of  good  health.  Rigors,  fever,  vomiting,  and  abdominal  pain  are  the 
first  symptoms.  However,  the  "  abdominal  stitch  "  seems  to  me  to  be 
more  marked  in  pneumococcia,  and,  on  the  other  hand,  the  greenish  vomit 
appears  to  be  more  frequent  in  streptococcia.  Hiccough  is  rare  in  both 
cases.  I  would  call  special  attention  to  the  diarrhoea.  It  is  too  often 
thought  that  constipation  is  the  usual  symptom  in  peritonitis.  Constipa- 
tion is  particularly  frequent  in  appendicular  peritonitis  and  in  peritonitis 
following  perforation  of  the  stomach  or  duodenum,  but  in  pneumococcal 
and  streptococcal  peritonitis  diarrhoea  is  the  rule.  In  pneumococcal  peri- 
tonitis, diarrhoea  appears  very  early  in  the  disease,  and  for  several  days 
the  stools  are  liquid,  frequent,  and  biHous.  In  streptococcal  peritonitis 
diarrhoea  is  found  in  almost  all  cases,  and  has  led  to  the  erroneous  diagnosis 
of  typhoid  fever. 

Summary. — In  pneumococcal  and  streptococcal  peritonitis  the  onset 
is  sudden,  and  certain  symptoms,  such  as  pain,  vomiting,  and  diarrhoea, 
are  common  to  both  diseases.  The  real  distinction  is  the  general  condition 
of  the  patient,  which  differs  from  the  first  in  the  two  cases.  In  streptococcal 
peritonitis  the  prostration,  the  acceleration  and  smallness  of  the  pulse,  the 
delirium  and  the  ataxo-adynamia,  and  the  rapid  tendency  to  collapse  and 
coma,  are  the  chief  features,  even  early  in  the  case.  With  few  exceptions, 
nothing  of  the  sort  occurs  in  pneumococcal  peritonitis,  which  may  last 
for  weeks  without  fatal  consequences. 

The  prognosis  in  streptococcal  peritonitis  is  more  serious  than  in  pneumo- 
coccal peritonitis.  In  the  latter  case  the  toxi-infection  remains  for  a  long 
time  abdominal,  and  does  not  aiTect  the  remainder  of  the  system,  whereas 
in  the  case  of  streptococcal  peritonitis  the  toxi-infection  is  severe  from  the 
outset.  It  is  the  rapid  poisoning  which  dominates  everything,  and  in  a 
few  days  leads  to  collapse,  coma,  and  death. 

This  parallel  between  pneumococcal  and  streptococcal  peritonitis  is 
applicable  in  the  great  majority  of  cases.  There  are,  however,  exceptions. 
On  the  one  hand,  streptococcal  peritonitis  may  be  neither  very  virulent 
nor  superacute  ;  it  may  run  a  slow  course,  and  be  cured  after  operation,  as 
in  the  case  reported  by  Lorrain.  On  the  other  hand,  pneumococcal  peri- 
tonitis, from  its  great  virulence  or  the  presence  of  other  organisms,  may 
be  as  severe  as  streptococcal  peritonitis.  Cases  of  this  kind  are  described 
mider  Pneumococcal  Peritonitis. 


860  TEXT-BOOK  OF  MEDICINE 

The  treatment  of  primary  streptococcal  peritonitis  is  early  surgical 
intervention.  The  operation  must  be  performed  as  quickly  as  possible, 
and  in  this  event  a  cure  may  be  hoped  for. 


VI.  CANCER  OF  THE  PERITONEUM— CANCEROUS  PERITONITIS. 

^Etiology. — The  great  omentum  is  the  only  peritoneal  fold  attacked  by 
primary  cancer.  Cancer  of  the  peritoneum  is  always  secondary,  and  has  the 
same  structure  as  the  primary  growth  (carcinoma,  epithehoma,  sarcoma, 
lymphadenoma).  This  question  has  been  carefully  discussed  in  Aslanian's 
thesis,  from  which  I  have  taken  the  following  statistics  : 

Cancer  of  the  stomach  invades  the  peritoneum  in  the  proportion  of  1  to  4  ;  cancer 
of  the  intestine  invades  the  peritoneum  in  the  proportion  of  1  to  8  ;  primary  cancer 
of  the  liver  invades  the  peritoneum  in  the  proportion  of  1  to  8  ;  primary  cancer  of  the 
biliary  passages  invades  the  peritoneum  in  the  proportion  of  1  to  2  ;  cancer  of  the 
pancreas  invades  the  peritoneum  in  the  proportion  of  1  to  3  ;  cancer  of  the  spleen  invades 
the  peritoneum  in  the  proportion  of  1  to  13  ;  cancer  of  the  kidney  invades  the  peritoneum 
in  the  proportion  of  1  to  15  ;  cancer  of  the  uterus  invades  the  peritoneum  in  the  pro- 
portion of  1  to  18  ;  carcinoma  and  sarcoma  are  rare  in  the  ovaries,  but  epithehoma  of 
a  papillary  type  is  common,  and  invades  the  peritoneum  in  the  proportion  of  1  to  3  ; 
cancers  of  the  thoracic  cavity  practically  never  spread  to  the  peritoneum,  but  cancer 
of  the  peritoneum  often  spreads  to  the  thoracic  organs,  glands,  pleurae,  and  lungs. 

Pathological  Anatomy. — The  cancerous  process  takes  place  in  two 
stages  :  it  commences  as  a  local  infection  near  the  pripiary  growth,  and  then 
becomes  general.  The  peritoneal  cavity  can  only  be  infected  when  the 
serous  membrane  around  the  cancerous  organ  is  involved.  The  seats  of 
election  of  the  peritoneal  infection  are  the  anterior  parietal  peritoneum,  the 
diaphragmatic  peritoneum,  the  pelvic  peritoneum,  and  the  large  omentum. 

In  the  miliary  form  cancer  takes  the  form  of  tubercles  as  large  as  a  pea, 
a  lentil,  or  a  nut.  In  the  ulcerous  form  the  tumours  present  crateriform 
ulcerations.  In  the  vegetating  form,  which  usually  follows  papillary  growths 
of  the  ovaries,  the  cancer  resembles  a  soft  mushroom,  bristHng  with  papillas 
that  may  be  as  large  as  a  walnut,  or  larger.  In  the  cystic  form,  which  is 
usually  secondary  to  cancer  of  the  ovaries,  but  which  may  also  occur 
primarily  in  the  great  omentum,  the  cancer  takes  the  form  of  cysts,  from 
the  size  of  a  pea  to  that  of  an  apple.  In  the  infiltrating  form,  which  is 
seen  especially  in  the  parietal  peritoneum  and  omentum,  the  cancer  takes 
the  form  of  hard  and  thick  patches,  or  of  infiltrated  sheets.  All  these  forms 
may  be  combined.  Carcinoma  of  the  peritoneum  is  accompanied  by  more 
or  less  intense  inflammation  of  the  serous  membrane.  Sometimes  we  find 
only  a  fibrinous  exudate,  with  matting  of  the  intestinal  coils  and  yellowish 
fluid  ;  but  at  other  times  the  cancerous  peritonitis  is  clearly  pronounced, 
and  there  are  numerous  adhesions  between  the  layers  of  the  peritoneum 


DISEASES  OF  THE  PERITONEU^I  861 

and  tlie  abdominal  organs.     These  neo-membranes  are  vascular,  sometimes 
hsemorrhagic,  and  often  invaded  by  the  cancerous  growth. 

These  cancerous  masses,  fused  with  the  organs  and  with  the  glands, 
and  themselves  attacked  by  cancerous  degeneration,  sometimes  form 
enormous  tumours. 

The  ascitic  fluid  in  cancerous  peritonitis  may  amount  to  several  pints. 
The  fluid  is  sometimes  citron- coloured  and  sero-fibrinous,  or  sometimes 
hsemorrhagic.  The  fluid  is  nearly  always  hsemorrhagic  in  papillomatous 
cancer  (Terrier).  The  sero-purulent  effusion  is  much  less  common,  and  an 
ascites  which  is  citron- coloured  at  the  first  puncture  may,  like  pleuritic 
fluid,  later  become  hsemorrhagic,  or  vice  versa. 

The  hsemorrhagic  fluid  may  be  rosy,  reddish,  brownish,  or  blackish. 
Ascites,  the  Hquid  being  citron-coloured  or  hsemorrhagic,  is  a  much  more 
frequent  complication  of  abdominal  neoplasms  than  the  invasion  of  the 
peritoneum  by  cancer.  "  In  ovarian  cysts  Terrier  found  twenty-nine  cases 
of  ascites,  and  only  six  cases  of  peritoneal  metastasis,  in  175  ovariotomies." 

Hanot  and  Gilbert,  in  their  researches  on  diseases  of  the  Hver,  found 
that  in  thirteen  cases  of  cancer  of  the  liver,  ascites  was  present  in  ten  cases, 
whilst  general  infection  of  the  peritoneum  existed  in  only  three  cases. 
"  Whatever  organ  be  invaded  by  the  cancer,  we  have  always  found  that 
ascites  predominated  over  peritoneal  metastasis  "  (Aslanian).  Ascites  is 
not  only  more  frequent  than  cancerous  metastasis  in  the  peritoneum,  but 
it  is  also  the  earliest  phenomenon,  and  seems  to  precede  the  appearance  of 
cancer  in  the  peritoneum. 

Description. — Cancerous  peritonitis  has  an  insidious  onset,  and  is  not 
ushered  in  by  any  acute  symptom.  The  abdomen  becomes  distended, 
ascites  appears,  the  patient  complains  of  pain,  and  it  may  be  said  that  the 
symptoms  of  peritonitis  are  subintrant  to  the  symptoms  of  cancerous 
infection. 

A  little  later,  in  the  stationary  stage,  these  symptonLs  are  more  clearly 
marked  :  the  abdomen  is  more  enlarged,  the  ascites  is  greater,  and  a  collateral 
circulation  often  appears  in  the  abdominal  wall.  Palpation  is  rarely  painful, 
l)ut  it  allows  us  to  make  out  indurations  and  tumours  of  various  forms 
and  dimensions,  especially  after  evacuation  of  the  fluid.  The  ascitic  fluid 
is  generally  free  in  the  peritoneal  cavity,  and  a  fluid  thrill  is  readily  obtained. 
The  inguinal  glands  may  be  attacked  by  the  cancerous  degeneration,  which 
may  also  be  met  with  in  other  regions  (supraclavicular  glands).  Numerous 
complications  may  appear  from  one  moment  to  another  (intestinal  occlusion, 
jaundice  from  compression,  retention  of  urine).  In  the  thorax  we  may  find 
malignant  growths  in  the  pleura,  lung,  or  mediastinum. 

Intraperitoneal  hrrmorrhage  is  so  frc(|uent  that  it  may  be  looked  upon 
as  a  symptom  rather  than  as  a  complication.     Fever  is  far  from  being 


862  TEXT-BOOK  OF  MEDICINE 

constant,  but  we  sometimes  see  the  temperature  rise  to  102°  or  103°  F. 
after  a  period  of  complete  apyrexia. 

The  patient  quickly  becomes  cachectic  ;  the  loss  of  flesh  and  asthenia 
make  rapid  progress.  The  yellow,  straw-coloured  complexion,  with  peri- 
pheral oedema,  appears,  and  death  supervenes  within  a  year  of  the  invasion 
of  the  peritoneum. 

VII.  HYDATID  CYSTS  OF  THE  PERITONEUM. 

Pathogenesis. — Hydatid  cysts  of  the  peritoneum  are  fairly  common. 
It  is  thought  that  the  embryo  reaches  the  peritoneum,  either  directly  by 
perforating  the  walls  of  the  intestine,  or  indirectly  through  the  bloodvessels 
and  lymphatics.  Peritoneal  cysts  are  sometimes  secondary  to  a  cyst  in 
another  organ.  In  some  cases  the  disease  may  be  grafted  on  the  peri- 
toneum by  the  heads  of  the  taeniae,  liberated  in  consequence  of  natural  or 
artificial  rupture  of  a  cyst  (Soupault).  We  have  then  to  deal  with  a  case 
of  secondary  echinococcia. 

Pathological  Anatomy. — The  hydatid  cyst  of  the  peritoneum  is  rarely 
solitary ;  we  usually  find  from  three  to  fifty  or  sixty  cysts,  and,  indeed, 
two  hundred  and  more  have  been  counted.  Their  size  varies  greatly.  The 
more  numerous  they  are,  the  smaller  their  size,  but  they  are  never  all  of 
the  same  size.  One  or  two  cysts  of  the  size  of  an  orange  are  sometimes  met 
with,  and  also  other  cysts  as  large  as  a  lentil,  a  grape;pip,  or  a  walnut. 

The  hydatid  is  found  in  the  omenta,  then  in  the  mesentery,  the  meso- 
colon, the  peritoneal  folds  of  the  pelvis,  and  the  broad  ligaments.  The 
cysts  may  be  discrete  or  confluent,  and  are  sometimes  aligned  in  chains, 
after  the  fashion  of  streptococci,  or  at  other  times  agglomerated  in  bundles, 
like  the  staphylococcus,  or,  lastly,  heaped  up  like  a  bunch  of  grapes.  Davaine 
and  Charcot  have  proved  that  the  cyst  never  develops  in  the  peritoneal 
cavity,  but  in  the  subserous  cellular  tissue.  The  peritoneum  covers  the  cyst, 
and  helps  to  form  the  pedicle  when  the  cyst  spreads  from  its  point  of  origin 
into  the  pelvis. 

The  structure  of  the  cyst  is  given  under  Hydatid  Cysts  of  the  Liver,  but 
the  peritoneal  cyst  is  surrounded  by  a  more  distinct  membrane,  formed 
by  the  subperitoneal  tissue,  and  covered  by  the  serous  membrane.  This 
covering  may  become  thick  and  fibrous,  thus  helping  to  isolate  and  fix  the 
cyst.  The  hydatid  cyst  may  give  rise  to  more  or  less  thickened  false  mem- 
branes, with  matting  of  the  intestinal  coils  and  fibrinous  bands.  It  is  not 
rare  to  find  ascites,  due  to  compression  of  the  portal  vein. 

Description. — Hydatid  cysts  of  the  peritoneum  develop  silently  for 
some  time.  Enlargement  of  the  belly  is  generally  the  first  sign  which  betrays 
their  presence.     The  belly  enlarges  and  becomes  deformed,  sometimes  in 


DISEASES  OF  THE  PERITONEUM  863 

one  region,  sometimes  in  another.  This  increase  in  size  is  soon  followed 
by  continuous  or  paroxysmal  pain.  Whatever  the  cause  of  the  pain  (torsion 
of  the  omenta,  peritoneal  traction,  attacks  of  peritonitis),  it  may  supervene 
in  crises,  accompanied  by  vomiting  and  constipation. 

As  the  cyst  grows,  it  provokes  many  and  varied  symptoms  of  com- 
pression. Compression  of  the  intestine  causes  constipation  and  occlusion  ; 
compression  of  the  portal  vein  gives  rise  to  ascites  and  collateral  circula- 
tion ;  compression  of  a  large  bile-duct  leads  to  icterus ;  compression  of  the 
inferior  vena  cava  is  the  cause  of  oedema  of  the  lower  half  of  the  body ; 
compression  of  the  ureters  brings  about  anuria  and  uraemia  ;  compression 
of  the  nerves  of  the  sacral  plexus  produces  intense  neuralgia.  The  abdomen, 
on  examination,  is  frequently  found  to  be  deformed  and  nodular  ;  percussion 
will  map  out  dull  and  resonant  regions.  Very  large  cysts  may  give  a 
sensation  of  fluctuation. 

When  peritoneal  cysts  grow  towards  the  diaphragm,  they  may  push  it 
upwards  into  the  thoracic  cavity,  and  provoke  symptoms  of  dyspnoea. 
Pregnancy  in  women  suffering  from  hydatid  cysts  of  the  peritoneum  has 
a  marked  effect  on  the  prognosis.  Porak  has  given  a  resume  of  twenty-four 
cases,  with  the  following  results :  Twice  the  accouchement  was  premature ; 
five  times  the  delivery  was  spontaneous,  but  difficult ;  and  eight  times  the 
cyst  had  to  be  punctured  during  labour.  The  cyst  broke  in  three  cases. 
Embryotomy  had  to  be  performed  in  two  cases,  and  Csesarean  section  in 
two  cases.  Cephalotripsy  was  performed  in  one  case,  and  in  two  cases 
delivery  was  impossible.  The  growth  of  hydatids  of  the  peritoneum  is 
generally  very  slow,  and  during  the  first  period  of  their  development  they 
occasion  no  appreciable  trouble.  The  symptoms  of  compression  appear 
later,  and  it  is  only  after  several  years  that  the  patient  reaches  the  cachectic 
stage,  with  loss  of  appetite,  progressive  wasting,  loss  of  strength,  and  peri- 
pheral oedema. 

The  appearance  of  fever  and  rigors  indicates  suppuration  in  one  or  more 
cysts.  Sweating  and  diarrhoea  complete  the  picture  of  hectic  fever,  and  the 
condition  brings  about  marasmus  and  death. 

The  rupture  of  a  hydatid  cyst  in  the  peritoneum  is  often  accompanied 
by  urticaria  and  symptoms  of  peritonitis,  which  is  not  always  fatal. 
Hydatid  disease  of  the  peritoneum  is  serious  because  the  cysts  are  almost 
always  multiple,  and,  supposing  that  one  of  them  recover,  either  spon- 
taneously or  after  surgical  intervention,  the  other  cysts  continue  to  grow, 
and  sooner  or  later  bring  on  the  complications  just  mentioned. 

Diagnosis. — The  diagnosis  is  beset  with  extreme  difficulties.  The 
iiidurations  and  tumours  which  the  hydatid  forms  resemble  those  of  tuber- 
cular or  cancerous  peritonitis.  Sometimes  the  cysts  give  the  sensation  of 
soft,  fluctuating  tumours,  and  at  other  times  they  give  the  impression  of 


864  TEXT-BOOK  OF  MEDICINE 

indurated  tumours  adherent  to  the  neighbouring  organs.  "  It  is  easily 
understood  that  the  hydatid  tumour  may  be  mistaken  for  a  distended 
bladder,  a  gravid  uterus,  fibro-cystic  fibroids,  peri-uterine  collections,  cystic 
tubes,  or  cysts  of  the  ovary  "  (Soupault).  Aspiratory  puncture  is  the  onlv 
means  of  arriving  at  a  diagnosis. 

Treatment. — The  treatment  does  not  give  such  good  results  as  are 
obtained  in  cysts  of  the  liver,  because  the  cysts  in  the  peritoneum  are  mul- 
tiple, of  different  ages,  and  develop  one  after  the  other  ;  and  even  if,  by  an 
aspiratory  puncture  or  by  laparotomy,  we  succeed  in  curing  one  or  two  of  the 
principal  cysts,  it  is  much  to  be  feared  that  the  other  cysts  will  continue 
to  grow.     TJno  avulso,  non  deficit  cdter, 

VIII.  ASCITES. 

ffitiology. — Ascites,  or  dropsy  of  the  peritoneum,  may  be  primary  or 
secondary.  Primary  ascites,  which  is  said  to  supervene  from  cold,  or 
without  apparent  cause,  has  been  alternately  admitted  and  rejected  by 
authors,  and  we  have  seen  the  con-ect  view  of  it  in  the  section  on  Tubercular 
Peritonitis.  Secondary  ascites  follows  on  mechanical  and  constitutional 
troubles.  Ascites  is  found  at  all  ages,  even  in  young  children.  The 
mechanical  troubles  are  those  which  offer  an  obstacle  to  the  circulation  in 
the  portal  vessels,  and  include  atrophic  cirrhosis  of  the  liver,  pylephlebitis, 
compression  of  the  portal  vein  by  tumours  of  the  peritoneum,  liver,  spleen, 
pancreas,  and  mesentery.  The  constitutional  troubles  are  those  seen  in 
Bright's  disease  and  cachexia.  Fluid  containing  sugar  may  occur  in 
diabetics. 

Pathological  Anatomy. — The  effusion  may  amount  to  as  much  as 
60  pints.  It  has  all  the  characteristics  of  dropsical  fluid,  being  transparent, 
fluid,  of  a  pale  yellow  colour,  and  contains  a  small  quantity  of  albumin. 

Description. — I  have  described  the  signs  and  symptoms  of  ascites 
under  Laennec's  Atrophic  Cirrhosis  and  Tubercular  Peritonitis.  I  will 
therefore  refer  the  reader  to  these  diseases,  and  will  merely  say  that  the 
course  and  the  duration  of  ascites  are  subordinate  to  its  cause.  In  some 
cases  (tuberculosis,  hypertrophic  alcohoHc  cirrhosis)  ascites  may  recover 
without  surgical  intervention,  but  most  frequently  it  is  persistent,  and  the 
liquid  is  subject  to  variations  which  rarely  end  in  recovery.  The  diagnosis  of 
ascites,  comprises  that  of  the  symptom  and  of  the  cause.  Ascites  must  not 
be  confounded  with  ovarian  cyst,  distended  bladder,  or  chronic  peri- 
tonitis. The  diagnosis  of  the  cause  is  sometimes  only  possible  after  evacua- 
tion of  the  Uquid.  The  treatment  of  ascites  has  been  given  under  Atrophic 
Cirrhosis.  Cyto-diagnosis  is  of  value,  although  the  results  are  not  as 
exact  in  ascites  as  in  pleurisy. 


DISEASES  OF  THE  PERITONEUM  865 


IX.  CHYLOUS,  CHYLIFORM,  LACTESCENT  ASCITES. 

History. — In  1700  we  find  the  first  mention  of  lactescent  ascites.  Vernage  made  a 
communication  to  the  Academie  Royale  des  Sciences  concerning  a  peculiar  case  of 
dropsy.  The  lacteais  had  just  beeil  discovered,  and  people  at  once  considered  the 
effusion  of  chyle  into  the  peritoneum  as  due  to  rupture  of  a  lacteal.  Subsequently, 
several  cases  were  pubUshed.  They  were  neither  collected  nor  compared,  and  no 
deduction  was  drawn  Goncerning  their  pathogenesis.  In  1874  Gueneau  de  Mussy, 
referring  to  two  cases  of  pleural  effusion  analogous  to  fatty  emulsion,  attributed  the 
aspect  of  the  fluid  to  fatty  changes  in  the  leucocytes  and  the  fibrinous  exudate.  Veil 
and  LetuUe  were  of  a  similar  opinion.  In  1880  Debove  described  the  existence  of  a 
special  variety  of  effusion  composed  of  emulsified  fats,  and  quite  distinct  from  serous, 
sero-fibrinous,  and  purulent  effusions.  This  theory  was  supported  in  the  thesis  of 
Madame  Perree.  In  1896  Strauss  described  a  typical  case  of  chylous  ascites  due  to 
communication  between  the  lacteais  and  the  peritoneal  cavity.  Lion  described  a  new 
variety  of  ascites,  which  had  only  the  milky  look,  and  differed  in  every  other  respect 
from  chyle.  The  colour  was  due  to  the  presence  of  a  special  albumin  closely  alUed  to 
casein.     Other  cases  support  this  interpretation  (Achard,  *Merklen,  Sainton,  Apert). 

Widal  and  Prosper  ^lerklen  have  shown  that  the  morphology  of  the  leucocytes  in 
the  effusion  is  of  great  importance  in  the  diagnosis  of  lactescent  ascites.  My  cUnical 
assistant,  Kahn,  has  pubhshed  two  cases  of  chyliform  ascites  in  my  wards  at  the  Hotel- 
Dieu.  In  these  two  cases  we  had  to  deal  with  secondary  cancer  of  the  peritoneum  and 
of  the  primary  lymphatic  passages,  and  in  one  of  them  he  proved  the  presence  of  the 
mono -nuclear  leucocytes  pointed  out  by  Widal. 

Examination  of  the  Lactescent  Fluid. — The  quantity  of  fluid  is  not  as  great  as  in 
common  ascites.  It  varies  from  2  to  20  Joints  (Schmidt),  and  in  one  case  only  did  it 
amount  to  30  pints.  The  hquid  has  a  tendency  to  reform.  As  its  name  indicates,  it 
has  the  appearance  of  chyle.  It  is  bluish-white  (Quincke),  milky,  or  creamj'^-white, 
like  an  emulsion  of  almonds  (Marsliall  Hughes).  Its  density  is  lower  than  that  of  blood- 
serum,  which  is  1028.  Hirtz  and  Merklen  give  the  following  figures  :  1007,  1023,  1020, 
1013.  Nearly  all  authors  agree  that  the  lactescent  fluid  is  quite  homogeneous,  and 
this  feature  persists  sometimes  for  a  fortnight  (Kahn).  One  of  its  most  remarkable 
characteristics  is  its  great  power  of  resisting  putrefaction.  Samples  have  been  kept 
for  some  weeks  in  summer  without  giving  off  the  least  smell.  In  the  long  run  the  fluid 
separates  into  two  layers — the  lower  one  serous  and  almost  limpid,  the  upper  one 
whitish  and  creamy.     The  reaction  is  neutral  or  shghtly  alkaline. 

On  chemical  examination,  the  proportion  of  fatty  matter  is  large  (15  parts  per  1,000), 
thougli  it  may  be  present  in  much  smaller  quantities.  It  is,  as  a  rule,  easily  soluble  in 
ether.  Albuminous  matter  also  enters  largely  into  the  composition  of  the  fluid  (30  parts 
per  1,000).  The  weiglit  of  tlie  mineral  salts  attains  the  average  of  5  parts  per  1,000. 
They  are  largely  composed  of  chlorides,  of  phosphates,  and  of  a  small  proportion  of 
sulphates.  In  very  rare  cases  the  presence  of  cholesterine  has  been  noticed.  Sugar  is 
often  found.  Bargebuhr  considers  the  presence  of  sugar  a  distinctive  sign  between 
true  chylous  and  chyliform  ascites,  but  his  sign  has  lost  its  vnluc,  since  Richard,  Roichel, 
and  Rotman  have  proved  that  all  pathological  fluids  poured  out  either  in  serous  cavities 
or  in  the  subcutaneous  cellular  tissue,  T^nth  the  exception  of  pus,  contain  sugar  in  vari- 
able proportion. 

On  microscopic  examination,  the  effusion  is  composed  of  a  large  number  of  very 
fine  rounded  granules,  isolated  from  one  another,  refractile,  and  sliowing  Brownian 
movements.  They  are  generally  very  small,  but  at  times  oily  drops  are  visible.  They 
dissolve  in  ether,  and  stain  brown  with  osmic  acid.  It  is  not  uncommon  to  find  degene- 
rated leucocytes.  Widal  and  Merklen  have  shown  the  importance  of  the  leucocytic 
formula  of  the  effusion  as  regards  the  origin  of  lactescent  ascites.     The  recognition  of 

55 


866  TEXT-BOOK  OF  MEDICINE 

the  mononuclear  leucocytes,  to  the  exclusion  of  every  other  variety  of  white  corpuscles, 
proves  the  lymiiliatic  nature  of  the  ascites.  The  white  mononuclear  corpuscles  are  the 
only  ones  transported  by  the  lymph.     Red  corpuscles  are  sometimes  seen. 

In  two  cases  the  patient's  serum  was  found  to  be  lactescent.  During  the  past  few 
years  some  cases  have  been  published  in  France  under  the  name  of  "  non-chylous  milky 
ascites."  The  iirst  is  due  to  Lion,  who  has  shown  that  ascites  may  be  lactescent  with- 
out containing  any  of  the  elements  of  chyle.  In  the  case  in  question  the  effusion 
appeared  in  a  woman  suffering  from  cancer  of  the  ovary.  The  fluid,  analyzed  by 
Winter,  did  not  contain  fat,  but  an  albuminoids  ubstance  analogous  to  casein,  which 
might  be  classed  amongst  the  glyco-proteids  of  Hammerstein.  Under  the  name  of 
"  non-chylous  milky  ascites,"  Achard  has  reported  a  case  in  wliich  the  fluid  contained 
only  an  infinitely  small  quantity  of  fat.  The  microscope  showed  innumerable  fine, 
refractile  granules,  unstained  with  osmic  acid,  and  similar  to  those  which  Widal  and 
Siccard  have  described  in  the  lactescent  serum  of  patients  suffering  from  albuminuria. 
Similar  granulations  have  been  found  by  Sainton  in  the  liquid  of  a  non-chylous  milky 
ascites  in  a  patient  suffering  from  cancer  of  the  pylorus.  Finally,  a  fourth  case,  entitled 
"  non-chyous  Imifky  ascites,"  has  been  published  by  Apert.  In  this  case  the  milky 
ascites  supervened  in  a  cardiac  patient,  and  was  characterized  by  the  complete  absence 
of  fat  globules,  and  by  the  presence  of  a  fine  powder  visible  only  with  very  high 
magnification. 

Pathological  Anatomy. — Lactescent  ascites  does  not  properly  belong 
to  any  abdominal  lesion.  It  may  be  observed  in  almost  all  the  affections 
which  cause  ascites,  with  or  without  lesions  of  the  peritoneum.  It  has  been 
noticed  in  alcoholic  atrophic  cirrhosis,  without  peritonitis  (Depoix,  Merklen, 
and  Widal).  In  another  case  Remond  and  Rispal  found  post  mortem  only 
chronic  nephritis.  The  lesions  of  a  concomitant  affection  and  lesions  of 
the  lymphatic  system,  such  as  rupture  of  the  lympha'tic  ducts,  compression 
by  tumours  or  by  glands,  are  generally  associated.  Tuberculosis  and  cancer 
of  the  peritoneum  are  the  most  frequent  causes  of  lactescent  ascites.  In 
tuberculosis  injection  and  pigmentation  of  the  serous  membrane  are  seen, 
and  near  Bauhin's  valve  a  very  fine  injection  of  the  chyliferous  vessels, 
without  appendicular  lesions,  is  often  noticed.  The  peritoneum  and  the 
intestinal  coils  adhere  at  the  level  of  the  two  layers  of  the  mesentery.  The 
lesions  of  the  lymphatic  system  include  constriction  and  obstruction  of 
the  lacteal  vessels,  which  are  twisted  and  distended,  but  rarely  ruptured ; 
presence  of  a  clot  in  the  thoracic  duct ;  and  fullness  of  the  intestinal  villi. 
Adenitis  is  constant. 

In  the  case  of  cancer  we  nearly  always  find  in  one  of  the  abdominal 
organs  a  primary  growth  which  has  spread  to  the  lymphatic  passages.  I 
had  in  my  wards  a  woman  suffering  from  lactescent  ascites.  The  primary 
cause  was  a  small  cancer  of  the  ovary.  Kahn  and  Nattan-Larrier  made 
the  inspection,  and  the  results  of  the  autopsy  were  as  follows  : 

The  entire  mesentery  was  much  thickened,  and  on  section  was  found  to  be  crammed 
with  glands  of  the  size  of  a  hazel-nut.  These  glands  were  hard,  and  yielded  but  little 
juice  on  scraping.  They  were  cancerous.  At  the  junction  of  the  small  intestine  with 
the  mesentery  the  lacteals  were  involved,  and  showed  three  principal  types :  (1)  The 


DISEASES  OF  THE  PERITONEUM  867 

lymphatic  duct  was,  as  it  were,  injected,  as  large  as  the  lash  of  a  whip,  indented, 
irregular,  and  tortuous.  It  was  cancerous,  though  not  corresponding  to  any  cancerous 
lesion  of  the  mucous  membrane.  (2)  There  was  distension,  but  no  cancerous  change 
in  the  lymphatics.  They  were  distended,  as  large  as  a  violin-string,  and  stood  out  in 
white  against  the  surface  of  the  serous  membrane.  They  showed  symmetrical  con- 
strictions, clearly  marking  the  situation  of  the  valves.  (3)  The  above-mentioned 
appearances  were  combined.  Sometimes  a  cancerous  lymphangitis  was  continued  to 
the  surface  of  the  intestine  by  a  large  l^Tnphatic  vessel  distended  with  lymph.  Some- 
times the  lymphatics  formed  long  and  fine  arches,  interrupted  at  certain  points  by  a 
short  portion  invaded  by  the  growth.  At  certain  points  there  were  diffuse  yellowish 
plaques  hke  a  thickening  of  the  serous  membrane,  but  due  to  general  dilatation  of  the 
fine  lymphatic  capillaries.  The  lymphatic  trunks,  which  ended  ia  the  receptaculum, 
though  not  invaded  by  the  cancer,  were  nevertheless  distended.  The  receptaculum 
was  greatly  distended  by  the  neoplasm,  and  appeared  as  a  nodular  canal  of  the  size  of 
a  penholder.  This  invasion  extended  for  a  distance  of  about  2  inches.  No  rupture 
was  visible. 

In  certain  cases  a  tear  of  the  thoracic  duct  or  of  the  chyliferous  vessels 
places  the  peritoneal  cavity  in  communication  with  the  lymphatic  circula- 
tion. Bussjr's  conclusions  must  certainly  not  be  accepted  without  reserve, 
when  he  says  that,  in  twenty-eight  cases  reported  by  him,  twenty-seven 
may  be  attributed  to  the  rupture  of  a  chyliferous  vessel.  It  is  correct  to 
make  allowance  for  tears  produced  at  the  post-mortem  examination,  but 
there  are  indisputable  cases  of  this  lesion,  as  in  Whitla's  case  : 

The  thoracic  canal,  in  its  inferior  third,  was  transformed  into  a  fibrous  obHterated 
cord.  Above  it  was  much  dilated,  and  below  there  was  a  perforation  of  the  size  of  a 
pea  at  a  point  where  the  walls  had  gradually  become  thin. 

Strauss  says  :  "  At  first  sight  I  did  not  perceive  any  chyliferous  vessels 
standing  out  in  rehef  on  the  surface  of  the  mesentery,  but  after  a  careful 
examination  I  saw  at  two  different  spots  a  whitish  liquid,  flowing  from  two 
little  openings  on  the  anterior  layer  of  the  mesentery.  The  fluid  was  exactly 
like  milk  or  chyle,  and  of  a  more  milky  colour  than  the  ascitic  fluid.  These 
openings  were  ruptures  of  the  lacteals  into  the  peritoneum.  The  point  of  a 
pipette  was  introduced  several  times  into  these  small  openings,  and  about 
a  cubic  centimetre  of  chyle  thus  aspirated.  I  wish  to  state  that  this  verifica- 
tion was  made  without  touching  the  intestine,  so  as  to  avoid  disturbing  the 
coils  and  producing  tears  in  the  mesentery.  It  is  certain  that  these  two 
small  orifices  were  not  caused  at  the  autopsy."  Quincke  has  observed  a 
similar  case.  It  is  in  consequence  of  these  cases  that  one  of  the  numerous 
pathogenic  theories  which  we  shall  now  study  has  been  built  up. 

Pathogenesis. — 1.  The  effusion  is  due  to  the  pas.sage  of  the  chyle  into 
the  peritoneal  cavity,  either  by  a  tear  or  by  an  obstacle  in  the  lymphatic 
system.  This  view  of  the  question  is  based  on  facts  of  incontestable  value. 
Strauss  made  use  of  a  most  ingenious  contrivance  to  prove  the  passage  of 
the  chyle  into  the  peritoneum  during  life.  The  patient,  who  was  placed  on 
an  ordinary  diet,  was  tapped,  and  the  ascitic  liquid  analyzed.     The  patient 

55—2 


868  TEXT-BOOK  OF  MEDICINE 

was  then  placed  on  strict  milk  diet,  and  an  emulsion  of  butter  was  given  in 
the  milk  as  strong  as  the  patient  could  take.  Fresh  effusion  appeared  at 
the  end  of  a  few  days.  The  patient  was  tapped,  and  the  analysis  of  the 
liquid  revealed  more  fatty  matter  than  at  the  first  tapping.  In  this  fatty 
matter  there  was  also  a  much  greater  quantity  of  butyrine.  It  is  therefore 
beyond  doubt  that  the  fat  absorbed  by  the  patient  passed  into  the  chyli- 
ferous  vessels,  and  from  them  into  the  cavity  of  the  peritoneum. 

Apart  from  the  cases  in  which  rupture  of  the  lymphatic  vessels  has  been 
proved,  can  the  transudation  of  the  chyle  through  the  chyliferous  vessels 
be  a  cause  of  lactescent  ascites  ?  Rokitansky,  Whitla,  Verdelli,  Bargebuhr, 
andWidal  admit  this;  but  an  objection  is  raised  against  this  theory,  because 
experiments  have  never  yet  succeeded  in  reproducing  chylous  efiusion. 
Potain,  in  speaking  of  this  subject,  insists  on  the  numerous  anastomoses 
of  the  large  lymphatics. 

2.  Lactescent  ascites  is  due  to  fatty  change  in  a  peritoneal  effusion 
(puralent  or  fibrinous).  Gueneau  de  Mussy  admits  that  the  chyliform 
effusion  into  the  pleura  results  from  the  slow  liquefaction  of  the  leucocytes 
of  the  pus  into  large  granulo-fatty  masses,  or  from  an  exaggerated  lipsemia. 
According  to  Robin,  when  the  pus  (which  contains  the  elements  of  the 
chyliform  liquid)  cannot  make  its  way  out,  it  undergoes  changes,  amongst 
which  fatty  degeneration  is  one  of  the  most  frequent.  The  peritoneal 
serum  is  said  to  have  an  emulsifying  action  (Veil). 

LetuUe  arrives  at  the  following  conclusions  :  (1)  All  cases  of  chyliform 
ascites  examined  post  mortem  are  cases  of  tubercular,  cancerous,  or  simply 
neo-membranous  peritonitis ;  (2)  the  existence  of  chronic  inflammatory 
lesions  represents,  then,  one  of  the  most  constant  elements  in  chyliform 
effusion  ;  (3)  granulo-fatty  degeneration  of  the  effused  inflammatory  pro- 
ducts (fibrine  and  leucocytes)  is  perhaps  sufficient  to  account  for  all  the 
emulsified  fat  in  suspension  in  the  peritoneal  serous  fluid.  This  conception 
serves  to  explain  the  presence  of  fat  in  chronically  inflamed  serous  mem- 
branes in  which  chyliferous  vessels  do  not  exist. 

3.  Debove  opposes  this  theory  with  an  argument  of  great  value  :  How 
are  we  to  explain  the  fact  that  the  liquid  preserves  its  chyliform  character 
when  it  recurs  so  soon  after  tapping  ?  In  order  to  explain  these  facts,  he 
proposes  a  theory  which  has  the  advantage  of  uniting  all  the  cases  without 
prejudging  any  one  of  them.  These  effusions,  says  he,  are  chyliform  from 
the  first,  in  the  same  manner  as  they  might  have  been  serous  or  purulent. 
The  word  "  chyliform  "  merely  shows  that  in  appearance  and  colour  the 
liquid  somewhat  resembles  chyle. 

4.  Parasitic  Theory.  —  In  some  cases  of  chyliform  ascites  Winckel 
observed  very  small  entozoa,  endowed  with  energetic  movements,  and  said 
to  be  filaria,  analogous  to  Bancroft's  species.     It  is  by  their  presence  that 


DISEASES  OF  THE  PERITONEUM  869 

Lancereaux  explains  milky  hydroceles,  and  Levois  lymphuria.  According 
to  Lancereaux,  the  parasite  causes  the  rupture  of  a  chyliferous  vessel. 

Finally,  the  experiments  of  Desombry  and  Porcher,  as  well  as  those  of 
Nocard,  show  that  the  intestinal  microbes  traverse  the  healthy  intestinal 
wall,  and  pass  into  the  serum  when  animals  have  been  given  fat  to  ingest. 
It  may  be  that  some  new  theory  will  withstand  the  attacks  that  have  shaken 
all  previous  hypotheses  (Fran9ois). 

Symptoms. — According  to  the  teaching  of  pathological  anatomy,  lac- 
tescent ascites  does  not  properly  belong  to  any  abdominal  affection  ;  it  may 
be  associated  with  any  disease  causing  effusion.  It  has  no  proper  symp- 
tomatology. Tapping  and  examination  of  the  liquid  alone  reveal  its 
presence.  In  the  stationary  stage,  inspection,  palpation,  and  percussion 
give  the  physical  signs  of  ordinary  ascites.  Lymphatic  varices  have  not  been 
found  in  any  case. 

After  tapping,  cancerous  or  tubercular  tumours  may  be  found  in  the 
peritoneum.  Ascites  which  is  lactescent  on  a  first  tapping  remains  so  on 
other  tappings.  Nevertheless,  it  has  been  found  first  limpid,  and  then 
milky  (Mery-Letulle)  ;  milky  and  then  limpid  (Siredey) ;  or  limpid,  then 
milky,  and  limpid  again  (Rendu).  Quenette  has  seen  it  associated  with 
pleurisy  of  a  like  nature. 

Course  —  Duration  —  Termination.  —  The  variety  of  the  affections 
accompanied  by  lactescent  ascites  explains  the  variable  course  of  this 
syndrome.  This  form  of  ascites  never  proceeds  in  an  identical  manner. 
The  stages  of  the  process  differ  in  aspect  and  in  duration,  but  the  termination 
is  always  fatal.  Momentary  arrest  and  remissions  have  been  observed. 
In  most  cases,  after  a  year  or  eighteen  months,  during  which  the  tappings 
follow  at  closer  and  closer  intervals,  the  patient  dies  of  cachexia.  This 
fatal  prognosis  is  perhaps  the  only  point  of  difference  between  lactescent 
and  ordinary  ascites.  Ascites  with  citron-like  effusion  can  recover  when 
the  causative  lesion  is  cured.  Such  cases  are  not  uncommon.*  Lactescent 
ascites  is  never  cured. 

Diagnosis. — ^Lactescent  ascites  may  be  diagnosed  by  examination  of 
the  liquid.  Fatty  granules  and  leucocytes  must  be  sought  for,  and  the 
formula  of  the  latter  must  be  determined.  Strauss's  experiment  (ingestion 
of  large  quantities  of  butter)  might  be  tried,  and  does  not  present  the 
slightest  danger.  As  to  the  diagnostic  value  of  lactescent  ascites,  it  is  of 
but  small  importance.  It  must  be  remembered,  however,  that  it  has  been 
specially  observed  in  tuberculosis  and  cancer  of  the  peritoneum. 

*  Di.iilafoy,  ('Uniques  de  I'Hutel-Dieu,  1898,  1899,  19'»    lecon. 


CHAPTER  VII 
DISEASES  OF  THE  LIVER 

I.  ANATOMY  AND  PHYSIOLOGY  OF  THE  LIVER. 

Anatomy.— Before  describing  the  lesions  of  the  hver,  the  cirrhoses  which  play  such  a 
large  part  in  the  pathology  of  this  organ,  the  degenerations  of  all  kinds  (fatty,  pig- 
mentary, amyloid)  which  affect  the  cell  in  various  ways,  the  changes  in  the  bloodvessels 
and  biUary  canals,  etc.,  it  is  essential  to  describe  briefly  its  normal  structure  and 
functions. 

The  hver  occupies  the  right  hypochondiium,  and  weighs  about  50  ounces.  It 
receives  two  kinds  of  afferent  vessels:  (1)  the  hepatic  artery  for  purposes  of  tissue 
nutrition  ;  and  (2)  the  portal  vein,  which  brings  the  venous  blood  from  the  intestine, 
stomach,  and  spleen  to  the  hver.  It  has  only  one  set  of  efferent  vessels— the 
hepatic  veins,  which  pour  the  blood  into  the  vena  cava.  In  a  section  of  the  liver  the 
portal  veins  may  be  easily  distinguished  from  the  hepatic  veins.  The  portal  veins  are 
accompanied  by  the  ramifications  of  Ghsson's  capsule,  do  not  adliere  to  the  tissue  of 
the  hver,  and  collapse,  whereas  the  hepatic  veins  adhere  to  the  tissue  of  the  hver  and 
remain  open.  On  section  of  the  Hver  we  can  observe  with  the  naked  eye  or  with  a 
low-power  microscope  a  number  of  small  islands,  coloured  deeper  at  the  centre  than 
at  the  circumference,  and  giving  to  the  liver  a  grained  appearance.  These  islands 
represent  the  hepatic  lobules. 

The  hver  is  formed  by  the  union  of  lobules,  and,  according  to  Sappey,  contains 
1,200,000.  If,  therefore,  we  know  the  structure  of  one  lobule,  we  know  the  structure 
of  the  whole  Uver.  The  hepatic  lobules  are  small  masses  1  milhmetre  wide  and  2  milH- 
metres  long,  and  fixed  on  to  the  divisions  of  the  hepatic  vein  hke  glandular  acini  to 
their  excretory  ducts.  The  polyhedral  form  of  the  lobules  is  due  to  mutual  pressure. 
They  are  separated  from  one  another  by  fissures  and  by  triangular  spaces  caused  by 
the  blunting  of  their  angles.  In  the  centre  of  the  lobule  we  find  the  suprahepatic  vein, 
which  is  adherent  to  the  tissue  of  the  Uver,  and  penetrates  the  lobule.  It  is  a  short 
branch  of  the  extralobular  hepatic  vein.  The  suprahepatic  vein  is  formed  of  fibro- 
elastic  tissue,  with  a  few  smooth  muscular  fibres,  and  is  hned  with  epithehum.  In 
pathological  conditions  this  fibrous  thickened  vein  is  an  important  histological  land- 
mark.  Around  the  lobule,  in  the  triangular  spaces  and  fissures,  are  the  portal  veins, 
the  hepatic  artery,  the  bihary  ducts,  and  the  lymphatic  vessels,  bound  together  by  con- 
nective tissue.  The  importance  of  these  fissures  and  spaces  in  the  pathological  anatomy 
of  the  Uver  will  be  already  apparent.  Between  the  hepatic  vein,  which  is  central,  and 
the  portal  veins,  which  are  peripheral,  we  find  capillaries  carrying  the  blood  from  the 
circumference  to  the  centre  of  the  lobule,  forming  a  venous  network  in  tlie  interior  of 
the  lobule,  and  united  with  one  another  by  transverse  anastomoses.  In  pathological 
conditions  these  capillaries  are  often  obstructed  by  red  corpuscles  and  microbes.  In 
the  meshes  of  this  capillary  network  are  the  hepatic  cells,  directly  connected  with  the 
network  of  the  biUary  canalicuU. 

S70 


DISEASES  OF  THE  LIVER  871 

1.  The  hepatic  cells  constitute  the  essential  and  specific  element  of  the  liver.  They 
are  small  blocks  of  a  soft  and  granular  substance,  and  their  variety  of  shape  is  due  to 
the  pressure  exerted  on  them  by  the  surroimding  cells  and  vessels.  After  a  fast  the 
cells  are  small  and  somewhat  ill-defined,  but  during  digestion  they  become  large  and 
very  distinct.  They  are  readily  isolated.  They  are  flattened,  polygonal,  so  that  each 
cell  is  in  contact  with  six  or  seven  of  its  neighbours,  as  well  as  with  the  blood  and  bile 
capillaries.  The  hepatic  cells  do  not  appear  to  have  an  envelope,  and  are  formed  of 
granular  protoplasm  containing  one  or  two  nuclei.  They  contain  yellow  gi'anules  of 
biliary  pigment,  with  red  granules  of  blood  pigment  and  fatty  granulations.  They 
contain  glycogen  and  the  ferment  by  which  the  glycogen  is  transformed  into  sugar. 
This  glycogenic  matter  is  especially  abundant  in  the  cells  at  the  centre  of  the  lobules. 
It  appears  in  Uttle  amorphous  masses,  wliich  are  almost  fluid,  and  turn  a  mahogany-red 
colour  with  tincture  of  iodine.  The  cells  radiate  from  the  centre  towards  the  circum- 
ference, thereby  following  the  disposition  of  the  vascular  meshes,  and  are  placed  in  a 
network  at  the  periphery  of  the  lobule  (Frey). 

The  radiation  of  the  cells  gives  them  the  appearance  of  little  columns,  sometimes 
called  trabeculae.  Eberth  has  compared  these  trabeculae  with  tubes,  the  tube  being 
formed  of  hepatic  cells  surroimded  by  a  membrane.  This  tubular  disposition  of  the 
liver,  which  exists  in  some  animals,  especially  in  the  seal,  is  seen  in  man  in  pathological 
conditions. 

2.  The  portal  veins  wliich  surround  the  hepatic  lobule  run  in  the  spaces  and  fissures 
between  the  lobules.  Each  lobule  is  penetrated  by  capillaries  derived  from  several 
portal  vessels.  These  capillaries  make  their  way  in  a  radial  direction  from  the  jjeriphery 
towards  the  centre  of  the  lobule  (KoUiker).  They  are  united  one  to  another  by  trans- 
verse anastomoses,  and  they  anastomose  with  the  capillaries  of  the  central  hepatic 
vein.  It  is  by  means  of  this  network  that  the  blood  of  the  peripheral  portal  veins, 
after  having  traversed  the  mass  of  the  cells,  pours  into  the  hepatic  vein.  It  is  in  this 
network  that  the  hepatic  cells  are  contained.  The  blood  capillaries  make  their  way 
in  the  gutters  hollowed  out  at  the  jimction  of  the  vertical  edges  of  the  hepatic  cells. 
Hence,  in  a  section  of  the  hver  perpendicular  to  the  capillaries  of  the  lobule,  the  hepatic 
cells  have  four  sides,  and  their  excavated  angles  receive  a  blood  capillary,  whereas 
the  bile  capillaries  travel  over  the  faces,  and  not  over  the  angles,  of  the  cells. 

3.  The  biliary  canals  surrounding  the  hepatic  lolmle  are  fonued  of  a  thin  enveloping 
membrane,  Uned  internally  by  cubical  epithelial  cells.  These  canals  are  the  terminal 
portions  of  the  intralobular  bifiary  canallculi.  The  intralobular  canalicuU  make  their 
way  through  the  hepatic  cells,  forming  narrow  meshes.  Their  path  is  rectiUnear,  and 
their  meshes  are  somewhat  elongated,  like  those  of  the  blood  capillaries.  "  The  biliary 
canaliculi  pass  between  the  faces  of  the  cells,  and  consequently  do  not  meet  the 
capillaries  of  the  blood,  from  which  they  are  distant  by  at  least  half  the  face  of  a 
hepatic  cell." 

Some  doubt  exists  regarding  the  structure  of  the  intralobular  canaliculi.  Some 
autliors  assign  to  them  a  wall  of  their  own,  formed  of  juxtaposed  flat  cells  (Legros)  ; 
others  say  that  they  have  only  a  borrowed  wall,  "  formed  by  the  condensation  of  tlio 
surface  of  the  hepatic  cells  into  a  cuticle."  The  hepatic  cell,  without  a  proper  wall, 
is  said  to  be  a  sim|)lo  modification  of  the  epithelium  of  the  biliary  canaliculi,  and  to 
circum3cril)e  them,  after  the  manner  of  the  secretory  cells  (Faraboeuf).  In  any  case, 
these  intralobular  canaliculi  serve  some  purpose  in  the  biUary  secretion.  They  receive 
the  bile  secreted  by  the  hepatic  lobule. 

4.  The  connective  tissue  of  the  hepatic  lolmle  is  derived  from  Glisson's  capsule. 
On  the  surface  of  the  liver  this  envelojje  is  formed  of  two  layers — the  one  superficial, 
serous,  and  covered  by  the  endothelial  cells  of  tlio  peritoneum  ;  the  other  deep,  thicker, 
and  formed  of  fibrous  tissue.  From  this  caiisule  bundles  of  connectfve  ti.ssuo  accom- 
pany the  interlobar  vessels,  and  help  to  fill  the  fissures  and  spaces  between  the  lobules. 


872  TEXT-BOOK  OF  MEDICINE 

The  perilobular  connective  tissue,  in  its  turn,  sends  out  an  intralobular  network  which 
is  adherent  to  the  wall  of  the  capillaries  or  extends  between  the  capillaries  in  the  form 
of  a  reticulated  tissue.  This  tissue,  united  with  the  blood  capillaries,  forms  a  woof 
supporting  the  hepatic  cells. 

The  perilobular  lymphatic  vessels  form  networks  that  accompany  the  portal  vein. 
These  lymphatic  vessels  are  probably  formed  by  lymphatic  capillaries  arising  in  the 
interior  of  the  lobule  (MacGillavry).  The  hepatic  artery  (nutrient  vessel)  supplies  the 
lobules  and  the  walls  of  the  veins  and  biliary  canals. 

The  hepatic  lobule  forms  an  anatomical  unit,  but  this  unit  in  no  way  corresponds 
to  the  ordination  of  pathological  lesions.  If  we  wish  to  discover  our  bearings  in  many 
lesions  of  the  liver,  we  must  come  back  to  the  conception  of  Eberth,  who  looks  upon 
this  organ  as  a  tubular  gland.  His  conception  is  borne  out  by  comparative  anatomy 
and  embryology.  The  hepatic  lobule  constitutes  in  the  human  species  the  anatomical 
unit,  but  the  pathological  unit  is  the  biliary  lobule  (Sabourin).  The  bihary  lobule, 
the  liver  being  considered  as  a  tubular  gland,  "  has  as  its  glandular  domain  the  paren- 
chyma grouped  around  a  portal  space — a  domain  extending  excentrically  as  far  as  the 
fii'st  system  of  subhepatic  veins.  This  domain  is  not  homogeneous,  because  it  is  com- 
posed of  several  hepatic  lobules.  Each  hepatic  lobule  is,  therefore,  formed  of  distinct 
segments,  each  one  belonging  to  different  biliary  lobules  "  (Sabourin). 

Physiology. — The  liver  joerforms  multiple  functions,  some  well  known,  others  still 
under  study.     I  shall  review  them  briefly. 

1.  The  liver  makes  bile.  It  is  not  made,  as  was  formerly  held,  by  the  biliary  glands 
contained  in  the  bihary  canals.  The  biliary  canals,  no  matter  what  their  size,  are  only 
excretory  ducts.  The  secretory  organ  of  the  bile  is  the  hepatic  cell.  Blligenesis  is 
one  of  the  most  important  functions  of  the  hepatic  cell,  which,  bathed  in  the  blood  of 
the  portal  vein,  extracts  and  elaborates  the  primary  matter  of  the  biliary  excrements. 
The  bile  made  by  the  cell  is  poured  into  the  bihary  canalicuh,  which  in  turn  lead  it 
into  the  larger  excretory  canals. 

It  is  chiefly  during  periods  of  fasting  that  the  liver  accomplishes  its  bihgenic  function, 
and  it  is  towards  the  end  of  the  meal  that  the  excretion  of  bile  into  the  intestine  takes 
place.  Man  secretes  about  40  ounces  of  bile  in  twenty-four  hours,  but  a  portion  is 
reabsorbed.  Fresh  bile  has  a  beautiful  yellow  colour,  due  to  bihrubin.  The  first  stage 
of  oxidation  causes  the  yellow  bile  to  become  green,  the  bihrubin  being  converted  into 
biUverdin.  Bilirubin  is  derived  from  the  htemoglobin  of  the  blood,  which  is  converted 
into  hsematin  by  the  biliary  acids,  takes  up  water,  and  loses  its  ferruginous  elements. 
Hsemoglobin  is  not  present  in  normal  bile.  In  the  spectroscope  bihrubin  extends  to 
the  left  of  Frauenhofer's  B  hne. 

The  bihary  acids  are  hkewise  formed  by  the  hepatic  cells.  Cholic  and  choleic  acids 
are  eliminated  as  salts  of  soda. 

The  bile  shares  with  the  pancreatic  juice  the  power  of  emulsification  and  absorp- 
tion of  fat.  A  fatty  condition  of  the  faecal  matter  is  therefore  seen  in  obstructive 
jaundice. 

As  the  bile  passes  through  the  intestine,  it  has  been  thought  to  act  as  an  antiseptic 
(Charrin  and  Roger). 

The  bile  is  a  toxic  Uquid,  and  the  intravenous  injection  in  an  animal  of  5  or  6  grammes 
of  bile  per  kilogramme  of  weight  produces  convulsions  and  death.  The  toxic  action 
depends  on  the  acids  and  colouring  matter. 

2.  The  liver  makes  glycogen,  and  the  hepatic  cell  is  charged  with  this  important 
fimction.  The  question  of  hepatic  glycogenesis,  first  discussed  by  Claude  Bernard,  will 
be  treated  in  greater  detail  under  Diabetes. 

The  liver  possesses  the  power  of  making  glycogen  from  every  kind  of  food.  I  say 
every  kind  advisedly,  because  the  formation  of  glycogen  takes  place  in  the  hepatic  cell, 
no  matter  what  the  kind  of  food  may  be,  and  apart  from  any  starch  and  sugar. 


DISEASES  OF  THE  LIVER  873 

Glycogen,  or  animal  starch,  is  not  the  simple  result  of  a  transformation,  but  of  a 
formation  which  is  effected  throughout  the  whole  animal  series  by  a  mechanism  analo- 
gous to  that  observed  in  the  vegetable  kingdom. 

The  sugar,  absorbed  by  the  intestine,  does  not  remain  in  the  liver  as  sugar,  but  is 
immediately  transformed  into  glycogen,  which  is  in  its  turn  transformed  into  glucose, 
and  poured  into  the  general  circulation  as  the  economy  demands  it  for  nutrition  and 
heat  production. 

In  the  formation  and  evolution  of  the  immediate  sugar  principle  there  are  two 
distinct  phenomena:  (1)  The  creation  of  the  amylaceous  matter  in  the  hepatic  cell — 
that  is  to  say,  the  secretion  of  glycogen ;  (2)  the  chemical  phenomenon,  causing  this 
principle  to  undergo  successive  transfcfrmations.  A  portion  of  the  glycogen  contained 
in  the  cell  is  stored  there  as  a  reserve  ration  ;  another  portion  is  continually  subject  to 
the  action  of  a  ferment  produced  in  the  liver.  By  this  ferment  the  glycogen  is  con- 
verted into  glucose,  which  passes  into  the  hepatic  veins,  and  so  to  the  whole  system, 
to  aid  in  the  general  nutrition  and  production  of  heat.  Glycogen  appears  to  undergo 
other  successive  transformations  (carbonic  acid,  lactic  acid,  and  no  doubt  fat). 

During  life  these  two  phenomena— the  secretion  of  glycogen  and  its  transformation 
by  the  ferment — take  place  at  the  same  time ;  after  death  the  secretion  of  glycogen, 
which  is  the  vital  act,  stops,  whilst  its  decomposition  into  secondary  products,  which 
is  the  chemical  act,  continues.  Accordingly,  the  liver  of  an  animal  may  be  washed 
several  times,  and  still  jaeld  traces  of  glucose. 

Writers  have  wished  to  make  the  glycogenic  function  general.  Rougey,  having 
found  glycogen  in  other  tissues — in  the  muscles,  for  example — though  only  in  small 
proportions,  wished  to  make  glycogenesis  a  general  nutritive  act,  and  not  a  particular 
function  of  the  liver.  I  cannot  enter  here  into  the  full  details  of  this  question,  but  it 
is  certain  that  the  presence  of  glycogen  in-  the  muscles,  testicles,  ovaries,  and  placenta 
has  not  the  importance  formerly  attributed  to  it.  "  These  are  phenomena  subject  to 
all  the  eventuahties  of  feeding,  and  to  all  the  varieties  that  are  observed  in  the  acci- 
dental phenomena  of  the  economy,  and  must  be  distinguished  from  the  constant 
functions  "  (Claude  Bernard).  The  constant,  invariable,  and  necessary  function  has 
devolved  on  the  Uver. 

3.  The  formation  cff  fat  in  the  liver  (I  am  not  speaking  of  fatty  degeneration)  seems 
to  result  from  a  change  in  the  glycogen  similar  to  the  production  of  wax  by  bees  which 
nourish  themselves  on  sugar,  and  the  production  of  fat  in  geese,  who,  after  an  exclusive 
diet  of  starch  and  sugar,  end  by  having  an  enormous  Hver  (Persoz).  The  formation 
has  not  its  exclusive  seat  in  the  liver,  but  this  organ  participates  largely  therein. 

4.  Lehmann's  view  that  the  liver  is  concerned  in  the  production  of  the  red  corpuscles 
is  no  longer  admitted.  It  is  now  held  that  the  Hver  is  an  organ  in  which  the  red  cor- 
puscles are  destroyed. 

5.  The  theory  advanced  by  several  authors,  and  notably  by  Murchison,  that  the 
liver  may  be  charged  with  the  production  of  urea,  lias  been  upheld  in  France  (Brouardel). 
According  to  the  old  theory,  urea,  considered  as  a  phenomenon  of  combustion,  or  as 
the  result  of  organic  splitting  up,  was  produced  in  the  tissues  of  the  whole  economy. 
According  to  the  new  theory,  urea,  considered  as  the  result  of  organic  splitting  up,  is 
produced  exclusively  in  the  hver.  We  see  the  deductions  which  result  tlujrcfrom. 
Pathological  condititjns,  which  exaggerate  the  normal  functions  of  the  organ,  favour  the 
increased  production  of  urea.  Pathological  conditions,  which  tend  to  impair  or  destroy 
the  function  of  the  liver  (acute  atrophy),  produce  a  noticeable  diminution  in  the  (juantity 
of  urea  excreted  in  the  urine.  We  shall  see  in  the  course  of  the  following  articles  that 
this  tlieory  is  not  absolutely  in  accordance  witli  facts,  l)ut  we  must  novertlicless  recog- 
nize that  physiologically  the  liver  takes  an  active  part  in  urogencsis. 

().  According  to  Schiff,  another  function  of  the  liver  is  to  arrest,  neutralize,  or 
destroy,  the  toxic  substances  absorbed  in  the  intestine  and  contained  in  the  portal 


874  TEXT-BOOK  OF  MEDICINE 

vein.  The  hepatic  cell  has  to  stop  in  part  the  alkaloids  resulting  from  the  putrid 
fermentation  that  goes  on  during  intestinal  digestion. 

"  In  the  intestine  infection  is  constant.  In  every  man  and  at  every  hour  the  agents 
of  intestinal  putrefaction  are  found  in  the  intestinal  cavity  giving  birth  to  toxic  products 
which  the  intestine  absorbs,  and  intoxication  in  various  degrees  is  extremely  frequent. 
If  this  intoxication  is  not  more  frequent,  or  if  it  is  not  of  daily  occurrence,  it  is  because 
the  organism  is  supplied  with  the  means  of  self -protection.  The  liver  arrests,  destroys, 
or  converts  a  part  of  the  poisons  absorbed  by  the  intestine ;  the  blood  burns  a  part,  and 
the  kidneys  ehminate  the  surplus  "  (Bouchard). 

"  The  poisons  of  the  gastro-intestinal  tract  are  to  a  large  extent  produced  by 
microbes  which  decompose  the  tertiary  and  quaternary  substances  of  food.  On  the 
other  hand,  these  very  microbes  produce  toxines,  so  that  infection  and  intoxication  are 
thus  intimately  connected"  (Hanot). 

"  The  intestine  is  generally  the  open  door  for  the  poisons  of  intoxication,  but  the 
liver  protects  the  organism  by  arresting  the  passage  of  the  poisons  in  order  to  neutralize 
them  or  to  return  them  into  the  intestine  "  (Bouchard). 

"  The  liver,  then,  is  not  only  the  storehouse  for  the  organism :  it  is  also  the  advance 
fortress  against  intoxication.  The  recognition  of  the  antitoxic  power  of  the  liver  and 
of  the  auto-intoxdcation  of  intestinal  origin  show  the  pathological  relations  between  the 
liver  and  the  intestine  "  (Hanot).  The  liver  arrests  the  vegetable  alkaloids  (morphia, 
quinine,  curare)  in  the  proportion  of  50  per  cent.  It  arrests  the  toxic  substances  of 
the  bile  which  have  been  reabsorbed  into  the  intestine. 


II.  CONGESTION  OF  THE  LIVER. 

The  extreme  vascularity  of  the  liver  and  the  richness  of  its  double 
system  of  capillaries,  interposed  between  the  general  venous  circulation 
and  the  heart,  are  favourable  to  congestion.  In  congestion  of  the  liver, 
as  in  that  of  the  lungs,  or  of  the  other  viscera,  we  have  not  to  describe  a 
definite  morbid  entity,  but  only  a  morbid  condition,  made  up  of  dissimilar 
elements.  This  chapter  in  pathology  is  therefore  an  enumeration  of  facts, 
most  of  which  have  no  connection  one  with  another,  and  in  order  to  group 
these  facts  it  is  customary  to  unite  them  into  active  and  passive  congestion. 
The  latter  has  acquired  such  an  importance  in  connection  with  "  the 
cardiac  liver  "  that  I  shall  devote  a  special  section  to  its  description. 

Active  Congestion. — Active  congestion  is  caused  by  an  excess  of 
pressure  in  the  afferent  vessels  (portal  veins).  The  fullness  of  these  vessels 
causes  a  marked  increase  in  the  size  of  the  liver.  Heavy  meals,  errors  of 
diet,  alcohohc  excess,  and  purgatives,  modify  the  portal  circulation  and 
stimulate  the  hepatic  cells,  causing  vaso-dilatation  and  congestion.  I  may 
say  the  same  of  afiections  of  the  small  intestine  (tuberculosis)  and  of  the 
colon  (dysentery),  in  which  case  the  portal  blood  carries  irritating  substances 
(microbes  or  toxines)  to  the  Hver.  Congestion  of  the  liver  is  frequent  in 
the  intermittent  fevers  and  in  the  bilious  remittent  fevers  of  hot  countries 
(Dutrouleau).  It  forms  the  first  stage  in  certain  diseases  of  the  organ 
(cirrhosis,  hepatitis).     Suppression  of  the  menses  or  of  a  hsemorrhoidal  flux 


DISEASES  OF  THE  LIVER  875 

may  cause  congestion  of  the  liver.  An  attack  of  gout  is  sometimes  preceded 
by  congestion  of  the  liver. 

Amongst  the  causes  which  produce  congestion  of  the  liver,  I  may  mention 
dyspeptic  troubles  and  auto-intoxication  of  gastro-intestinal  origin. 

Dilatation  of  the  stomach  enters  into  the  pathogenesis  of  hepatic  con- 
gestion. "  In  389  personal  observations  of  dilatation  of  the  stomach," 
says  Bouchard,  "  I  found  swelHng  of  the  liver  in  the  proportion  of  23  per 
cent." 

Congestion  of  the  liver  shows  itself  by  a  feeling  of  discomfort  and  heavi- 
ness in  the  right  hypochondrium.  Shght  jaundice  may  be  present,  and  the 
urine  contains  urobilin  or  biliary  pigments.  The  Uver  is  tender  on  pressure, 
and  can  be  felt  beyond  the  false  ribs.  Percussion  gives  an  increase  of  several 
centimetres  in  the  vertical  diameter.  This  swelling  increases  or  diminishes  ; 
it  is  subject  to  recurrences,  and  is  sometimes  the  first  stage  of  a  commencing 
cirrhosis. 

The  treatment  of  hepatic  congestion  varies  according  to  the  cause. 

III.  PASSIVE  CONGESTION— CARDIAC  LIVER. 

Pathogenesis. — Passive  congestion  of  the  liver  is  caused  by  increased 
pressure  in  the  efferent  vessels  (sublbbular  veins,  vena  cava).  This  venous 
stasis  is  due  to  many  causes — diseases  of  the  heart  (lesions  of  the  mitral 
and  tricuspid  valves),  diseases  of  the  lungs,  which  diminish  the  field  of 
hsematosis  (emphysema  and  fibrosis),  intrathoracic  tumours,  which  impede 
the  circulation  in  the  inferior  vena  cava — but  the  most  frequent  causes 
are  lesions  of  tlie  mitral  valve  and  changes  in  the  cardiac  muscle.  When 
mitral  lesions  are  ill-compensated,  when  the  cardiac  muscle  Ls  affected,  and 
the  left  auricle  is  not  completely  emptied,  there  results  an  obstruction 
which  extends  throughout  the  whole  of  the  lesser  circulation  to  the  vessels 
of  the  lungs,  the  right  ventricle,  and  the  right  auricle.  This  blood-stasis 
hinders  the  return  circulation  in  the  inferior  vena  cava,  and  the  hepatic  veins 
and  causes  congestion  of  the  liver.  This  congestion,  which  is  at  first 
temporary,  ends  by  becoming  permanent,  and  causes  the  anatomical  changes 
of  the  cardiac  liver. 

Tlie  value  of  this  mechanical  theory  for  the  cardiac  liver,  as  created  by 
Beau  and  Gendrin,  must  not  be  exaggerated.  Defective  hydraulics,  due  to 
the  cardiac  lesion,  certainly  play  a  large  part  in  the  determination  of  the 
hepatic  changes,  but  the  mechanical  obstacle  to  the  circulation  is  not  the 
only  cause.  It  is  not  rare  to  find  people  suffering  from  disease  of  the  heart 
in  whom  the  liver  is  attacked  before  the  intermediary  circulation — that  of 
the  lungs,  for  instance— and  before  the  peripheral  circulation  (cwloma  of 
the  legs)  has  been  influenced  by  the  cardiac  lesion.    In  such  a  case  it  might 


876  TEXT-BOOK  OF  MEDICINE 

be  held  that  the  liver,  having,  under  the  influence  of  multiple  causes,  become 
an  organ  of  minoris  resistentice,  is  more  liable  than  the  other  organs  to 
feel  the  cardiac  lesions. 

These  considerations  are  absolutely  applicable  to  the  auto-intoxications 
of  intestinal  origin,  prolonged  gastro-intestinal  dyspepsia,  alcoholism, 
malaria,  gall-stones,  and  more  or  less  general  arterio-sclerosis.  The  liver 
withstands  the  effect  of  the  cardiac  lesions  the  better  as  it  is  prepared  by 
its  relations. 

Symptoms. — The  clinical  picture  of  the  cardiac  liver  varies.  Let  us 
select  the  most  common  types.  In  one  variety  the  cardiac  lesion  is  not 
advanced.  The  patient  suffers  slightly  from  palpitation,  and  can  neither 
ascend  a  staircase  nor  walk  quickly  without  getting  out  of  breath.  Malleolar 
oedema  is  common,  but  there  are  as  yet  no  serious  symptoms.  Later,  in 
consequence  of  fatigue,  of  excesses  in  the  use  of  drink  and  food,  or  even 
without  any  appreciable  cause,  the  patient  suddenly  experiences  digestive 
troubles,  distension  of  the  belly,  and  a  feeling  of  weight  in  the  liver.  He 
complains  of  sharp  pains  in  the  right  hypochondrium,  and  has  "  a  weight 
on  his  stomach."  The  dyspnoea  and  the  cardiac  arrhythmia  grow  worse, 
as  if  the  liver,  in  its  turn,  reacted  on  the  cardio-pulmonary  circulation 
(Potain).  On  examining  the  patient,  we  notice  a  yellowish  tint  of  the  con- 
junctivae and  the  face,  but  the  urine  does  not  always  contain  bile  pigment. 
There  is  no  ascites,  but  the  oedema  of  the  lower  limbs  progresses.  On 
auscultating  the  heart,  a  mitral  lesion  is  found,  and 'in  the  lungs  rales,  due 
to  congestion  and  oedema,  are  heard  at  both  bases.  The  urine  is  scanty, 
of  a  red-brown  colour,  and  contains  urobilin.  At  this  period  the  liver  is 
large  and  but  slightly  indurated,  being  as  yet  only  congested.  It  is  known 
as  the  nutmeg  liver,  and  only  becomes  hard  and  cirrhotic  (red  atrophy) 
later,  if  the  hepatic  lesion  persists,  or  if  it  is  complicated  by  further  changes. 
If  we  institute  efficient  measures,  such  as  leeches  or  wet- cupping  to  the 
hepatic  region,  a  milk  diet,  and  diuretic  wine  or  small  doses  of  digitalis,  in 
a  little  while  the  congestion  of  the  liver  will  disappear,  and  for  the  time 
being  the  danger  is  removed. 

In  another  patient  events  may  take  a  different  course.  The  hepatic 
mischief  is  more  advanced,  the  mitral  lesion  is  of  longer  duration,  and  the 
cardiac  muscle  is  losing  its  strength.  The  lungs  are  much  congested,  the 
kidneys  act  badly,  the  urine  is  of  a  deep  colour,  and  contains  a  brownish 
pigment,  the  yellow  colour  of  the  skin  is  more  evident,  and  the  oedema 
tends  to  become  general.  Palpation  and  percussion  show  that  the  liver 
is  hard  and  painful ;  in  size  it  is  either  enlarged  or  normal,  but  the  ascites 
often  makes  exact  examination  impossible.  The  treatment  referred  to 
above  is  put  into  practice,  but  does  not  produce  the  same  effect,  because  the 
cardiac  liver  is  now  cirrhotic. 


DISEASES  OF  THE  LIVER  877 

In  short,  the  hepatic  congestion  of  cardiac  patients  is  transitory  before 
becoming  permanent.  It  may  be  considerable  during  the  attacks  of 
asystole.  Feelings  of  heaviness  and  of  pain  in  the  hypochondrium,  a 
yellowish  colour  of  the  skin,  and  dyspeptic  troubles  are  rarely  absent.  The 
liver  is  tender  on  pressure,  and  increased  in  size.  Later  the  cirrhosed  liver 
may  diminish  in  size,  the  symptoms  become  more  severe,  ascites  is  frequent, 
and  symptoms  of  icterus  gravis  often  supervene. 

In  certain  cardiac  cases  the  hepatic  troubles  precede  the  other  mani- 
festations of  heart  disease  ;  in  others  (tricuspid  insufficiency)  the  reflux  of 
the  blood  produces  hepatic  pulsation  (Potain). 

Pathological  Anatomy. — The  cardiac  Hver  varies  according  to  the  period 
at  which  it  is  examined.  In  the  first  period  it  is  congested,  hypertrophied, 
and  weighs  4  to  6  pounds,  while  its  sharp  edge  becomes  rounded  and  its 
surface  is  smooth.  On  section,  the  lobules  are  increased  in  size,  and  form 
islets,  red  in  the  centre  and  greyish  at  the  periphery.  This  double  colora- 
tion, which  is  only  an  exaggeration  of  the  normal  condition,  gives  the  liver 
a  granular  appearance,  whence  the  name  of  nutmeg  liver.  Under  the 
microscope  the  central  part  of  the  lobule  is  of  a  mahogany-red  colour,  from 
the  dilatation  and  congestion  of  the  hepatic  vein,  from  the  enlargement  and 
fullness  of  the  neighbouring  capillaries,  and  from  the  changes  in  the  flattened 
and  atrophied  Uver  cells,  the  protoplasm  often  containing  granules  of 
pigment  and  crystals  of  hgematoidin.  The  peripheral  portion  of  the 
lobule  is  greyish  or  opaque,  because  it  is  relatively  anaemic,  and  also  because 
many  of  the  hepatic  cells  are  spherical  and  rich  in  fatty  granules,  the  blood 
in  the  portal  veins  becoming  stagnant  at  the  periphery  of  the  lobule,  and 
leaving  the  fat  derived  from  digestion  in  the  peripheral  cells.  At  a  more 
advanced  period  the  liver  may  atrophy  (red  atrophy)  ;  its  surface  becomes 
slightly  granulated,  and  the  double  colouring  of  the  islets  is  less  dLstinctly 
defined.  Under  the  microscope  we  see  that  the  central  vein  and  the  central 
capillaries  are  dilated  and  congested  with  blood,  so  as  to  resemble  the  blood 
tumours  of  the  liver  ;  hence  the  name  of  "  red  atrophy  "  given  to  this  stage 
of  the  cardiac  liver.  The  hepatic  cells  of  the  central  zone  have  partially 
disappeared,  and  are  replaced  by  young  connective  tissue,  with  periphlebitis 
and  thickening  of  the  external  coat  of  the  vessels.  The  liver  is  also  indurated, 
and  this  fibrous  change  in  the  congested  cardiac  liver  has  given  to  the  lesion 
the  name  of  cardiac  cirrhosis. 

Some  authors  do  not  admit  this  central  fibrosis  of  the  hepatic  lobule, 
or,  at  least,  they  consider  it  inconstant,  rudimentary,  and  limited  to  the 
walls  of  the  hepatic  vein  only,  whilst  there  is  at  the  periphery  of  the  hepatic 
lobule  a  fibrosis  which  accompanies  the  ramifications  of  the  pf)rtal  vein, 
and  is  somewhat  analogous  to  the  lesioiLs  of  Laeunec's  atrophic  cir- 
rhosis. Thus  understood,  cirrhosis  in  the  cardiac  liver  would  be  a  bivenous 


878  TEXT-BOOK  OF  MEDICINE 

cirrhosis,  and  the  hepatic  lobule  would  be  invaded  from  all  sides — at  its 
centre  from  the  hepatic  vein,  and  at  its  periphery  from  the  portal  veins. 
We  should  find,  therefore,  endo-periarteritis  of  the  hepatic  arterioles.  This 
opinion  has  been  upheld  by  Wickham  Legg  and  Talamon., 

Recent  researches  have  given  to  each  of  these  changes  their  proper 
value.  As  a  matter  of  fact,  perilobular  fibrosis  and  endo-periarteritis  are 
found  amongst  the  lesions  in  the  cardiac  liver,  but  this  peripheral  fibrosis 
is  not  directly  associated  with  the  lesions  of  the  cardiac  liver,  properly  so 
called.  They  are  superadded  fibrous  lesions,  and  form  a  part  of  a  more 
general  fibrous  process.  Thus,  to  quote  examples,  patients  attacked  with 
these  bastard  forms  of  cardiac  cirrhosis  suffer  at  the  same  time  either  from 
Bright's  disease,  or  are  alcoholics,  and  have  in  consequence  more  or  less 
general  arterio -sclerosis.  The  characteristic  lesion  of  the  nutmeg  (period 
of  vascular  enlargement)  and  cirrhotic  liver  (period  of  connective  tissue 
formation)  chiefly  affects  the  centre  of  the  hepatic  lobule — that  is  to  say, 
the  area  of  the  hepatic  veins.  The  lesions  are  more  or  less  extensive,  accord- 
ing as  the  process  that  produces  the  cardiac  liver  is  cortical,  subcapsular, 
or  general. 

In  "  this  complete  remodelling  of  the  hepatic  parenchyma  "  (Chauffard) 
the  microscopic  appearance  of  the  sections  presents  certain  peculiarities, 
carefully  described  by  Sabourin.  We  see  hepatic  islets  which  have  no  longer 
the  hepatic  vein  in  the  centre  of  the  islet,  but  a  porto-biliary  space,  and 
around  these  islets  zones  of  trabecular  atrophy  form  a  network  in  which, 
at  the  points  of  convergence,  the  hepatic  veins  are  found.  The  type  of  the 
normal  hepatic  lobule  is  thus  reversed,  and  the  porto-biliary  canal  actually 
forms  the  centre  of  the  figure." 

The  lesions  of  the  cardiac  liver  are  sometimes  accompanied  by  catarrh 
of  the  bile-ducts  and  jaundice. 

The  treatment  of  passive  congestion  of  the  liver  consists  in  lowering 
the  blood-pressure  in  the  venae  cavae  and  hepatic  veins.  Diuretic  drinks, 
milk  diet,  Trousseau's  diuretic  wine,  digitalis,  leeches  applied  to  the  anus, 
leeches  and  wet-cupping  over  the  liver,  saline  purgatives,  and  Vichy, 
Carlsbad,  or  Tharasp  water,  are  the  means  most  employed. 


IV.  CIRRHOSIS  OF  THE  LIVER  IN  GENERAL. 

The  word  cirrhosis  has  been  preserved  to  conform  to  the  usage  established  by 
Laennec.  Cirrhosis  of  the  hver,  otherwise  called  sclerosis,  or  chronic  hepatitis,  forms 
a  large  part  of  the  pathology  of  this  organ.  It  is  characterized  by  the  overgrowth  of 
the  normal  connective  tissue,  extending  from  Glisson's  capsule  into  the  hepatic  lobules. 
In  the  first  stage  the  fibroplastic  tissue  is  embryonic,  and  formed  of  cells  analogous  to 
leucocytes.  In  this  embryonic  connective  tissue  flat  cells  and  bundles  of  fibrils  appear, 
and  the  morbid  process,  continuing  its  growth,  ends  in  a  morbid  tissue  which  is  more 


DISEASES  OF  THE  LIVER  879 

or  less  invading,  more  or  less  dense,  and  more  or  less  fibrous  and  retractile,  as  the  case 
may  be. 

The  formation  of  cirrhotic  tissue  is  not  a  matter  of  chance,  and  the  fibrous  tissue 
is  not  produced  here  or  there  in  an  indeterminate  manner.  It  is  almost  systematic  in 
its  invasion.  Thus,  according  to  the  case,  the  cirrhosis  follows  the  coiurse  of  the  veins, 
the  bihary  canaficuh,  or  the  arterioles.  Venous  cirrhosis  is  associated  either  with 
lesions  of  the  central  vein  of  the  lobule  (cardiac  fiver),  with  the  combined  lesions  of 
the  peripheral  portal  veins,  or  with  the  combined  lesions  of  the  central  and  peripheral 
veins  (bivenous  cirrhosis,  Laennec's  atrophic  cirrhosis,  hypertrophic  alcohohc  cirrhosis). 
Bihary  cirrhosis  is  associated  with  the  lesions  of  the  bifiary  canals,  and  the  most  im- 
portant variety  is  called  hypertrophic  bihary  cirrhosis.  In  many  circumstances  the 
toxic  agent  attacks  the  hepatic  cells  themselves,  and  produces  divers  changes.  It  was 
formerly  said  that  the  fibrous  lesions  might  arise  from  changes  in  the  cells  of  the  hepatic 
lobule,  and  that  there  was  a  double  lesion — Interstitial  hepatitis,  having  its  origin  in 
the  connective  tissue ;  and  parenchymatous  hepatitis,  or  visceral  cirrhosis,  having  its 
origin  in  the  hepatic  cells.  The  epithehal  change  is  now  denied.  "  In  reahty,  the 
doctrine  of  epithehal  cirrhosis  has  had  its  day  "  (Letulle). 

These  varieties  of  origin,  extension,  topography,  and  evolution  of  the  morbid  con- 
nective tissue  are  associated  with  the  condition  of  the  cells  (atrophy,  disappearance, 
fatty  degeneration,  pigmentation,  or  adenoma)  that  imprints  on  fibrosis  of  the  fiver  its 
pecufiar  characteristics. 

Division. — Fibroses  of  the  fiver  may  be  partial  or  general,  primary  or  secondary, 
and  isolated  or  associated  with  other  diseases,  such  as  syphifis,  alcohofism,  malaria, 
diabetes,  arterio-sclerosis,  or  diseases  of  the  heart  and  kidneys. 

1.  Partial  fibroses  occur  as  secondary  lesions  in  several  diseases  of  the  fiver.  Fibrous 
tissue  is  found  around  tumours,  in  the  neighbourhood  of  syphifitic  gummata,  hydatids, 
or  angiomata.  In  these  examples  of  partial  fibrosis  the  overgrowth  of  connective  tissue 
is  not  of  great  interest. 

2.  Fibrosis  in  some  cases  occurs  at  the  same  time  as  some  other  lesion  of  the  fiver. 
We  meet  with  fatty  fivers  which  are  hkewise  fibrous,  and  side  by  side  with,  the  cells 
filled  with  fat  we  find  hyperplasia  of  the  connective  tissue,  which  sometimes  penetrates 
the  interior  of  the  lobule.  The  liver  is  indurated,  smooth  on  section,  and  increased  in 
size.  I  shall  describe  a  type  of  tins  variety  later  under  the  name  of  hypertrophic  fatty 
cirrhosis  (Hutinel-Sabourin  type).  I  shall  also  describe  cirrliosis  associated  with  tuber- 
culosis of  the  fiver.  When  fibrosis  is  combined  witli  amyloid  degeneration,  the  hver 
has  not  the  enormous  size  of  the  purely  lardaceous  organ,  and  is  perhaps  even  below 
the  normal  size. 

3.  We  find  bastard  secondary  fibroses  in  which  the  lesion  in  the  fiver  is  associated 
with  disease  of  the  In-art  and  kidneys.  I  have  described  elsewhere  the  changes  found 
in  tlie  cardiac  liver,  so  tiiat  I  need  not  return  to  tliem.  We  shall  see  later  under  Diseases 
of  the  Kidneys  that  iiepatic  cirrliosis  may  accompany  the  complex  process  of  Bright's 
disease.    This  form,  as  also  malarial  and  diabetic  cirrhosis,  will  be  described  in  duo  course. 

4.  For  the  time  being  I  will  fimit  the  description  of  cirrhosis  of  the  liver  to  certain 
well-defined  varieties — viz.,  Laennec's  atrophic  cirrhosis,  hypertrophic  alcohofic  cir- 
rhosis, hypertropliic  biliary  cirrhosis,  and  syphifitic  cirrhosis — but  yet  some  of  these 
varieties  are  not  alwaj's  dearly  defined,  and  may  give  rise  to  mixed  or  intermediate 
forms. 

5.  Adenoma  is  in  some  cases  associated  witii  cirrhotic  lesions.  Tiio  adenoma  is 
sometimes  discrete,  but  at  other  times  it  takes  a  most  important  place. 

Tlio  question  of  the  regeneration  of  the  fiver  will  also  claim  our  attention  (com- 
pensatory hyperplasia). 

Before  describing  cirrhosis  of  the  fiver,  it  will  bo  useful  to  give  a  iiisturical  sketch 
of  this  question. 


880  TEXT-BOOK  OF  MEDICINE 

History. — The  history  of  cirrhosis  of  the  liver  dates  from  Laennec's  time,  and  it 
may  even  be  said  that,  following  Laennec's  example,  only  one  variety  of  hepatitis  was 
for  a  long  time  described — viz.,  atrophic  cirrhosis.  Laennec  used  the  name  cirrhosis 
{Kippos,  red)  on  account  of  the  coloitr  of  the  cirrhotic  liver.  Although  this  term  is 
imperfect  in  that  it  only  applies  to  an  inconstant  trait  of  the  lesion,  and  although  the 
name  sclerosis  (ctkAt^pos,  hard),  or  chronic  hepatitis,  might  be  substituted,  I  shall 
nevertheless  retain  the  name,  so  as  to  conform  to  custom.  Laennec  was  mistaken  as 
to  the  nature  of  the  lesion,  because  cirrhosis,  in  his  mind,  represented  a  production 
which  he  called  "  cirrhosis,"  and  which  he  believed  to  be  analogous  with  sciiThus  ;  but 
in  all  other  points  his  description  is  typical.  With  admirable  precision  he  sketched  in 
a  few  words  the  characters  and  the  course  of  a  disease  previously  unknown.  Hanot 
had  the  happy  idea  of  giving  to  this  disease  the  name  of  Laermec's  cirrhosis. 

In  the  year  1827  Bright  stated  positive  ideas  with  regard  to  sclerotic  hepatitis.  He 
cites  as  a  cause  alcohohsm.  As  lesions,  he  describes  the  changes  in  the  liver,  fibrous 
peritonitis,  sclerosis  of  the  intestine,  and  the  illustrations  in  his  book  show  several 
types  of  cirrhosis.  He  noticed  that  the  lesions  "  produce  general  obstruction  of  the 
circulation  through  the  branches  of  the  portal  vein,  and  thus  become  the  immediate 
cause  of  the  ascites,  independently  of  the  morbid  conditions  which  may  affect  the 
blood  from  the  fact  that  it  has  not  left  behind  in  the  liver  the  substances  which  ought 
to  be  eliminated  by  the  bile." 

With  Kieman  the  pathological  anatomy  of  cirrhosis  takes  a  decided  step  forward. 
The  Enghsh  author,  in  his  remarkable  "  Researches  on  the  Structure  of  the  Liver," 
proves  the  normal  existence  of  a  connective  web  which  surrounds  and  penetrates  the 
hepatic  lobule,  and  he  attributes  cirrhosis  to  the  abnormal  development  of  this  web. 
In  Gubler's  thesis  for  the  Fellowship,  which  bears  the  date  1853,  the  ideas  common 
to  that  period  are  collected.  It  shows  us  that  up  to  that  time  only  one  variety  of 
cirrhosis,  with  very  few  exceptions,  was  admitted — viz.,  that  which  ended  in  atrophy 
of  the  Uver.  We  see  that  the  cirrhotic  Hver  may  show  itself  in  the  hypertrophic  form, 
but  for  a  long  time  to  come  Laennec's  atrophic  cirrhosis  was  the  only  variety  known. 
Nevertheless,  post-mortem  examinations  revealed  enlarged  and  cirrhotic  livers  that  had 
not  the  appearance  of  common  cirrhosis  ;  but,  as  the  profession  was  convinced  that 
cirrhosis,  even  when  it  commences  with  hypertrophy,  must  end  in  atrophy,  all  enlarged 
livers  were  considered  to  represent  the  initial  pliase  of  ordinary  cirrhosis,  the  morbid 
process  commencing  with  hypertrophy  of  the  organ,  and  ending  with  atrophy.  More- 
over, this  manner  of  regarding  matters  has  been  admitted  by  certain  (.^erman  authors 
(Birch-Hirschfeld).  This  interpretation  perpetuates  an  error.  I  do  not  say  that 
atrophic  cirrhosis  cannot  commence  with  temporary  hypertrophy  ;  I  do  not  say  that 
in  certain  mixed  forms  which  we  shall  study  later  Laennec's  cirrhotic  hver  may  not 
weigh  more  than  normal ;  but  these  cases  are  in  no  way  opposed  to  the  existence  of 
so-called  hypertrophic  cirrhosis,  where  the  liver  remains  increased  in  size  during  the 
whole  disease. 

The  autonomy  of  hypertrophic  cirrhosis  had  been  foreseen  by  Requin,  and  clearly 
formulated  by  Told.  Jaccoud  had  observed  and  discussed  it,  but  it  was  only  accepted 
in  France  after  the  publication  of  OlHver's  monograph,  in  which  he  points  out  the 
chnical  characters  of  this  affection,  and  assigns  to  it  anatomical  characters  previously 
indicated  by  Charcot  and  Luys. 

From  this  epoch  hypertrophic  cirrhosis  served  as  a  text  for  numerous  works. 
Hayem  studied  the  disposition  of  the  sclerotic  tissue.  Cornil  observed  the  inflamma- 
tion, the  dilatation  of  the  bihary  canahcuh,  and  the  formation  of  an  intra-  and  extra- 
lobular  network  of  bile-ducts.  Hanot  proved  that  the  inflammation  of  the  small 
bihary  canals  in  the  portal  spaces  is  the  starting-point  for  the  lesions.  He  created 
hypertropliic  bihary  cirrhosis,  to  which  the  name  of  "  Hanot's  disease  "  has  been  rightly 
given. 


DISEASES  OF  THE  LIVER  881 

On  the  other  hand,  the  experiments  begun  by  Legg  and  coniijieted  by  Cliarcot  and 
Gombault  prove  that  permanent  hgature  of  the  common  bile-duct  produces  in  animals 
angiochoUtis  and  periangiocholitis,  and  consequently  connective  hyperplasia,  somewhat 
analogous  to  the  change  seen  in  hypertrophic  biliary  cirrhosis.  Hypertrophic  cirrhosis 
is,  therefore,  an  absolutely  distinct  variety.  Its  pathogenesis  and  its  anatomical  and 
clinical  characters  differentiate  it  from  Laennec's  atrophic  cirrhosis,  and  are  so  distinct 
that  it  seems  impossible  to  reconcile  these  two  species.  The  distinctive  characteristics 
may  be  thus  stated  : 

1.  Laennec's  atrophic  cirrhosis  is  of  bivenous  origin  (periportal  and  hepatic).  This 
cirrhosis  is  annular,  multilobular,  and  extralobular.  The  hver  is  atrophied  and  granular. 
The  clinical  characteristics  are  as  follows  :  ascites,  the  development  of  a  collateral  cir- 
culation, frequent  haemorrhage,  absence  of  jaundice,  and  average  duration  twelve  to 
eighteen  months. 

2.  Hypertrophic  biliary  cirrhosis  is  of  biliary  origin — that  is  to  say,  the  process 
commences  vrith  angiochohtis  of  the  bile-ducts.  The  sclerosis  is  monolobular,  insular, 
extra-  and  intralobular.  The  hver  shows  general  enlargement.  The  clinical  charac- 
teristics are  as  follows :  progressive  and  persistent  jaundice,  enormous  enlargement  of 
the  liver,  enlarged  spleen,  absence  of  ascites  and  collateral  circulation,  httle  haemor- 
rhage, average  duration  three  to  eight  years.  Do  these  two  cirrhoses  really  form  two 
distinct  types  ?  Are  not  their  lesions  and  their  symptoms  often  combined  ?  Cannot 
they  give  rise  to  mixed  and  various  forms  ?  I  shall  attempt  to  answer  these  questions, 
but  I  may  state  at  the  outset : 

1.  Side  by  side  with  Laennec's  atrophic  cirrhosis  there  is  room  for  other  atropliic 
varieties  of  cirrhcsis. 

2.  Side  by  side  with  hypertrophic  biliary  cirrhosis  there  is  room  for  other  forms  of 
hypertrophic  cirrhosis,  with  or  without  jaundice. 

3.  Between  the  atrophic  bivenous  type  of  cirrhosis  and  the  hypertrophic  biliary 
type  there  is  room  for  intermediate  formB.  This  question  will  be  discussed  under  Mixed 
Cirrhoses. 


V.    VENOUS    CIRRHOSIS— L,AJi:NNEC'S    ATROPHIC    CIRRHOSIS- 
CIRRHOSIS  BY  GASTRO-INTESTINAL  AUTO-INTOXICATION. 

Pathological  Anatomy.  —  In  atrophic  cirrhosis  the  hver  is  always 
dimiriLshed  in  size,  and  the  atrophy  principally  affects  the  left  lobe  (Freichs). 
The  theory  that  atrophic  cirrhosis  commences  with  hypertrophy  must  not 
be  rejected  altogether,  for  there  are  cases  in  which  the  initial  congestion 
increases  the  size  of  the  organ.  At  an  advanced  period  the  liver  is  atrophied 
and  may  not  weigh  more  than  half  the  normal  weight.  Its  colour  is  l)r(>wn, 
reddish  {Kippo<i,  red),  yellowish,  or  greyish,  according  to  the  predominance 
of  the  biliary  or  fatty  elements.  The  edge  of  the  hver  is  blunted,  and  often 
furrowed  by  fibrous  bands.  The  surface  of  the  liver  is  nodular,  and  studded 
with  little  hard  mas.ses  that  are  mammillated,  of  a  ruddv  yellow,  and  varying 
in  size  from  a  pin's  head  to  a  hazel-nut.  These  granulations  are  formed 
by  larger  or  smaller  masses  of  hepatic  lobules,  surrounded  by  fibrous  tissue. 
These  details  are  better  seen  after  removal  of  Glisson's  capsule,  which  is 
generally  adherent,  opaque,  and  thickened.  The  granulations  sometimes 
resemble  the  heads  of  naUs,  whence  the  name  hobnailed  liver  of  English 


882  TEXT-BOOK  OF  MEDICINE 

writers.  In  some  cases  the  parencliyma  is  strangled  by  tlie  fibrous  zones, 
protrudes  like  a  cauliflower,  and  the  liver  is  thus  divided  into  lobes. 

The  tissue  of  a  cirrhotic  liver  is  not  easily  torn.  It  is  hard,  creaks  under 
the  knife,  and  is  not  friable.  On  section,  granules  of  various  sizes  are  found, 
similar  to  those  on  the  surface.  They  are  surrounded  by  fibrous  tissue, 
which  forms  rings  around  them,  and  from  which  they  emerge,  as  though 
they  were  about  to  become  enucleated.  The  granules  may  be  enucleated 
when  the  specimen  is  macerated  in  water. 

Histological  Examination. — Atrophic  cirrhosis  of  the  liver  consists  in 
hyperplasia  of  the  connective  tissue  in  various  phases  of  growth — em- 
bryonic cells,  fusiform  cells,  fibrillary  and  fibrous  tissue.  The  process 
commences  as  an  embryonic  neoplasia,  and  ends  in  fibrous  retractile  tissue. 

The  fibrous  tissue  of  atrophic  cirrhosis  is  formed  in  the  portal  spaces 
around  the  portal  veins,  and  in  the  centre  of  the  lobules  around  the  hepatic 
veins.  These  two  cirrhotic  systems,  the  one  peripheral  and  the  other 
central,  occur  together,  and  are  united  by  numerous  anastomoses.  The 
cirrhosis  is  thus  bivenous. 

In  the  midst  of  the  fibrous  connective  tissue  around  the  portal  spaces, 
which  stains  red  with  picrocarmine,  the  portal  veins,  biliary  canaliculi,  and 
capillaries  are  seen.  The  portal  veins,  attacked  by  phlebitis  and  peri- 
phlebitis, are  particularly  striking ;  but  the  biliary  canaliculi,  so  prominent 
in  hypertrophic  cirrhosis,  where  they  are  attacked  by  angiocholitis,  are 
here  much  less  apparent  than  the  veins. 

The  fibrous  tissue  surrounds  a  certain  number  of  hepatic  lobules  en  Uoc, 
and  thus  forms  large  granulations,  whence  secondary  tracts  arise  and  form 
smaller  ones.  Even  the  smallest  granulations  are  nearly  always  made  up 
of  several  hepatic  lobules,  whence  the  name  "  multilobular  cirrhosis."  They 
are  often  surrounded  by  a  ring  of  cirrhotic  tissue,  whence  the  name  of 
"  annular  cirrhosis." 

In  many  specimens  orientation  becomes  impossible,  because  the  normal 
topography  of  the  lobule  is  completely  changed.  The  hepatic  lobules  in 
cirrhosis  are  more  or  less  fused  together.  Neither  the  spaces  nor  the  fissures 
are  seen,  as  in  the  normal  condition.  "  Orientation  is  made  the  more 
difficult  because  the  central  vein,  the  landmark  par  excellence  in  physiological 
conditions,  is  here  very  difficult  to  find."  In  the  interior  of  the  lobules  there 
is  the  same  disorder  ;  the  trabeculse  have  no  longer  their  radial  disposition, 
and  some  of  the  lobules  are  cut  ofi  and,  represented  by  only  a  few  cells. 

This  complete  recasting  of  the  lobules  produces  an  unnatural  topography, 
even  at  the  commencement  of  the  lesions. 

Under  the  influence  of  the  sclerogenous  process,  what  becomes  of  the 
different  elements  in  the  hepatic  lobule  ? 

1.  The  hepatic  cells  lose  their  radial  disposition  in  the  lobule,  and 


DISEASES  OF  THE  LIVER  683 

leave  no  free  space  between  their  columns.  They  are  heaped  up,  over- 
turned, and  deformed,  especially  at  the  periphery.  Some  of  them  show 
simple  atrophy;  others  are  infiltrated  with  fat  and  bile  pigment.  This 
atrophy  of  the  cells,  which  is  the  rule  at  some  period  in  atrophic  cirrhosis, 
is  the  exception  in  hypertrophic  biliary  cirrhosis,  where  the  cells  are  hjrper- 
trophied,  preserving,  as  a  rule,  their  normal  characteristics,  being  neither 
injfiltrated  with  fat  nor  with  pigment  (Hanot). 

2.  The  ramifications  of  the  portal  vein  in  the  portal  spaces  are  in- 
vaded by  phlebitis  and  periphlebitis.  They  are  dilated  at  the  commence- 
ment of  the  cirrhosis,  during  the  period  of  embryonic  growth.  Later  they 
are  thickened,  lose  their  elasticity,  and  become  the  seat  of  coagulation,  and 
occasionally  of  extensive  thrombosis.  When  the  cirrhotic  tissue  has  become 
fibrous,  the  tissue  is  still  vascular,  tortuous  vessels  of  new  formation  being 
seen.  "  They  are  canals,  hollowed  out  in  the  indurated  connective  tissue, 
and  their  walls,  modified  by  the  inflammation,  have  become  blended  with 
the  neighbouring  tissue,  so  as  to  form  one  structure  with  it."  According  to 
most  authors,  this  vascular  network  is  formed  at  the  expense  of  the  portal 
vein.  According  to  others  (Frerichs,  Ackermann),  a  rarefaction  of  the 
portal  network  takes  place,  and  the  arterial  network  (hepatic  artery)  tends 
to  substitute  itself  for  the  portal  ven.ules  in  which  the  circulation  is  embar- 
rassed. However  this  may  be,  the  obstacle  to  the  circulation  of  the  blood 
in  the  Hver  arises  from  several  causes — lesions  of  the  portal  veins,  throm- 
boses in  their  interior,  and  changes  in  the  vessel  walls,  entailing  loss  of 
elasticity  and  contractility  in  the  vessels.  Injections  of  fluid  in  the  cir- 
rhotic liver  pass  from  the  portal  to  the  hepatic  veins  with  some  difficulty, 
and  it  is  partly  from  this  circulatory  embarrassment  in  the  portal  system 
that  a  collateral  development  of  supplementary  veins  takes  place. 

3.  The  hepatic  veins  are  attacked  by  obliterating  phlebitis.  Their 
internal  coat  is  fibroid  and  granular,  and  their  lumen  is  constricted  or 
obliterated.  In  some  cases  the  cirrhosis,  instead  of  being  bivenous,  is  so 
clearly  localized  to  the  portal  or  hepatic  system  that  it  may  be  called  mono- 
venous. 

4.  In  the  sclerosed  portal  spaces  a  fairly  large  number  of  biliary  canali- 
culi  are  seen.  The  canaliculi  of  a  certain  size  are  not  attacked  by  angio- 
cholitls  and  periangiocholitis,  as  in  hypertrophic  biliary  cirrhosis,  but  the 
development  of  biliary  capillaries  is  found  here,  as  in  all  foruLS  of  hepatitis. 
The  mode  of  formation  of  this  biliary  network  will  be  studied^under  Hyper- 
trophic Cirrhosis,  in  which  it  attains  its  greatest  development.  The  more 
or  less  obliterating  catarrh  seen  in  some  of  the  biliary  canaliculi  explains  the 
slight  jaundice  found  in  some  cases  of  atrophic  cirrhosis  (Hanot). 

5.  Cirrhosis  is  sometimes  associated  with  nodules,  forming  a  tumour. 
They  have  been  described  as  adenomata.     According   to  circumstances, 

56—2 


884  TEXT-BOOK  OF  MEDICINE 

the  adenoma  has  the  size  of  a  millet-seed,  a  hazel-nut,  or  a  small  egg,  and 
invades  the  liver  in  a  more  or  less  considerable  degree.  The  discrete  or 
confluent  islets  of  adenoma  do  not  project  on  section,  like  those  of  cirrhosis. 
They  are  homogeneous,  yellowish,  old,  or  soft  like  mastic  (Sabourin),  and 
sometimes  so  little  adherent  to  the  wall  around  them  that  they  escape 
on  gentle  washing. 

Adenoma  is  essentially  an  infecting  production  of  epithelial  origin, 
and  will  be  studied  later  under  Primary  Cancer  of  the  Liver.  The  proof  of 
its  malignant  nature  lies  in  the  fact  that  it  spreads  to  the  peritoneum  and 
to  the  lungs.  The  lymphatic  glands  are,  however,  not  af?ected.  In  the 
liver,  as  elsewhere  (kidneys,  uterus,  stomach),  the  association  of  cirrhosis 
and  adenoma  is  not  rare,  and  it  is  the  association  of  adenoma  with  hepatic 
cirrhosis  which  hastens  the  course  of  the  disease  and  makes  the  prognosis 
worse. 

The  systematization  of  cirrhosis  and  its  commencement  in  the  vascular 
system  of  the  liver  are  now  called  in  question.  Several  authors  would  assign 
a  more  important  part  to  the  hepatic  cell.  "  In  most  diseases  of  the  liver 
the  fibrosis  is  not  systematic,  and  always  has  as  a  primordial  cause  a  change 
in  the  hepatic  cell." 

To  sum  up,  in  the  words  of  Brault,  "it  is  not  always  necessary  to  look 
upon  fibrosis  of  a  viscus  as  being  derived  from  fibrosis  of  its  vessels,  and 
it  is  indeed  more  natural  to  admit  a  simultaneous  fibrosis  affecting  the 
vessel-walls  and  the  interstitial  tissue  of  the  viscus.  To  be  sure,  "  the 
reaction  of  the  interstitial  on  the  epithelial  lesions,  and  vice  versa,^''  must 
be  accepted,  but  it  is  more  natural  to  admit  that  the  different  parts  of  the 
viscus,  its  vessels  and  connective  tissue,  are  attacked  simultaneously  by 
the  toxic-infectious  process,  which  shows  itself  in  different  ways,  according 
to  the  element  invaded. 

Finally,  as  far  as  alcoholic  cirrhosis  is  concerned,  whether  the  poison 
(alcohol)  attacks  the  cell  at  the  same  time  or  before  it  attacks  the  veins, 
and  at  the  same  time  or  after  the  connective  tissue,  it  is  none  the  less  carried 
to  the  liver  by  the  portal  veins,  the  cirrhosis  being  of  venous  origin. 

6.  The  quantity  of  liquid  in  the  peritoneal  cavity  (ascites)  is  more  or 
less  considerable.  The  perihepatic  peritoneum  is  almost  always  affected, 
and  this  partial  peritonitis  is  sometimes  characterized  by  villous  filaments, 
or  at  other  times  by  free  or  adherent  membranes.  Adhesive  perihepatic 
peritonitis  establishes  communications  between  the  liver  and  the  abdominal 
walls,  and  these  adhesions  are  furrowed  with  veins,  which,  in  their  turn, 
serve  for  the  re-establishment  of  the  complementary  circulation.  The 
whole  radicular  system  of  the  portal  vein  may  show  changes,  which  I  shall 
discuss  under  Ascites..  The  intestine  is  sometimes  shortened  and  thickened, 
and  the  mesentery  is  retracted. 


DISEASES  OF  THE  LIVER  885 

Pleurisy  must  be  mentioned  :  it  may  be  dry  or  accompanied  by  effusion, 
which  is  rarely  hsemorrhagic.  The  spleen  is  enlarged  in  half  the  number 
of  cases,  but  not  as  much  as  in  hypertrophic  cirrhosis.  This  swelling  is 
not  solely  due  to  blood  stasis  in  the  portal  system,  but  to  an  active  splenitis. 
The  lesions  of  the  kidneys  are  concomitant  with,  and  not  dependent  on, 
those  of  the  liver.  The  varicose  dilatation  of  the  veins  of  the  oesophagus 
is  explained  by  the  fact  that  the  veins  of  its  lower  two-thirds  empty  into  the 
portal  vein.     Grave  haemorrhages  sometimes  result  therefrom. 

Symptoms. — The  initial  symptoms  of  atrophic  cirrhosis  are  insidious 
and  variable.  Most  frequently  the  patient  during  this  indefinite  phase 
experiences  anorexia,  nausea,  heaviness  in  the  right  hypochondrium,  and 
alternating  diarrhoea  and  constipation.  Itching,  epistaxis,  and  haemor- 
rhoids are  often  present  in  this  initial  phase.  In  some  patients  the  cirrhosis 
announces  itself  by  congestion  and  pain  in  the  liver.  In  many  cases  before 
any  trace  of  ascites,  the  belly  is  distended  and  tympanitic.  "  The  wind 
precedes  the  rain,"  as  Portal  says,  and,  as  a  matter  of  fact,  nothing  is  more 
frequent  than  this  initial  tympanites.  Even  in  the  initial  period  the  decay 
of  the  hepatic  cell  is  shown  by  ahmentary  glycosuria,  urobilin  in  the  urine, 
and  pigmentary  acholia. 

To  sum  up,  "  Dyspeptic  troubles,  meteorism,  constipation,  urobilinuria, 
a  jaundiced  or  bronzed  tint,  pigmentary  acholia,  alimentary  glycosuria, 
pruritus,  epistaxis,  haemorrhages  from  the  gums,  haemorrhoids,  localized 
oedema,  and  diarrhoea,"  are  the  symptoms  of  the  precirrhotic  period.  Hanot 
has  given  to  them  the  name  of  hepatism,  by  analogy  with  the  symptoms 
which  I  have  denominated  Brightism. 

In  some  cases  the  usual  symptoms  of  the  onset  are  absent,  or,  at  least, 
they  pass  unnoticed,  and  ascites  is  the  first  sign,  accompanied  or  not  by 
abdominal  tympanites  and  complementary  circulation.  Sometimes  oedema 
of  the  lower  limbs  is  the  first  apparent  sign.  Loss  of  flesh  may  also  precede 
the  other  symptoms.  Whatever  may  be  the  mode  of  onset,  a  time  comes 
when  the  patient's  aspect  is  characteristic.  The  skin  is  dry  and  earthy, 
the  face  Is  marked  by  small  dilated  veins,  the  loss  of  flesh  is  rapid,  the 
digestive  troubles  increase  in  severity,  the  belly  is  distended,  and  the  oedema 
invades  the  lower  limbs.  The  urine  is  brown,  rich  in  urates,  and  poor  in 
urea  (Brouardel),  and  sooner  or  later  three  chief  symptoms  usually  appear  : 
(1)  ascites  ;  (2)  development  of  a  complementary  circulation  ;  (3)  diminu- 
tion in  the  size  of  the  liver.     The  spleen  sometimes  increases  in  size. 

1.  Ascites. — Ascites  must  first  demand  our  attention.  Ascites,  how- 
ever, is  almost  always  preceded  or  accompanied  by  abdominal  tympanites, 
to  which  I  attach  great  value.  Sometimes  the  meteorism  is  so  marked 
that  the  ascites  is  of  minor  importance.  The  tympanites  gives  an  exag- 
gerated resonance  on  percussion,  and  interferes  with  the  exact  delimitation 


886  TEXT-BOOK  OF  MEDICINE 

of  the  liver.  Ascites  generally  takes  several  weeks  to  develop,  and  increases 
slowly.  Sometimes  its  appearance  is  so  sudden  that  the  amount  of  fluid 
is  large  in  a  few  days.  When  the  ascites  is  considerable  (20  to  30  pints), 
the  abdomen  has  a  peculiar  shape.  When  the  patient  lies  down,  the 
umbilicus  protrudes,  and  the  bulging  flanks  recall  the  belly  of  the  bac- 
trachians.  A  slight  tap  on  the  side  of  the  abdomen,  whilst  the  other  hand  is 
applied  to  the  opposite  side,  gives  a  fluid  wave.  The  dullness  is  complete 
over  the  whole  region  invaded  by  the  fluid,  and  unless  there  is  very  great 
fullness  the  fluid  can  be  readily  displaced.  This  sign  is  obtained  by  making 
the  patient  He  alternately  on  the  left  and  then  on  the  right  side.  Per- 
cussion of  the  flanks  shows  that  each  side  is  dull  and  resonant  in  turn. 
The  area  and  limits  of  the  dullness  change  if  the  patient  stands  up.  Ausculta- 
tion sometimes  shows  the  transmission  of  the  heart  and  lung  sounds  to  the 
lower  part  of  the  belly  (Widal). 

Owing  to  its  increase,  ascites  becomes  one  of  the  most  painful  symptoms. 
It  interferes  with  movement  and  with  respiration.  Although  it  has  but 
little  tendency  to  absorption,  it  has  been  observed  to  diminish  temporarily 
or  permanently  through  the  action  of  purgatives  and  diuretic  drugs.  It 
may  be  cured  by  tapping  of  the  abdomen. 

The  pathogenesis  of  ascites  in  atrophic  cirrhosis  is  not  clearly  known. 
For  a  long  time  the  following  mechanical  theory  obtained  :  The  changes  of 
the  portal  veins  in  the  liver,  the  transformation  of  their  walls,  the  con- 
striction of  their  lumen,  and  their  obliteration  by  thrombosis,  are  an  obstacle 
to  the  intrahepatic  circulation,  so  that  effusion  may  take  place  into  the 
peritoneum,  just  as  cedema  forms  in  the  cellular  tissue  of  the  leg  when  the 
chief  veins  are  obliterated.  There  is,  however,  a  corrective  for  this  obstacle 
to  the  intrahepatic  venous  circulation — viz.,  the  complementary  circulation, 
which  retards  or  lessens  the  production  of  ascitic  fluid.  And  in  order  to 
make  the  theory  complete,  a  kind  of  equihbrium  between  the  production 
of  ascites  and  the  development  of  the  complementary  circulation  has  been 
admitted,  the  ascites  becoming  less  marked  as  the  collateral  circulation 
becomes  more  developed. 

The  influence  of  these  mechanical  causes  on  the  production  of  ascites 
cannot  be  denied,  and  yet  we  must  recognize  that  this  theory  is  frequently 
at  fault.  In  the  first  place,  ascites  sometimes  appears  as  the  initial  symp- 
tom of  cirrhosis  when  the  intrahepatic  circulation  is  so  little  affected  that 
it  excites  no  complementary  extrahepatic  circulation.  In  such  a  case, 
therefore,  it  cannot  be  said  that  the  ascites  comes  from  a  mechanical 
obstruction.  On  the  other  hand,  cirrhosis  of  the  liver  may  reach  the 
atrophic  stage  without  the  production  of  any  ascites,  as  is  clearly  shown 
by  the  post-mortem  records  published  on  this  subject  (Hanot  and  Lecorche). 
If  ascites  were  only  the  result  of  a  mechanical  obstruction  to  the  intra- 


DISEASES  OF  THE  LIVER  887 

hepatic  circulation,  it  would  have  occurred  in  the  cases  in  question,  the  more 
readily  in  that  there  was  not  any  complementary  circulation. 

If  the  mechanical  obstacle  in  the  intrahepatic  circulation  cannot  alone 
explain  the  formation  of  ascites,  where  are  we  to  seek  for  its  causes  ? 
Peritoneal  lesions  have  been  suggested.  As  a  matter  of  fact,  perihepatic 
and  peritoneal  lesions  are  always  found  post  mortem,  and  may  assist  in  the 
production  of  ascites.  In  addition  to  peritoneal  inflammations  directly 
associated  with  hepatic  cirrhosis,  Leudet  has  described  chronic  peritonitis 
in  alcoholic  patients,  which  appeared  on  its  own  account  (the  Uver  not  being 
in  fault),  or  which  may  appear  at  the  same  time  as  the  cirrhotic  lesions 
in  the  Uver.  This  latent  peritonitis  betrays  itself  sooner  or  later  by  abundant 
ascites. 

Another  Cause  of  Ascites. — Cirrhosis  of  the  liver  is  fairly  frequently  asso- 
ciated with  tuberculosis.  I  do  not  merely  allude  to  one  of  the  forms  of 
hypertrophic  cirrhosis,  which  I  shall  describe  in  the  following  section.  I 
refer  to  those  cases  in  which  we  find  post  mortem  old  tuberculosis  of  the 
lung,  which  may  be  very  limited,  or  even  healthy  lungs,  the  tubercular 
lesion  affecting  only  the  liver  and  the  peritoneum.  This  lesion  consists 
sometimes  of  a  few  miliary  granulations  or  greyish  patches  that  are  hardly 
visible  to  the  naked  eye,  and  appear  under  the  microscope  in  the  form  of 
tubercular  follicles  with  giant  cells  and  tubercle  bacilli.  These  peritoneal 
lesions  have  their  share  in  the  production  of  ascites. 

The  recognition  of  these  facts  show  the  part  of  the  peritoneum  in  the 
production  of  ascites  in  atrophic  cirrhosis.  The  question,  however,  is  not 
exhausted.  I  ask  whether  ascites  in  cirrhotic  patients  is  not  caused  by 
lesions  in  the  mesenteric  and  peritoneal  tributaries  of  the  portal  vein  ? 
While  the  researches  of  Giraudeau  and  myself  do  not  give  an  affirmative 
answer,  they  deserve  notice. 

In  a  patient  who  had  died  of  atrophic  cirrhosis  without  peritonitis  we  found  in  the 
Btoraach,  intestine,  and  mesentery  phlebitis  of  the  small  veins,  which  were  at  least 
2  miUimetres  in  diameter.  At  some  points  the  external  coat  of  the  small  veins  was 
double  or  treble  its  normal  size,  while  the  other  coats  were  atrophied  or  had  disap- 
peared. In  the  moat  diseased  portions  the  periphlebitis  of  the  tributaries  of  the  portal 
vein  gave  rise  to  fibrous  prolongations,  which  joined  the  tracts  arising  around  the 
neighbouring  veins,  and  enclosed  the  arteriole  and  the  nerves  in  the  vicinity.  If  new 
discoveries  confirm  these  data,  they  may  prove  that  the  systematic  venous  inflamma- 
tion which  dominates  the  process  of  atrophic  cirrhosis,  affects  the  tributaries  to  the 
same  extent  as  the  terminals  of  the  portal  vein.  They  would  also  help  to  explain 
certain  early  symptoms  (haemorrhage  from  the  oesophagus,  stomach,  or  intestine,  and 
intestinal  discharges),  which  would  not  then  be  set  down  to  blood  stasis  alone.  Thoy 
would  have  their  share  in  the  pathogenesis  of  ascites. 

Let  me  add  that  cold  may  have  some  influence  in  the  production  of 
ascites  in  cirrhosis  (Potaiu). 

2.  Collateral  Circulation. — Whilst  the  circulation   Ls   impeded  in  tho 


888  TEXTBOOK  OF  MEDICINE 

interior  of  the  cirrhotic  liver,  we  find  a  collateral  circulation  outside  the 
organ,  which  serves  to  return  to  the  heart  by  a  roundabout  way  the  blood 
arrested  in  the  portal  system  of  the  liver.  This  collateral .  circulation  is 
thus  established.  In  addition  to  the  blood  received  from  the  portal  vein, 
the  liver  also  receives  venous  blood  from  various  small  veins.  These  veins, 
collected  into  five  groups  by  Sappey,  form  the  accessory  portal  system. 

They  arise  in  organs  or  regions  other  than  the  digestive  system,  and  end 
in  the  liver  or  in  the  portal  vein  where  it  enters  the  liver,  so  that  each 
accessory  vein  represents  a  small  portal  system.  The  fourth  group  arises 
in  the  diaphragm,  passes  through  the  suspensory  ligament,  and  empties 
into  the  lobules  of  the  liver,  to  which  this  hgament  is  adherent.  This 
group  anastomoses,  on  the  one  hand,  in  the  liver,  with  the  branches  of  the 
portal  vein,  and,  on  the  other,  with  the  diaphragmatic  and  subcutaneous 
thoracic  veins.  It  may  thus  serve  to  establish  a  circulation  between  the 
liver  and  the  veins  of  the  thorax.  The  fifth  group  arises  from  the  sub- 
umbilical  portion  of  the  anterior  wall  of  the  abdomen,  and  in  part  empties 
itself  into  the  left  branch  of  the  portal  vein.  The  small  veins  of  this  group 
unite  the  trunk  of  the  portal  vein  with  the  deep  epigastric  and  internal 
mammary  veins,  and  with  the  cutaneous  veins  of  the  abdomen. 

The  accessory  portal  veins,  which  are  but  slightly  developed  in  the  normal 
condition,  are  much  developed  in  obstruction  of  the  portal  vein.  It  is  by 
them  that  the  circulation  is  partly  re-established.  Let  us  suppose  an 
obstacle  caused  by  cirrhosis  :  the  blood  of  the  portal  vein  creates  new  routes 
for  itseK,  and  a  portion  of  the  blood  flows  back  from  the  liver  through  the 
accessory  veins  of  the  fourth  group  into  the  mammary  and  intercostal 
veins,  which  carry  it  into  the  azygos  veins.  In  the  collateral  circulation 
effected  by  this  group  the  course  of  the  blood  is  from  below  upwards. 
Another  portion  of  the  blood  in  the  portal  vein  finds  a  new  route  by  flowing 
back  from  the  trunk  of  the  portal  vein  into  the  veins  of  the  fifth  group, 
which  lead  it  to  the  epigastric  and  subcutaneous  abdominal  veins,  the  former 
emptying  into  the  iliac  and  the  latter  into  the  saphena  veins.  In  the 
collateral  circulation  effected  by  this  group  the  course  of  the  blood  in  the 
veins  of  the  abdominal  walls  is  from  above  downwards.  Let  me  finally 
mention  the  veins  in  the  adhesions  that  are  sometimes  found  between  the 
peritoneum  and  the  abdominal  wall  and  the  diaphragm. 

The  dilatation  of  the  subcutaneous  veins  of  the  abdomen  gives  rise  in 
some  patients  to  a  varicose  plexus  at  the  umbilicus,  and  a  well-marked 
venous  network  between  the  xiphoid  cartilage  and  the  pubis,  especially  on 
the  right  side  and  towards  the  upper  half  of  the  abdomen.  In  certain  cases 
a  thrill  is  felt  and  a  murmur  is  heard  in  the  dilated  veins.  The  congestion 
of  the  saphena  vein  from  backward  pressure  plays  some  part  in  the  oedema 
of  the  lower  limbs. 


DISEASES  OF  THE  LIVER  889 

This  collateral  circulation  may  retard,  but  does  not  prevent,  the  appear- 
ance of  the  ascites,  and  though  these  venous  dilatations  seem  to  be  the 
result  of  a  mechanical  obstacle  to  the  blood  in  its  passage  through  the 
liver,  there  are  nevertheless  cases  of  atrophic  cirrhosis  in  which  a  collateral 
circulation  is  absent.  Furthermore,  we  do  not  always  find  the  equilibrium 
between  the  ascites  and  the  circulation  necessitated  by  an  entirely  mechanical 
theory.  It  would  seem,  as  a  matter  of  fact,  that  if  we  are  to  rely  on  the 
mechanical  production  of  ascites  and  of  the  collateral  circulation,  there 
ought  to  be  more  intimate  bonds  between  these  two  symptoms.  This 
is  not  the  case,  and  close  observation  shows  that  each  of  them  enjoys  a 
certain  independence. 

3.  Atrophy  of  the  Liver,  which  depends  less  on  the  retractile  power 
of  the  fibrous  tissue  than  on  the  disappearance  or  atrophy  of  a  large 
number  of  hepatic  cells,  is  a  constant  symptom  in  advanced  cirrhosis,  but 
it  is  not  always  easy  to  discover  the  atrophy  on  account  of  the  tympanites 
and  ascites.  It  is  sometimes  possible  to  feel  the  lower  edge  of  the  liver, 
and  to  make  certain  that  it  has  become  blunted  and  irregular. 

Besides  the  symptoms  just  described,  others  occur  in  the  course  of 
atrophic  cirrhosis,  and  are  of  great  value.  The  spleen  becomes  hyper- 
trophied  in  half  the  number  of  cases  (Frerichs),  and  sometimes  atrophied. 
Some  subjects  suffer  from  oedema  of  the  lower  limbs,  which,  as  I  have 
already  said,  precedes  or  accompanies  the  development  of  ascites.  This 
oedema  sometimes  develops  early,  and,  as  it  becomes  considerable,  it  may 
lead  to  the  supposition,  through  lack  of  care,  that  there  is  a  cardiac 
lesion. 

4.  Attacks  of  haemorrhage  are  frequent,  and  epistaxis,  hsematemesis, 
melsena,  purpura,  haemoptysis,  or  haemorrhage  from  the  pleura  and  peri- 
toneum, may  be  seen.  Haemorrhage  appears  at  all  periods  of  the  disease ; 
it  may,  indeed,  occur  as  a  symptom  of  the  onset.  Gastro-intestinal 
hemorrhage  is  the  most  terrible  ;  the  hsematemesis  may  be  fulminant.  I 
had  in  hospital  a  cirrhotic  patient  who  succumbed  in  a  quarter  of  an  hour 
from  hsematemesis,  caused  by  rupture  of  the  oesophageal  varices.  In 
other  patients  haematemesis  occurs  several  times  a  day  and  on  several 
successive  days  ;  it  then  ceases,  or  reappears  some  days  or  weeks  later.  I 
had  in  my  wards  a  cirrhotic  patient  in  whom  ascites  and  copious  haema- 
temesis were  the  two  principal  symptoms.  Immediately  after  evacuation 
of  the  ascitic  liquid  the  haematemesis  ceased  ;  the  fluid  did  not  return,  and 
the  patient  was  able  to  leave  the  hospital. 

Nsevi  are  frequent  in  cirrhotic  patients.  I  have  seen  in  one  of  my 
patients  at  the  Necker  Hospital  obstinate  haemorrhage,  caused  by  an 
ulcerated  najvus  at  the  angle  of  the  nostril.  I  had  in  the  Hotel-Dieu  a 
cirrhotic  patient,  suffering  with  haemorrhage  from  the  larynx,  as  proved 


890  TEXT-BOOK  OF  MEDICINE 

by  laryngoscopic  examination.  Another  case  of  this  nature  has  been 
published  by  Lubet-Barbon. 

What  are  these  haemorrhages  in  cirrhotic  patients  due  to  ?  According 
to  certain  authors,  the  obstacle  which  the  blood  meets  in  the  liver  causes 
stasis  of  the  circulation  in  the  stomach  or  intestine,  and  haemorrhage.  It 
is  certain  that  the  mechanical  influence  of  the  obstruction  in  the  portal 
system  cannot  fail  to  be  recognized,  for  the  hsemorrhagic  erosions  of  the 
mucosa  of  the  stomach,  and  the  varices  of  the  oesophagus  and  of  the  stomach 
are  evidence  to  this  effect.  But  this  mechanical  cause  seems  to  me  to  play 
a  part  only  in  the  pathogenesis  of  haemorrhage  in  atrophic  cirrhosis. 

Haemorrhage  may  appear  so  soon  after  the  commencement  of  the  disease 
that  mechanical  stasis  of  the  blood  cannot  be  the  cause.  Certain  patients 
are  seized  with  haematemesis  or  melaena  before  any  other  symptom,  and 
as  a  precursory  sign  at  an  epoch  when  as  yet  neither  collateral  circulation, 
nor  ascites,  nor  any  of  the  usual  indications  of  obstruction  in  the  hepatic 
circulation  are  present ;  writers,  in  order  to  explain  these  haemorrhages, 
invoke  a  blood  dyscrasia  due  to  the  alteration  in  the  hepatic  functions. 
This  dyscrasia,  which  is  most  marked  in  icterus  gravis,  and  which  cannot 
be  denied  in  cases  of  advanced  cirrhosis,  seems  to  me  to  be  scarcely  ad- 
missible at  the  very  commencement  of  the  hepatic  lesion.  Other  causes 
must  therefore  be  sought,  and  the  question  may  be  put  as  to  whether  the 
radicles  of  the  portal  system — i.e.,  the  peripheral  venules  of  the  stomach 
and  of  the  intestine — may  not  from  the  onset  of  the'  disease  be  the  seat  of 
changes  that  cause  friability  of  these  vessels. 

Icterus  is  not  a  symptom  of  atrophic  cirrhosis,  and  when  it  appears  it 
is  usually  shght,  and  due  to  urobilin.  Some  patients  with  atrophic  cir- 
rhosis, after  swallowing  5  ounces  of  syrup  of  sugar,  suffer  from  temporary 
glycosuria.  The  sugar,  absorbed  in  the  intestine,  passes  into  the  general 
circulation  and  into  the  urine,  without  having  been  arrested  in  the  Mver. 
This  experimental  glycosuria  is  due  either  to  obstruction  in  the  portal  system 
or  to  changes  in  the  hepatic  cells.  Lowering  of  the  quantity  of  urea  is 
another  sign  of  hepatic  insufficiency.  Hanot  has  noticed  the  existence  of 
abdominal  lymphatic  varices. 

Course — Termination— Duration. — In  its  typical  form  atrophic  cir- 
rhosis is  an  apyretic  and  chronic  disease.  In  certain  cases  it  runs  its 
course  without  acute  symptoms,  and  surprise  is  expressed  when  atrophic 
cirrhosis  is  discovered  in  patients  who  have  died  of  some  other  disease.  It 
usually  lasts  one  or  two  years,  but  it  may  be  checked  by  efficient  treatment. 
Sometimes  the  patient  dies  of  cachexia  ;  at  other  times  the  end  is  hastened 
by  hepatic  adenoma,  by  complications,  or  by  some  intercurrent  disease,  such 
as  peritonitis,  pneumonia,  erysipelas,  infective  endocarditis,  suppurative 
cholecystitis,  abscess   of  the   liver,   nephritis,   phlebitis,  hemorrhage,   or 


DISEASES  OF  THE  LIVER  831 

tuberculosis  affecting  the  liver,  peritoneum,  etc.  (Rendu).  Some  patients 
succumb  with  profuse  diarrhoea,  algid  condition,  coma,  and  secondary 
infection  due  to  the  coli  bacillus  (Hanot),  Finally,  symptoms  of  icterus 
gravis  may  appear,  and  prove  rapidly  fatal.  In  the  section  on  Icterus  Gravis 
we  shall  see  that  the  liver,  already  unable  to  defend  itself,  is  invaded  by 
the  toxines  and  infections  which  produce  secondary  icterus  gravis. 

Atrophic  cirrhosis  is  not  absolutely  fatal.  In  some  cases  it  may  be 
cured,  but  these  fortunate  cases  are  chiefly  met  with  in  the  hypertrophic 
form  of  alcoholic  cirrhosis,  which  I  shall  describe  in  the  following  section. 

Acute  Atrophic  Cirrhosis. — Atrophic  cirrhosis  has  not  always  the 
common  and  chronic  form  just  described.  Hanot  has  published  four  cases 
in  which  the  cirrhosis  ran  a  febrile  and  rapid  course,  lasting  from  two  to 
six  months.  From  the  commencement,  says  Hanot,  more  or  less  sharp 
pains  are  noticed  in  the  right  hypochondrium.  Ascites  may  appear  before 
any  abnormal  development  of  the  subcutaneous  abdominal  veins.  Con- 
siderable oedema  of  the  lower  and  upper  limbs  is  soon  seen.  Jaundice, 
haemorrhage  from  the  mucosae,  and  subcutaneous  haematomata,  although 
not  as  severe  as  in  acute  yellow  atrophy,  are  more  frequent  and  more 
pronounced  than  in  ordinary  atrophic  cirrhosis.  Death  supervenes  in  the 
midst  of  the  symptom-complex,  called  acholia. 

Post  mortem,  the  liver  is  found  to  be  more  or  less  atrophied,  granular, 
hard,  and  consequently  comparable  with  the  liver  in  common  atrophic 
cirrhosis.  Histological  examination,  however,  reveals  essential  differences. 
These  differences  are  not  seen  in  the  distribution  of  the  fibrous  tissue,  for 
it  is  systematically  distributed  as  in  ordinary  cirrhosis.  The  differences 
are  due  to  the  lesions  in  the  hepatic  cells.  In  common  cirrhosis  the  change 
in  the  protoplasm  of  the  cells  is  slow,  late,  and  incomplete,  but  in  acute 
cirrhosis  the  cellular  degeneration  is  rapid,  general,  and  complete.  A 
large  number  of  cells  are  converted  into  fat  globules,  and  it  might  be  said 
that  yellow  atrophy  has  complicated  cirrhosis.  Moreover,  as  the  important 
functions  of  the  liver  are  rapidly  abolished,  the  clinical  picture  of  icterus 
gravis  and  of  acholia  supervenes.  This  proves  once  more  that  "  in  cases 
of  cirrhosis,  from  the  anatomo-pathological  point  of  view,  the  diagnosis 
depends  on  tho.  topography  of  the  connective  neo-formation,  and  the 
prognosis  on  tlie  condition  of  the  hepatic  cell  "  (Hanot). 

Diagnosis. — At  first  the  diagnosis  of  atrophic  cirrhosis  of  the  liver  is 
hardly  })Ossible  through  lack  of  signs.  Later  it  is  more  easy,  on  account  of 
the  appearance  of  ascites,  and  of  the  com])lementary  circulation,  but  yet  it 
still  presents  some  difficulties.  Thus,  chronic  tubercular  peritonitis  has 
symptoms  in  common  with  cirrhosis — viz.,  digestive  troubles,  })rogreHsive 
loss  of  Hcsh,  meteorism,  and  ascites  ;  and  as  it  is  not  always  possible  to  prove 
atrophy  of  the  hver,  oa  the  one  hand,  and,  on  the  other  hand,  lesions  of  the 


892  TEXT-BOOK  OF  MEDICINE 

peritoneum,  the  data  for  a  diagnosis  must  be  sought  elsewhere.  In  chronic 
tubercular  peritonitis  the  fluid  is  less  abundant  and  less  easy  to  displace 
than  in  cirrhosis.  The  flanks  are  less  spread  out,  the  periumbilical  region 
is  less  prominent,  and  the  sensation  of  a  fluid  wave  is  less  clear.  The  com- 
plementary circulation,  which  is  only  an  initial  stage  in  peritonitis,  is  often 
well  developed  in  cirrhosis.  Haemorrhage,  hypertrophy  of  the  spleen,  and 
jaundice  belong  rather  to  cirrhosis.  Finally,  the  subject  suffering  from 
abdominal  tuberculosis  is,  as  a  rule,  afiected  with  pulmonary  tuberculosis. 

The  chronic  peritonitis  of  alcoholics  has  also  several  signs  in  common 
with  cirrhosis  of  the  liver  (ascites,  dyspeptic  troubles).  The  error  is  some- 
times the  more  difficult  to  avoid,  in  that  cirrhotic  patients  are  most  fre- 
quently alcoholics. 

Cancer  of  the  peritoneum  may  be  accompanied  by  ascites  and  collateral 
circulation,  but  these  symptoms  are  much  less  marked  than  in  cirrhosis. 
Palpation  reveals  nodules  or  indurations,  and  the  fluid,  withdrawn  by 
tapping,  often  has  a  haemorrhagic  tint. 

The  early  appearance  or  the  severity  of  haematemesis  and  of  melaena 
is  sometimes  a  cause  of  error.  These  symptoms  are  too  frequently  attri- 
buted to  ulcers  or  cancerous  lesions  in  the  stomach  and  intestine,  when  they 
are  really  the  precursors  of  hepatic  cirrhosis.  The  same  remark  applies  to 
oedema  of  the  lower  limbs,  which  occurs  early,  and  must  not  be  attributed 
to  a  cardiac  lesion. 

Pylephlebitis  (inflammation  of  the  portal  vein)  causes  much  ascites 
and  well-marked  collateral  circulation,  but  the  acute  course  of  pylephle- 
bitis and  the  accompanying  jaundice  are  sufficient  to  clear  up  the  diagnosis. 

Finally,  we  must  distinguish  true  atrophic  cirrhosis  from  fibrous  hepatitis 
associated  with  diseases  of  the  kidneys  and  heart. 

etiology. — Atrophic  cirrhosis  is  a  disease  of  adult  age.  It  is  frequent 
in  France,  and  still  more  common  amongst  the  people  of  the  Northern 
countries,  especially  England.  As  regards  its  causes,  one  stands  out  pro- 
minently— viz.,  alcoholism  in  aU  its  forms  ;  and  the  disease  is  also  called 
alcoholic  cirrhosis.  The  mechanism  of  the  lesion  is  readily  understood, 
the  poison  being  carried  to  the  liver  by  the  portal  veins. 

Alcoholism  is  sometimes  produced  by  wine,  and  the  patient,  prior  to 
the  appearance  of  cirrhosis,  has  morning  vomiting,  trembling  of  the  hands, 
and  nightmare.  At  other  times  alcohohsm  is  caused  by  spirituous  liquors 
rich  in  aromatic  essences.  The  two  causes  are  often  joined,  and  the  better 
the  individual  stands  drink,  the  more  he  takes,  and  the  more  surely  will 
he  suffer  from  cirrhosis.     Children  may  suffer  from  alcoholic  cirrhosis. 

Numerous  attempts  have  been  made  to  produce  alcoholic  cirrhosis  in 
animals,  but  the  results  obtained  are  not  constant — a  further  proof  that  it 
is  often  difficult  to  draw  conclusions  from  animals  and  apply  them  to  man- 


DISEASES  OF  THE  LIVER  893 

kind.  Sabourin  saturated  guinea-pigs  with  increasing  doses  of  alcohol  for 
several  weeks,  and  on  examining  the  Hver,  found  capillary  phlebitis  around 
the  hepatic  veins  and  centro-lobular  steatosis.  The  results  obtained  by- 
Strauss  and  Blocq  are  different.  Prolonged  alcoholic  intoxication  was 
produced  in  rabbits.  The  histological  examination  of  the  liver  in  these 
animals  showed  a  systematic  portal  cirrhosis,  though  no  trace  of  hepatic 
central  cirrhosis  was  found.  Laffite,  in  his  experiments  on  rabbits,  found, 
after  examination  of  the  hver,  cellular  and  not  vascular,  lesions. 

Cirrhosis  from  Gastro-intestinal  Auto-infection.— Alcoholism  has  been 
assigned  too  much  importance  in  the  pathogenesis  of  cirrhosis.  While 
alcohol  produces  fibrous  changes,  it  is  far  from  being  the  only  cause.  Many 
patients  are  not  alcoholic,  and  we  must  therefore  search  elsewhere  for  the 
cause  of  the  cirrhosis.  This  cause  appears  to  exist  in  the  poisons  present 
throughout  the  entire  length  of  the  gastro-intestinal  tract.  In  some  cir- 
cumstances they  become  the  source  of  auto- infection,  reacting  directly  on 
the  liver. 

The  poisons  of  the  digestive  tube  are  of  multiple  origin.  Some  come 
from  food — putrid  meat,  pork,  fish,  or  shell-fish,  bad  water,  etc.  Under  the 
influence  of  the  microbes  in  the  alimentary  canal,  the  gastro-intestinal 
ferments  give  rise  to  a  series  of  poisons — butyric,  acetic,  valerianic,  lactic, 
and  oxalic  acid,  etc.,  without  counting  indol,  skatol,  phenol,  and  the  toxines 
manufactured  by  the  microbic  agents,  notably  by  the  coli  bacillus. 

Boix  has  carried  out  experiments  with  all  these  acids  on  rabbits,  taking 
care  that  the  acids  were  ingested  in  small  doses  and  over  long  periods. 
By  ingestion  of  butyric  acid  he  was  able  to  induce  Laennec's  atrophic 
cirrhosis  ;  by  the  ingestion  of  lactic  and  of  valerianic  acid  he  was  also  able 
to  cause  cirrhotic  lesions.  The  ingestion  of  acetic  acid  produced  even 
more  marked  fibrous  lesions  in  the  liver.  Analogous  results  have  been 
obtained  with  living  cultures  and  with  the  toxines  of  the  Bacillus  coli.  To 
sum  up :  "  The  very  interesting  researches  of  Boix,"  says  Hanot,  "  prove 
that  the  organic  acids  of  digestion  may  produce  hepatic  cirrhosis,  some  more 
easily  than  others.  In  the  normal  state  the  liver  resists  these  daily  poisons. 
If  it  grows  feeble,  or  if  it  is  already  weak  ah  ovo,  the  toxic  action  takes 
place,  and  hepatic  cirrhosis  by  auto-infection  of  a  gastro-intestinal  origin 
supervenes." 

It  is  evident  that  the  question  differs  somewhat  in  man,  and  many 
factors  must  be  considered,  such  as  heredity,  disorganization  of  the  liver  by 
anterior  or  concomitant  infections,  and  the  tendency,  which  is  perhaps  the 
result  of  arthritism,  to  make  fibrous  tissue.  Here,  as  elsewhere,  the  patho- 
genic problem  is  often  complex,  and  yet,  logically  and  experimentally,  we 
cannot  deny  tiiat  gastro-intcstino-hepatic  intoxication  plays  a  very  impor- 
tant part  in  the  determination  of  cirrhosis. 


894  TEXT-BOOK  OF  MEDICINE 

While  the  gastro-intestino-hepatic  process  does  not  always  end  in  con- 
firmed cirrhosis,  it  often  causes  congestive  cirrhotic  lesions  in  the  liver,  of 
which  the  following  are  the  principal  varieties  : 

In  a  first  variety  the  liver  is  rather  congested  than  cirrhotic,  being 
enlarged,  and  tender  on  pressure.  The  patient  experiences  a  feeHng  of 
heaviness  in  the  right  hypochondrium,  and  has  slight  jaundice.  The  size 
of  the  liver  increases  or  diminishes  according  as  the  patient  passes  through 
the  phases  of  more  or  less  marked  dyspepsia.  "  In  389  personal  observa- 
tions of  dilatation  of  the  stomach,"  says  Bouchard,  "  I  have  found  that 
swelling  of  the  liver  is  seen  in  the  proportion  of  23  per  cent.,  and,  in  order 
to  prejudge  nothing,  I  have  given  to  this  change  the  name  of  enlarged 
liver."  This  is  an  example  of  the  enlarged  dyspeptic  liver  (Boix),  the 
word  "dyspepsia"  signifying  by  abbreviation  the  change  in  the  liver  resulting 
from  dyspeptic  troubles. 

In  this  variety  of  enlarged  dyspeptic  liver,  in  adults  as  well  as  in  children, 
the  liver  suffers  from  congestion,  and  a  long  interval  elapses  before  the 
appearance  of  cirrhosis. 

The  cirrhotic  liver  of  intestinal  auto- infection  is  enlarged,  hard,  and  not 
painful.  Jaundice,  ascites,  collateral  circulation,  and  splenomegaly  are  not 
seen.  The  liver  reaches  some  inches  below  the  false  ribs,  and  measures 
8  to  10  inches  in  the  nipple  line.  It  has  a  smooth  surface,  is  remarkably 
hard  and  wooden.  This  ligneous  hypertrophy  of  the  Hver  persists  for 
years  without  causing  grave  signs,  and  the  organ  continues  to  fulfil  its 
functions  sufficiently  well.  Sometimes  acute  attacks  are  noticed,  and  are 
characterized  by  dyspeptic  troubles,  pains  in  the  hypochondrium,  and  the 
appearance  of  urobiHn  in  the  urine.  In  this  variety  of  cirrhosis  the  liver 
remains  enlarged,  and  need  not  necessarily  end  in  atrophy  (in  experi- 
mental cases  the  liver  becomes  atrophied).  In  these  cases  we  cannot  find 
alcoholism,  malaria,  syphilis,  diabetes,  tuberculosis,  or,  indeed,  any  cause 
to  explain  this  cirrhosis.  And  yet  we  have  certainly  to  deal  with  cirrhosis, 
for  ill  one  case  it  has  been  possible  to  make  the  histological  examination  of 
a  cirrhotic  liver  due  to  intestinal  auto-infection.  The  lesions  of  bivenous 
cirrhosis  were  present:  fibrosis  of  the  porto-biliary  spaces  invading  the 
hepatic  lobule,  the  central  vein  of  the  lobule,  and  the  portal  capillaries. 
In  some  instances  the  lumen  of  the  portal  vein  had  completely  disappeared. 
In  consequence  of  the  relations  between  the  appendix  and  the  liver 
(see  the  chapter  on  the  Appendicular  Liver),  I  am  quite  prepared  to  add 
appendicitis  to  the  intestinal  intoxications  which  may  cause  cirrhosis  of  the 
Hver,     Cirrhosis  of  the  hver  from  lead-poisoning  has  also  been  described. 

Treatment. — The  prognosis  of  cirrhosis  of  the  Hver  is  not  so  fatal 
as  was  supposed  a  few  years  ago,  provided  that  efficient  treatment  is  em- 
ployed.     Local  treatment  must  not  be  neglected — i.e.,  dry- cupping,  the 


DISEASES  OF  THE  LIVER  895 

actual  cautery  or  blisters  applied  over  tlie  hepatic  region.  Milk  diet,  iodide 
of  potassium,  and  hydrotherapy,  form  the  general  treatment. 

Personally,  I  know  of  no  treatment  so  efficacious  as  milk  diet :  5  pints 
of  milk  daily,  and  milk  foods,  for  six  months.  I  further  discuss  this  treat- 
ment under  Curabihty  of  Cirrhosis  of  the  Liver.  I  prescribe  iodide  of 
potassium,  but  in  very  small  doses  (3  grains  daily),  without  intermission 
for  a  year.  It  is  evident  that  the  chances  of  success  are  best  if  the  disease 
is  treated  as  early  as  possible. 

What  is  the  best  treatment  for  ascites  ?  If  the  effusion  is  abundant, 
and  the  diaphragm  is  pushed  up  so  as  to  interfere  with^the  normal  function 
of  the  lungs,  paracentesis  becomes  necessary.  The  best  spot  for  para- 
centesis is  the  middle  of  a  line  joining  the  umbilicus  and  the  antero-superior 
iliac  spine.  I  recommend  a  small-size  trocar,  previously  sterilized.  When 
the  puncture  has  been  made,  a  tube  is  attached  to  the  cannula  of  the  trocar, 
so  as  to  siphon  off  the  Hquid  in  a  slow  and  continuous  manner.  This 
operation,  though  quite  simple,  is  sometimes  followed  by  compUcations, 
some  immediate,  such  as  syncope,  and  others  more  remote,  such  as  ery- 
sipelas, starting  in  the  wound,  and  extending  as  far  as  the  peritoneum. 
These  compUcations  can  always  be  avoided  if  paracentesis  is  performed 
with  a  trocar  of  average  size  and^  with  proper  aseptic  precautions.  I 
admit  that  with  a  large  trocar  the  operation  is  finished  quicker,  but  to  the 
detriment  of  the  patient,  because  the  rapid  flow  of  the  liquid  more  readily 
causes  sjmcope,  the  wound  remains  open,  and  secondary  infection,  caused 
through  the  want  of  care,  spreads  more  readily  from  the  puncture  to  the 
peritoneum.  The  operation  concluded,  the  dressings  are  applied.  The  patient 
must  remain  on  his  back  for  several  hours,  or  on  the  side  opposite  to  the 
puncture,  the  object  being  to  prevent  oozing  from  the  wound. 

Evacuation  of  the  fluid  affords  the  patient  great  reUef,  but  the  fluid 
usually  reforms  after  a  few  days  or  weeks.  The  operation  is  again  per- 
formed as  soon  as  may  be  necessary.  In  some  cases,  however,  after  two  or 
three  tappings,  the  ascites  does  not  reappear,  and,  indeed,  restoration  to 
health  may  be  possible.  The  question  of  the  definite  disappearance  of  ascites 
and  of  the  curability  of  cirrhosis  will  be  referred  to  later. 

Surgical  treatment  of  cirrhosis  of  the  liver  has  been  employed  (Talma 
and  Morrison's  ojjeration).  It  has  been  thought  that  a  good  result  would 
be  obtained  if  a  means  were  found  to  deflect  the  circulation  of  the  portal 
vein  by  removing  the  obstacle  met  with  in  the  cirrhotic  liver.  This  hypo- 
thesis, however,  leaves  something  to  be  desired,  Eck  proposed  to  establish 
direct  communication  between  the  portal  vein  and  the  inferior  vena  cava. 
This  operation  has  not  been  adopted. 

Talma  proposed  as  a  remedy  for  the  obstacles  in  the  portal  circulation 
the  establishing  of  venous  anastomoses  between  the  splanchnic  portal  veins 


896  TEXT-BOOK  OF  MEDICINE 

and  the  veins  in  the  abdominal  wall.  In  order  to  do  this  he  fixed  the  great 
omentum  to  the  wall  of  the  abdomen.  Morrison  tried  to  obtain  widespread 
adhesion.  The  results  of  the  operation  have  been  disputed  :  some  say  that 
they  have  been  favourable,  others  say  that  they  have  been  bad.  The  fact 
is  that  the  question  has  still  to  be  settled. 

VI.  HYPERTROPHIC  ALCOHOLIC  CIRRHOSIS— REGENERATION 

OF  THE  LIVER. 

Hypertrophic  alcoholic  cirrhosis  does  not  form  a  clearly  defined  morbid 
entity.  Many  intermediate  forms  are  found  between  the  atrophied  cirrhotic 
organ  and  the  hypertrophic  one  ;  and  yet  I  cannot  see  how  the  same  factor 
(alcohol)  can  produce  in  one  case  the  atrophic  liver  and  the  fatal  cirrhosis 
of  Laennec,  and  in  another  case  the  enlarged  liver  of  curable  hypertrophic 
cirrhosis.  I  have,  therefore,  doubts  as  to  the  pathogenesis.  Clinical 
medicine,  however,  teaches  us  that  the  enlarged  alcoholic  liver  remains 
enlarged  after  the  ascites  is  cured,  and  experiments  teach  us  that  the  hyper- 
toxic  urine,  which  causes  convulsions  in  the  case  of  atrophic  cirrhosis,  is  of 
normal  toxicity  in  the  case  of  hypertrophic  cirrhosis.  While  the  existence  of 
initial  hypertrophy  in  atrophic  cirrhosis  is  not  improbable,  it  may  be  con- 
sidered as  exceptional.  When  the  liver  is  hypertrophied  in  alcoholic 
patients,  suspected  of  cirrhosis,  we  generally  see  one  of  the  following  results  : 
the  organ  either  contracts  to  its  normal  size  or  remains  enlarged.  In  the 
latter  case  the  cirrhosis  is  hypertrophic  (Hanot  and  Gilbert).  The  initial 
symptoms  as  well  as  the  aetiology  do  not  differ  in  the  slightest  from  common 
cirrhosis.  Later,  in  the  stationary  stage,  hypertrophic,  like  atrophic,  cir- 
rhosis may  be  lacking  in  such  cardinal  symptoms  as  collateral  circulation 
or  ascites.  It  may  be  rich  in  symptoms.  "  Dyspeptic  troubles,  alteration 
in  the  colour  of  the  faeces,  physiological  and  chemical  changes  in  the  urine, 
the  yellow  tint  of  the  skin,  the  appearance  of  varicose  veins  and  of  vascular 
naevi,  haemorrhages  from  diverse  tracts  (especially  epistaxis  and  gastror- 
rhagia),  ascites,  dilatation  of  the  subcutaneous  abdominal  veins,  haemor- 
rhoids, splenomegaly,  loss  of  strength  and  of  flesh,  belong  to  the  hypertrophic 
as  well  as  to  the  atrophic  forms  of  alcohoUc  cirrhosis  "  (Hanot  and  Gilbert). 
The  dilatation  of  the  subcutaneous  abdominal  veins  is  sometimes  slight  or 
absent.     It  is  only  in  exceptional  cases  that  it  shows  great  development. 

The  liver  extends  below  the  costal  margin  by  the  width  of  several 
fingers.  It  is  firm  ;  its  edge  is  rounded,  and  the  surface  may  be  studded  with 
nodules.  The  diagnosis  must  be  made  from  syphilitic,  malarial,  and  fatty 
liver. 

The  recognition  of  hypertrophic  alcoholic  cirrhosis  is  especially  interesting 
from  the  point  of  view  of  the  prognosis.     We  know  that  in  the  curabihty 


DISEASES  OF  THE  LIVER  897 

of  cirrhosis  has  recently  been  under  discussion  and  that  two-thirds  of  the 
cases  quoted  as  improved  or  cured  belong  to  the  form  under  description.  The 
ascites  diminishes ;  the  subcutaneous  and  heemorrhoidal  vessels  become 
small.  The  liver  may  contract,  but  as  a  rule  incompletely.  Millard  has 
quoted  a  case  in  which  the  spleen  contracted.  It  must  be  remembered  that 
the  curability  may  be  only  transient,  and  that  ascites  may  reappear  as  a 
result  of  alcoholic  excess.  Finally,  we  see  cases  in  which  cirrhosis  with  an 
enlarged  liver  may  cause  death,  after  the  manner  of  atrophic  cirrhosis. 

The  anatomical  characters  are  as  follows :  The  weight  of  the  liver  may 
be  5  or  6  pounds  ;  the  edges  are  rounded,  and  the  colour  is  of  a  rosy  yellow. 
The  surface,  after  removal  of  Glisson's  capsule,  presents  uneven  nodules, 
less  numerous,  however,  than  in  atrophic  cirrhosis.  The  surface  of  the 
section  is  smoother  than  in  Laennec's  cirrhosis,  but  is  divided  into  yellowish 
granules  by  reddish  fibrous  rings.  "  The  cirrhotic  rings  occupy  the  whole 
of  the  portal  spaces  and  the  majority  of  the  veins  of  the  hepatic  system." 
The  sclerotic  tissue  is  furrowed  with  capillary  angiectases  and  newly-formed 
bile-ducts. 

Hypertrophic  alcoholic  cirrhosis,  like  atrophic  cirrhosis,  is,  then,  an 
annular  and  perivenous  fibrosis.  Where  are  we  to  look  for  the  cause  of  the 
enlargement  of  the  liver  ?  Perhaps'  in  the  numerous  capillary  angiectases 
which  furrow  the  fibrous  rings,  or  perhaps  in  the  hypertrophy  of  the  hepatic 
cells  which  tend  to  the  concentric  orientation  seen  in  nodular  hepatitis. 

The  first  condition  in  treatment  is  the  suppression  of  alcohol.  Strict 
milk  diet,  continued  for  a  long  time,  iodides  in  small  doses,  diuretics,  and 
hydrotherapy,  may  bring  about  a  cure. 

Regeneration  of  the  Liver. — Hypertrophic  cirrhosis  is  of  the  same 
nature  as  atrophic  cirrhosis.  Both  diseases  present  the  same  topography 
of  the  connective  neo-formation.  Both  have  the  same  aetiology,  which 
often  is  alcoholism,  and  both  have  the  same  symptomatology  (ascites, 
dilatation  of  the  subcutaneous  abdominal  veins,  splenomegaly,  etc.),  and 
their  course  alone  is  dift'erent.  Hypertrophic  cirrhosis,  as  proved  by 
examples,  has  a  natural  tendency  to  recover.  What  is  the  cause  of  this 
relative  benignity  ?  Attempts  have  been  made  to  explain  it.  Relying 
on  experiments,  and  comparing  the  facts  observed  in  certain  affections  of 
the  liver,  authors  who  have  studied  the  question  admit  that  h}'pertrophic 
alcoholic  cirrhosis  is  an  example  of  compensatory  hy^aerplasia,  and  that 
we  have  to  deal  with  a  phenomenon  of  regeneration,  recently  made  clear. 
It  will  be  well  to  give  some  details  of  this  view,  which  is  destined,  I  think, 
to  play  a  great  part  in  the  conception  and  the  classification  of  cirrhosis. 

Experiments  prove  that  the  liver  possesses  in  a  high  degree  the  faculty 
of  regeneration.  Ponfick,  van  Merstcr,  Ploeck,  and  Krctz,  show  that  it  ia 
possible,  without  danger  to  the  life  of  the  animal  (dog,  rabbit,  rat),  to  remove 

57 


898  TEXT-BOOK  OF  MEDICINE 

half,  or  even  three-quarters,  of  the  liver.  The  animal  regains  its  appetite, 
and  gradually  recovers.  The  remainder  of  the  liver  becomes  double  or 
treble  its  si^e  in  three  or  four  weeks.  At  the  end  of  twenty-six  days,  on 
an  average,  the  hepatic  tissue  is  regenerated  to  such  an  extent  that  the 
newly- formed  tissue  may  weigh  more  than  the  normal  liver.  This  regenera- 
tion results  from  the  hypertrophy  of  the  organ,  and  especially  from  the 
hypertrophy  of  the  hepatic  cells.  The  lobules  attain  a  size  three  or  four 
times  larger  than  normal,  and  may  be  recognized  with  the  naked  eye. 
The  cellular  proliferation  commences  in  the  periphery  of  the  lobule,  and 
advances  progressively  towards  the  centre.  This  proliferation  is  regular, 
and  the  newly-formed  parts  retain  the  primary  anatomical  type.  Histo- 
logical examination  proves  that  the  process  is  one  of  true  hyperplasia,  and 
the  percentages  of  urea  seem  well  to  justify  the  name  of  compensatory. 
After  ablation  of  the  liver,  the  quantity  of  urea  Is  lowered.  This  diminu- 
tion is  proportional  to  the  amount  of  liver  removed.  Some  time  after  the 
operation  (ten  to  fifteen  days)  the  amount  of  urea  rises,  and  reaches  the 
normal  figure. 

These  experimental  results  have  been  applied  to  human  pathology. 
Hydatid  cysts  of  the  liver  furnished  the  first  example  of  regeneration  (Durug, 
Hanot,  Chauffard,  Kahn).  As  a  matter  of  fact,  these  parasitic  affections 
almost  realize  the  conditions  of  Ponfick's  experiments.  A  portion  of  the 
hepatic  2>arenchyma — most  frequently  the  right  lobe— is  destroyed  by  the 
tumour.  In  all  observed  cases  there  was  vicarious  hypertrophy  of  the  left 
lobe.  In  one  of  these  cases  this  lobe  alone  weighed  more  than  the  entire 
normal  liver.  The  increase  in  size  of  the  lobules  is  apparent  to  the  naked 
eye.  Under  the  microscope  the  hepatic  trabeculae  are  hypertrophied  and 
composed  of  cells  larger  than  normal,  and  containing  two,  three,  or  even 
four  nuclei,  in  which  karyoldnesis  can  be  distmguished.  It  is  a  remark- 
able fact  that  the  colunms  of  the  hepatic  cells  do  not  preserve  their  normal 
relation,  and  here,  as  in  experimental  cases,  the  lobule  no  longer  exists. 
The  rows  in  some  cases  are  sinuous,  and  arranged  without  regular  order ; 
in  other  cases — and  these  are  the  more  common — the  rows  have  a  tendency 
to  the  concentric  arrangement  observed  in  nodular  hyperplasia. 

This  process  of  regeneration  which  exists  in  hydatid  cysts  of  the  Hver, 
and  which  I  have  described  in  Hydatid  Cysts  of  the  Spleen,  has  been  found 
to  be  well  marked  in  hypertrophic  cirrhosis.  It  supplies  us  with  the  key 
to  the  different  evolution  of  the  atrophic  and  hypertrophic  forms  of  alcoholic 
cirrhosis.  In  the  former  most  of  the  cells  are  destroyed  or  are  on  the  way  to 
fatty  degeneration ;  in  the  latter,  not  only  do  the  cells  show  no  change,  but 
we  find  in  places  foci  of  hyperplasia,  cells  with  karyokinetic  proliferation 
and  concentric  nodules,  comparable  in  every  way  with  those  seen  in  the  case 
of  hydatid  cysts.      Here  again  the  idea  of  compensation  in  hypertrophic 


DISEASES  OF  THE  LIVER  899 

alcoholic  cirrhosis  is  verified  by  clinical  evidence.  We  have  seen,  as  a  matter 
of  fact,  that  the  urinary  toxicity,  instead  of  being  increased,  as  in  the 
atrophic  form,  remains  normal.  Furthermore,  researches  upon  urobihnuria 
and  alimentary  glycosuria  show  the  perfect  condition  of  the  cell.  In  alco- 
holic cirrhosis  this  regeneration  may  be  diffuse,  and  give  the  microscopic 
appearance  just  described.  The  hypertrophy  affects  the  liver  as  a  whole, 
or  is  confined  either  to  one  lobe  or  to  a  part  of  a  lobe.  All  these  varieties 
of  one  and  the  same  pathological  condition  differ  in  their  microscopic  aspect, 
but  they  are  blended  in  the  condition  of  the  living  and  regenerated  cell 
that  is  peculiar  to  them.  The  condition  of  the  cell  must  serve  to  classify 
cirrhoses,  for  it  commands  the  evolution,  while  the  prognosis  is  closely 
related  to  it.  The  proximate  causes  of  this  reaction  by  the  organism  are 
still  obscure  in  certain  cases.  The  regenerative  process  has  been  noticed 
particularly  in  young  arthritic  individuals.  We  shall  meet  mth  this  com- 
pensatory hyperplasia  when  we  study  other  kinds  of  cirrhosis,  such  as 
hypertrophic  biliary  cirrhosis,  in  which,  as  far  as  Hanot  is  concerned,  it 
explains  the  course  of  events.  It  manifests  itself  especially  by  the  forma- 
tion of  concentric  nodules.  ''  Similarly,  it  is  admissible  that  the  lesion 
described  by  Kelsch  and  Kiener  and  by  Sabourin  under  the  name  of  hyper- 
plastic nodular  hepatitis  in  certain,  cases  of  malarial  and  tubercular  cir- 
rhosis with  enlargement  of  the  liver,  is  only  the  expression  of  a  process  of 
more  or  less  developed,  though  often  insufl&cient,  regeneration." 


VII.  CURABILITY  OF  CIRRHOTIC  ASCITES  AND  CIRRHOSIS. 

Cirrhosis  and  cirrhotic  ascites  were  considered  to  be  incurable,  and 
every  individual  with  cirrhosis  of  the  liver  was  doomed  in  almost  the  same 
manner  as  an  individual  suffering  from  cancer.  These  opinions  must  be 
modified.  In  1886  Troisier  made  an  interesting  communication  to  the 
Societe  Medicale  des  Hopitaux  on  the  curability  of  cirrhotic  ascites,  and 
mentioned  with  regard  to  this  subject  the  work  of  Lendet  and  Ribeton. 
The  following  examples  give  an  idea  of  this  process  : 

Troisier  :  A  man  was  admitted  to  hosijital  for  ascites,  oedema  of  the  lower  limbs,  and 
collateral  circulation.  The  quantity  of  fluid  in  the  peritoneum  was  estimated  at 
about  12  pints.  The  Uver  seemed  to  be  enlarged,  and  the  spleen  was  hypertrophied. 
The  diagnosis  pointed  to  alcoholic  cirrhosis,  and  absolute  milk  diet  was  jirescribed. 
Under  the  influence  of  this  treatment  the  urine  rose  to  5  pints,  the  ascites  disappeared 
in  a  few  weeks,  as  did  the  oedema  of  the  lower  Umbs.  Since  then  the  ascites  has  not 
returned,  and  the  patient  is  in  excellent  health. 

Descoust :  A  patient  was  suffering  from  considerable  ascites,  with  d  ckiua  of  the 
legs,  and  jaundice.  The  urine  was  scanty,  but  did  not  contain  albumin  ;  tlic  lieart  was 
healthy.  The  man  had  for  a  long  time  been  addicted  to  drink,  and  tlio  cUagnosis  of 
cirrhosis  with  ascites  was  made.  Ascites,  ccdema  of  the  lower  limbs,  and  jaundice  had 
appeared  four  years  before,  but  had  disappeared  as  long  as  the  patient  abstained  from 

57—2 


900  TEXT-BOOK  OF  MEDICINE 

alcohol.  Vulpian,  who  saw  the  patient  at  the  time  of  his  second  attack,  gave  a  very 
grave  prognosis.  Soon  after  this  consultation  the  patient  left  for  the  country.  No  news 
was  received  from  him,  and  it  was  thought  that  he  was  dead.  Great  was  the  surprise 
of  Descoust  to  see  him  walk  into  his  consulting-room,  completely  recovered. 

Seailles :  A  blacksmith,  of  alcohohc  habits,  was  taken  ill  with  ascites  and  oedema 
of  the  legs.  The  hver  was  enlarged  and  extended  beyond  the  false  ribs  by  2  inches. 
The  case  was  one  of  alcohohc  cirrhosis,  with  enlarged  hver.  The  abdomen  was  tapi)ed, 
and  18  pints  of  a  citrine  Hquid  were  removed.  The  reproduction  of  the  liquid  was  so 
rapid  that,  between  January  28, 1885,and  November  5  of  the  same  year,  eighteen  tappings 
were  necessary,  and  gave  a  total  of  360  pints.  Each  tapping  was  followed  by  rehef, 
but  the  cachectic  condition  became  more  pronounced  and  the  patient  began  to  waste. 
From  the  commencement  of  treatment  absolute  milk  diet  had  been  prescribed.  After 
the  eighteenth  tapping  the  ascites  again  recurred  ;  and  then  the  urine  became  abundant, 
the  circumference  of  the  abdomen  fell  from  45  to  40  inches,  and  the  ascites  disappeared, 
although  the  hver  remained  hypertrophied.  In  a  few  weeks  he  regained  his  health, 
and  went  back  to  his  trade  as  a  blacksmith  ;  his  appetite  was  good,  but,  as  regards 
drink,  he  replaced  wine  by  milk. 

]\Iillard  :  This  was  a  case  of  a  man  of  alcoholic  habits.  After  a  prodromal  phase, 
lasting  a  year  and  a  half  (diarrhoea,  tympanites,  yellow  complexion,  and  emaciation), 
oedema  of  the  lower  limbs,  and  soon  afterwards  ascites,  appeared.  A  doctor  tapped  him, 
and  drew  off  16  pints  of  clear  fluid.  The  effusion  rapidly  reappeared.  Millard  found 
considerable  ascites  ;  the  liver  was  enlarged,  and  the  spleen  was  hypertrophied.  An 
exclusive  milk  diet  was  prescribed.  From  that  time  the  ascites  diminished  progres- 
sively, and  the  liver  and  spleen  decreased  in  size.  The  improvement  was  maintained, 
and  health  was  regained  in  a  few  months.  The  ascites  completely  disappeared,  the 
liver  and  spleen  resumed  their  normal  size,  and  the  man  was  cured  of  ascites  and  of 
alcoholic  cirrhosis. 

Kahn  :  A  woman,  of  alcoholic  habits,  noticed  a  gradual  enlargement  of  the 
abdomen.  Soon  afterwards  she  suffered  from  shght  jaundice,  oedema  of  the  lower  limbs, 
and  difficulty  in  breathing.  She  went  into  Hanot's  ward.  Considerable  ascites  and 
a  well-marked  collateral  circulation  were  found  ;  the  lower  Umbs  were  cedematous  ;  the 
face  was  cedematous ;  the  stools  were  almost  clay-coloured ;  and  she  experienced 
dyspnoea  on  the  least  exertion.  The  urine  contained  neither  albumin  nor  sugar, 
though  urobilin  and  red  pigment  were  foimd.  Paracentesis  was  performed,  and 
30  pints  of  yellowish  fluid  were  removed.  The  patient  was  placed  on  a  strict  milk  diet. 
After  tapping,  the  size  of  the  liver  was  more  easily  appreciated,  the  organ  being  much 
enlarged.  The  diagnosis  of  hypertrophic  alcohohc  cirrhosis  was  made.  The  hquid  was 
rapidly  reproduced,  and  a  second  tapping  was  necessary  in  three  weeks'  time,  34  pints 
being  withdrawn.  Other  tappings  were  performed  on  the  following  dates  :  April  3, 
42  pints  ;  April  20,  41  pints  ;  May  6,  41  pints ;  May  25,  40  pints  ;  June  26,  37  pints ; 
August  16,  34  pints  ;  October  10,  ninth  and  last  tapping,  withdrawal  of  36  pints. 
From  this  date  the  ascites  did  not  return,  the  hver  gradually  diminished  in  size,  the 
general  condition  became  excellent,  and  the  patient  finally  recovered.  The  saUent 
feature  is  that  she  was  seen  three  years  later  in  good  health. 

At  the  Hotel-Dieu  I  had  two  patients  whose  history  I  have  given  in  a  chnical  lecture* 
on  "  The  Curabihty  of  Ascites  and  Cirrhosis."  Resume  :  A  woman  was  admitted 
into  my  wards  for  ascites  estimated  at  about  24  pints.  The  patient  told  us  that  the 
trouble  began  seven  months  before,  in  August,  1897.  She  noticed  that  it  caused  her 
pain  to  put  on  her  corset,  and  that  her  stomach  was  more  swollen  than  usual.  As  regards 
digestive  troubles,  she  had  occasional  vomiting.  In  November  shght  oedema  of  the 
lower  limbs  made  its  appearance,  and  quickly  increased,  so  as  to  make  walking 

*  Clinique  Medicale  de  VHotd-Dieu,  1897,  19™^  legon. 


DISEASES  OF  THE  LIVER  901 

impossible.  Micturition  became  difficult.  She  was  admitted  in  this  condition  to  a 
surgical  ward  on  February  2,  1898,  the  diagnosis  being  ascites,  following  a  cystic  lesion 
of  the  ovary. 

On  February  5  an  incision  was  made  in  the  median  line  below  the  umbilicus,  and 
about  30  pints  of  serous  liquid  withdrawn.  The  ovaries  were  examined,  but  were 
healthy,  so  that  the  ascites  was  not  due  to  an  ovarian  lesion.  The  peritoneum  was  care- 
fully examined,  but  was  healthy,  so  that  the  ascitic  form  of  tuberculosis  was  out  of  the 
question.  The  diagnosis  of  cirrhotic  ascites  was,  therefore,  made,  and,  as  soon  as  the 
abdominal  wound  had  healed,  the  patient  was  sent  over  to  the  medical  wards,  under 
Chauffard.  For  some  time  after  the  evacuation  of  the  fluid  the  patient  felt  better,  and 
breathed  more  freely,  and  the  legs  were  less  oedematous.  She  was  placed  on  a  milk 
diet,  and  oxymel  scillae  was  prescribed.  On  February  15  (ten  days  after  laparotomy) 
ascites  was  again  present ;  the  oedema  of  the  legs  had  increased,  and  the  urine  was  less 
abundant.  On  March  2,  27  pints  of  yellowish  liquid  were  withdrawTi.  The  oedema 
of  the  legs  diminished  rapidly  and  the  patient  left  the  Cochin  Hospital  on  March  6 
for  home.  To  her  great  despair,  the  cedema  reappeared,  and  the  belly  again  swelled,  so 
that  she  was  compelled  to  keep  to  her  bed. 

On  March  15  she  was  admitted  to  my  wards,  complaining,  as  before,  of  the  size  of 
her  belly,  of  cedema  of  the  legs,  and  of  difficulty  in  micturition.  On  examination  I 
found  the  recent  cicatrix  of  the  median  laparotomy.  The  ascitic  hquid  was  very 
abundant  and  free  in  the  peritoneal  cavity.  The  size  of  the  belly  and  the  displacement 
of  the  intestinal  coils  made  the  measurement  of  the  liver  impossible.  Palpation 
revealed  neither  tumour  nor  induration.  A  well-marked  collateral  circulation  was 
evident  in  the  right  flank  and  the  epigastrium.  The  urine  contained  neither  all  urain, 
sugar,  nor  urobihn  ;  examination  for  ahmentary  glycosuria  remained  negative.  The 
existence  of  haemorrhoids  was  noticed. 

The  previous  operation  simplified  the  diagnosis  greatly,  and  I  knew  that  neither 
cystic  degeneration  nor  peritoneal  tuberculosis  had  been  found,  so  that  I  could  only 
agree  with  the  previous  diagnosis  of  cirrhotic  ascites.  Moreover,  the  patient  had  "  a 
hepatic  past,"  which  must  always  be  taken  into  account.  A  few  years  previously 
she  had  had  jaundice.  Again,  she  had  managed  a  wine-shop,  which  in  itself  is  an 
invitation  to  drink.  My  chagnosis  was,  therefore,  profuse  ascites,  hepatic  cirrhosis, 
relative  integrity  of  the  hepatic  cells  ;  bladder  troubles  caused  by  the  amount  of  the 
ascites.  The  patient  was  placed  on  a  strict  milk  diet.  Iodide  of  potassium  was  given 
only  for  a  short  time. 

On  March  27  tapping  became  necessary.  Thirty  pints  of  albuminous  yellow  hquid 
were  withdrawn  ;  the  lower  edge  of  the  liver  was  then  found  to  be  smooth.  Percussion 
gave  a  vertical  dullness  of  5  inches.  The  cirrhosis  was  therefore  not  atrophic,  but  had, 
rather,  a  hypertrophic  tendency.  During  the  next  few  weeks  the  ascites  slowly 
reappeared,  and  the  oedema  of  the  legs  persisted.  On  May  16  a  fresh  puncture  was  made, 
and  26  pints  of  yellowish  liquid  were  withdrawTi.  The  patient  continued  her  milk  diet, 
and  felt  much  better.  During  the  next  few  months  the  situation  comph^toly  changed  : 
the  cedema  of  the  legs  became  insignificant,  and  the  increase  in  quantity  of  the 
peritoneal  fluid  was  so  slow  that  in  two  months  and  a  half  the  belly  contained  only  a 
few  pints.  Nevertheless,  on  August  2  I  tapped  again,  15  pints  of  fhiid  being  withdrawn. 
From  that  dat,(!  not  the  slightest  peritoneal  effusion  was  noticed  ;  the  ondema  of  the  legs 
disappeared  r;omplotoly,  and  the  woman  felt  in  perfect  health  ;  but  I  kept  her  in  bed  on 
a  milk  diet.  On  October  15  I  allowed  the  patient  to  get  up,  and  I  added  eggs  and 
vegetables  to  her  milk  diet.  She  left  the  hospital  on  November  I,  promising  to 
continue  her  diet.  She  came  back  to  see  us  on  several  occasions,  and  we  found  her  in 
the  best  of  health.  She  ate  almost  all  kinds  of  food,  but  she  drank  only  milk.  There 
has  not  btH?n  a  trace  of  oedema  in  the  legs,  the  ascites  has  never  rea})i)eared,  and  the 
liver  has  gone  back  to  its  normal  size.     Summary  :   In  this  case  of  ascitic  cirrhosis 


902  TEXT-BOOK  OF  MEDICINE 

134  pints  of  fluid  had  been  withdrawn  in  six  months.     After  the  last  tapping  the  cure 
remained  permanent. 

I  saw  a  similar  case  at  the  Hotel-Dieu.  A  wine-broker  was  admitted  into  my 
wards  for  ascites.  He  told  me  that  the  belly  had  commenced  to  swell  three  months 
previously,  and  that  it  became  enormous  in  six  weeks.  The  appearance  of  the  ascites 
was  preceded  by  precirrhotic  symptoms — loss  of  appetite,  irregularity  of  the  bowels, 
appearance  of  haemorrhoids,  tympanites,  epistaxis,  wasting,  and  loss  of  strength.  On 
examination  I  found  that  he  had  an  earthy  complexion,  and  that  his  conjunctivae  were 
yellowish.  The  belly  was  much  enlarged,  and  measured  50  inches  around  the  umbilicus, 
which  was  very  prominent.  The  flanks  were  bulging,  and  the  skin  was  covered  with 
dilated  veins,  indicating  a  collateral  circulation.  Dullness  was  complete  in  the  flanks 
and  hypogastrium,  and  the  resonance  only  appeared  to  start  from  the  umbiUcus.  The 
sensation  of  fluid  was  very  clear.  I  estimated  the  quantity  of  fluid  in  the  peritoneum 
at  about  20  pints.  In  spite  of  the  distension  of  the  abdomen  the  enlargement  of  the 
liver  was  perceptible  ;  on  dipping  it  was  found  to  extend  an  inch  below  the  false  ribs. 
The  hypertrophy  was  Ukewise  shown  by  the  vertical  dullness,  measuring  6  inches. 
The  spleen  was  enlarged.  The  urine  was  of  normal  quantity,  and  contained  urobihn  in 
small  amount.     The  legs  were  not  oedematous.     The  heart  was  normal. 

The  man  was  an  alcohoUc,  drinking  some  12  pints  of  wine  a  day.  He  had  followed 
the  wine  trade  for  twenty-five  years.  Chronic  alcoholism  showed  itself  by  such 
symptoms  as  dyspeptic  troubles,  nightmare,  pains  and  cramps  in  the  legs,  and  tremors 
of  the  hands  and  tongue.  The  diagnosis  of  ascites,  associated  with  hypertrophic 
alcoholic  cirrhosis,  was  obvious.  The  large  size  of  the  Uver  was  not  antagonistic  to  this 
diagnosis  ;  on  the  contrar^^  an  enlarged  hver  is  frequently  characteristic  of  alcoholic 
cirrhosis. 

In  spite  of  the  ascites,  I  postponed  tapping,  and  ordered  complete  rest  and  milk 
diet,  to  which  a  tablespoonful  of  Trousseau's  diuretic  wine  was  added  daily.  The 
urine  became  more  abundant,  and  the  general  condition  improved.  After  a  month's 
treatment  the  belly  was  more  supple,  and  grew  smaller.  Strict'  treatment  was  continued, 
and  gradually  cured  the  ascites  and  the  cirrhosis.  Whilst  the  size  of  the  belly  diminished, 
the  urine,  which  amounted  to  3  pints  daily,  no  longer  contained  urobilin. 

After  the  disappearance  of  the  fluid  the  hypertrophied  liver  could  be  more  easily 
felt.  Improvement  ended  in  cure,  and  when  the  patient  left  the  hospital,  the  ascites  had 
completely  disappeared,  and  the  general  condition  was  excellent.  His  food  consisted 
of  white  meats,  bread,  and  vegetables  ;  the  wine  was  cut  off,  and  replaced  by  4  pints  of 
milk.  I  saw  the  patient  after  he  had  left  the  hospital :  the  Hver  had  regained  its  normal 
size  ;  the  cure  was  maintained. 

These  cases  prove  that  cirrhotic  ascites  is  curable.  Eecovery  has 
occurred  after  five  tappings  (my  first  patient),  after  eighteen  tappings 
(Seailles),  after  nine  tappings  (Kahn),  and  one  tapping  (Millard),  and  cure 
sometimes  results  without  tapping  (Troisier's  case  and  my  second  patient). 
This  cure  of  ascites  is  not  spontaneous,  but  is  due  to  an  exclusive  milk  diet, 
to  diuretic  medicines,  and  to  the  absolute  suppression  of  alcohol.  Two 
factors  contribute  to  the  cure  of  ascites — diuresis,  on  the  one  hand,  and,  on 
the  other  hand,  total  suppression  of  alcohol. 

Cirrhotic  ascites  is  curable.  Is  cirrhosis  of  the  liver  also  capable  of 
cure  ?  Cirrhosis  of  the  liver  may  be  cured.  I  am  of  opinion  that  the  more 
it  resembles  the  type  described  by  Hanot  and  Gilbert  as  "  alcoholic  and 
hypertrophic  cirrhosis  "  (the  type  described  in  the  preceding  section),  the 


DISEASES  OF  THE  LIVER  903 

more  easily  will  it  be  curable  ;  and  tlie  farther  it  is  removed  from  this  type, 
the  less  curable  it  will  be.  Let  me  explain  :  In  cirrhosis  with  an  atrophic 
tendency  the  hepatic  lobules  undergo  such  destruction  that  the  disease 
is  incurable  ;  but  there  are  cases  of  alcoholic  cirrhosis  with  compensatory 
hyperplasia.  By  this  hypertrophy  the  losses  sustained  through  the  cirrhotic 
process  are  more  than  compensated  by  the  new  formation  of  liver  substance. 

This  fact  was  proved  in  one  of  my  patiente  who  recovered  from  cirrhosis  and  ascites, 
finally  dying  of  erysipelas.  The  examination  of  his  hver  was  of  exceptional  interest. 
The  liver  weighed  over  4  pounds.  The  histological  examination  showed  the  existence 
of  bivenous  cirrhosis  ;  the  portal  lesions  were  of  especial  interest.  The  intrahepatic 
capillaries  were  enormously  developed,  both  in  the  fibrous  tissue  and  in  the  lobules, 
the  portal  circulation  being  completely  re-established. 

Furthermore,  the  numerous  centres  of  cellular  regeneration  found  ex- 
plained the  disappearance  of  the  signs  of  hepatic  insufficiency.  The 
remedy,  therefore,  exists  side  by  side  with  the  disease  ;  the  regenerative 
process  supplants  the  degeneration,  and  the  liver,  instead  of  becoming 
atrophied,  may  finally  be  much  larger  than  normal.  The  curability  of 
ascites  and  of  hepatic  cirrhosis  by  suitable  treatment  is  more  likely  when 
the  cirrhosis  approaches  the  type  of  alcoholic  cirrhosis  with  an  enlarged 
liver.  Clinically  this  type  differs  slightly  from  Laennec's  cirrhosis.  The 
course  is  less  rapid  ;  there  is  less  cachexia,  and  the  liver  is  enlarged. 

If  we  refer  to  the  preceding  cases  that  prove  the  curability  of  ascites 
and  of  cirrhosis,  we  see  that  hypertrophy  of  the  liver  was  present.  In  the 
case  of  Troisier's  patient  the  liver  seemed  to  be  increased  in  size.  In  one 
of  Letulle's  patients  the  liver  was  very  much  enlarged,  and  on  percussion 
showed  dullness  of  6  inches  in  the  nipple  line.  In  Seailles's  patient  the  liver 
was  larger  than  normal,  and  reached  below  the  false  ribs.  In  Millard's 
three  cases  the  liver  was  very  much  enlarged,  and  in  two  of  my  patients  it 
was  increased  in  size.  The  curability  refers  not  only  to  the  ascites,  but 
also  to  the  cirrhosis,  provided  the  treatment  is  continued  for  a  long  time. 
Nevertheless,  I  repeat,  all  kinds  of  cirrhosis  are  not  apt  to  be  cured,  but 
recovery  is  the  more  probable,  the  more  the  cirrhosis  approaches  the  hyper- 
trophic alcoholic  type. 

The  treatment  is  very  sim.ple.  It  consists  in  suppressing  alcohol  in 
any  form  (Millard).  The  patient  must  be  placed  on  absolute  milk  diet 
and  wator  (Vittel  or  Evian  water),  with  or  without  lactose.  Rest  in  bed  is 
essential.  If  the  ascites  is  considerable,  the  fluid  must  be  removed,  and  if 
it  reforms  rapidly,  tapping  must  be  done  as  often  as  necessary.  Improve- 
ment and  euro  may  sometimes  be  obtained.  On  the  other  hand,  recovery 
is  sometimes  slow  :  after  the  fifth  tapping  in  my  first  patient ;  after  the 
ninth  tapping  in  TIanot's  ])atient ;  or  after  the  eighteenth  tapping  in 
Seailles's  j)ationt. 


904  TEXT-BOOK  OF  MEDICINE 


VIII.  HYPERTROPHIC  CIRRHOSES. 

Hypertrophic  biliary  cirrhosis  does  not  sum  up  the  entire  history  of 
hypertrophic  cirrhoses.  Besides  hypertrophic  biliary  cirrhosis  there  are 
other  varieties  of  hypertrophied  liver,  which  I  shall  now  mention. 

1.  First  of  all,  we  find  malarial  hypertrophic  cirrhosis,  described  by 
Kelsch  and  Kiener,  who  found  in  the  liver  of  patients  dying  from  per- 
nicious fever  "  that  not  only  the  portal  vessels  and  the  capillaries  of  the 
islets  contained  white  pigmented  corpuscles,  but  that  the  endothelial  cells 
of  these  vessels  contained  also  black  pigment.  In  patients  who  died  from 
intermittent  fevers  of  long  duration  or  from  malarial  cachexia  these  authors 
have  seen  different  forms  of  cirrhosis,  generally  with  hypertrophy  of  the 
liver,  the  lobules  being  affected  by  nodular  parenchymatous  hepatitis 
(regeneration  of  the  liver)  with  adenomatous  growths,  as  well  as  with  more 
or  less  marked  pigmentation  of  the  new  connective  tissue  and  of  the  hepatic 
cells  "  (Cornil  and  Ranvier). 

2.  There  is  a  hypertrophic  alcoholic  bivenous  cirrhosis,  described  in 
one  of  the  preceding  sections. 

3.  There  is  a  bivenous  hypertrophic  cirrhosis  due  to  auto-intoxication  of 
gastro-intestinal  origin. 

4.  Fatty  degeneration  of  the  liver,  with  increase  in  size  of  the  organ,  is 
sometimes  accompanied  by  a  cirrhotic  lesion,  which  allows  us  to  describe  a 
fatty  hypertrophic  cirrhosis.  This  variety  is  especially  seen  in  alcoholics, 
or  in  patients  who  are  alcoholic  and  tubercular  at  the  same  time.  This 
variety  will  be  described  under  Tuberculosis  of  the  Liver. 

5.  Amyloid  degeneration  of  the  liver,  with  or  without  previous  syphilis, 
will  be  discussed  later.  It  is  sometimes  associated  with  cirrhosis,  which 
may  be  hypertrophic  or  atrophic. 

6.  We  find  in  some  patients  with  diabetes  cirrhosis  which  is  almost 
always  hypertrophic,  and  presents  special  characters.  It  will  be  dealt  with 
in  the  next  section. 


IX.  PIGMENTARY  HYPERTROPHIC  CIRRHOSIS— PIGMENTARY 

CACHEXIA. 

The  disease,  "with  which  I  am  going  to  deal  in  this  section,  has  received  diverse  names. 
It  has  been  called  pigmentary  hypertrophic  cirrhosis,  which  is  not  absolutely  true, 
because  the  pigmented  hver  may  not  be  hypertrophied.  It  has  also  been  called 
bronzed  diabetes,  which  does  not  answer  to  the  sum-total  of  the  cases,  because  diabetes 
and  bronzed  skin  may  be  absent  in  pigmentary  cirrhosis.  The  more  vague  name  of 
"  pigmentary  cachexia  "  would  be  more  in  accordance  with  the  actual  facts. 

I  had  in  my  wards  a  patient  suffering  from  this  pigmentary  cachexia.  On 
admission  I  was  struck  with  the  extreme  pallor  of  his  face,  while  the  skin  of  the  forehead, 


DISEASES  OF  THE  LIVER  905 

the  orbits,  and  the  cheeks  were  of  a  bistre  colour,  somewhat  resembhng  the  bronzed  tint 
of  Addison's  disease.  He  could  hardly  stand  erect,  because  he  was  so  weak.  I  examined 
him,  and  was  confronted  by  a  most  difficult  diagnosis.  On  the  one  hand  the  patient 
was  covered  with  large  purpuric  ecchymoses,  and  on  the  other  the  liver  was  enormous. 
The  urine  contained  neither  sugar  nor  albumin.  The  analysis  of  the  blood  showed  that 
there  was  no  increase  in  the  number  of  the  leucocytes.  The  clotting  was  normal.  The 
enormous  Uver  and  the  bistre  tint  of  a  jjortion  of  the  face  rather  pointed  to  bronzed 
hypertropliic  cirrhosis, .  and  I  made  this  diagnosis  -with  reserve.  It  was,  however, 
correct.     A  few  days  later  the  patient  died. 

The  post-mortem  examination  revealed  some  interesting  features.  The  Uver  was 
enlarged,  but  it  was  heavier  in  proportion,  because  it  weighed  110  ounces,  instead  of 
50  ounces.  It  was  hard  and  creaked  under  the  scalpel,  even  more  than  an  ordinary 
cirrhotic  liver.  It  seemed  as  though  the  knife  were  crushing  grains  of  sand.  Finally, 
and  this  was  the  particular  point  which  arrested  my  attention,  the  liver  had  a  sjiecial 
tint  ;  it  was  the  colour  of  rust.  Granules  of  cirrhosis  were  observed  in  the  sections, 
which  were  of  a  rusty  colour.  These  granules  and  the  intermediary  tissue  were  coloured 
with  two  different  tints  of  rust.  These  macroscopic  characters  already  showed  that 
the  liver  was  affected  with  the  cui'ious  lesion  called  "  pigmentary  cirrhosis." 

The  microscopic  and  chemical  examinations  fully  confirmed  the  diagnosis  of 
pigmentary  cirrhosis.  The  sections  showed  large  bands  of  fibrous  tissue,  forming 
irregular  rings,  di\ading  the  lobules  and  surrounding  the  hepatic  veins,  as  well  as  the 
portal  spaces.  In  short,  the  lesion  had  the  aspect  of  a  bivenous  cirrhosis.  The  hepatic 
lobules  were  let  into  the  cirrhotic  tissue,  and  in  places  the  cells  were  affected  with 
vesiculo-fatty  degeneration.  The  characteristic  feature  of  the  lesion,  however,  was  the 
presence  of  irregular  polyspherical  granules  of  a  golden-yellow  colour  in  the  bands  of 
the  fibrous  tissue  ;  in  the  interior  of  the  hepatic  cells  granules  of  the  same  colom-,  though 
much  smaller,  were  found.  In  the  cells  they  were  almost  regularly  divided,  but  they 
formed  tracts  in  the  fibrous  bands,  and  were  united  into  compact  masses  in  some  places. 

These  granules  had  very  peculiar  micro-chemical  characteristics,  and  in  spite  of 
staining  with  many  reagents  they  preserved  their  yellow  colour  in  the  midst  of  tissues 
coloured  pink,  red,  or  blue.  Even  in  very  thin  sections,  cleared  with  balsam,  they 
appeared  bright  yellow,  while  the  tissues  were  so  transparent  as  to  be  almost  invisible. 
Acids  or  alkaUs  did  not  atTect  the  yellow  colour.  They  were,  therefore,  rebellious  to  all 
colouring  and  decolouring  organic  materials.  On  the  other  hand,  with  sulphide  of 
ammonia  they  assumed  the  black  tint  of  sulphide  of  iron,  and  with  ferrocyanide  of 
potassium  and  hydrocliloric  acid  they  gave  the  beautiful  blue  colour  of  ferrocyanide 
of  iron  (Prussian  blue).     The  granules  were,  therefore,  formed  of  an  iron  pigment. 

Summary  :  The  liver  was  affected  with  hypertrophic  cirrhosis,  and  was  infiltrated 
with  pigment,  giving  the  reactions  of  iron.  There  was,  therefore,  no  doubt  tliat  it 
was  a  case  of  tlio  pigment  called  ochre  pigment  and  of  the  lesion  knowTi  as  pigmentary 
hypertrophic  cirrhosis. 

The  lesion  and  the  disease  that  it  causes  have  for  some  years  been  tlie  object  of 
much  investigation  that  tends  to  modify  former  conceptions.  A  recent  discussion  at 
the  Societe  Medicale  des  Hopitaux  showed  great  difference  of  opinion  with  regard  to 
this  subject.  In  this  di.seaso  it  is  the  rule  that  the  liver  is  not  the  only  organ  infiltrated 
with  tlie  jtigment  ;  the  pancn^as,  the  salivary  glands,  the  supranmal  capsules,  the 
myocardium,  and  the  lymphatic  glands  (corresponding  to  the  diseased  organs  are  often 
infiltrated  with  pigment.  The  more  active  the  cells  the  more  apt  are  they  to  bo  loaded 
with  iron  pigment. 

Description. — This  disease  was  first  described  by  Trousseau.  Tii  a 
man  with  dialx'tes  brought  on  by  overwork  and  privation,  Trousseau  was 
struck  with  the  brouze-liJ<e  colour  of  the  face  and  the  blackisli  colitur  of 


906  TEXT-BOOK  OF  MEDICINE 

tlie  penis.  "  At  the  post-mortem  examination,"  says  Trousseau,  "  we 
found  no  lesion  in  the  suprarenal  capsules.  The  liver,  however,  was  twice 
its  normal  size,  and  the  whole  surface  of  the  organ  was  granular,  of  a  uniform 
yellowish-grey  colour,  and  of  considerable  density.  It  resisted  pressure, 
and  did  not  break  down  between  the  fingers.  It  creaked  under  the  scalpel, 
and  the  cut  surface,  instead  of  being  smooth,  w<is  granular.  There  was 
evident  cirrhosis,  but  it  was  hypertrophic." 

Hanot  and  ChaufEard  thus  sum  up  the  symptomatology  of  the  disease  : 
(1)  Signs  of  diabetes  (glycosuria,  polyuria,  polyphagia,  polydipsia,  impo- 
tence, boils,  gingivitis,  etc.) ;  (2)  signs  of  cirrhosis  (ascites,  collateral  circula- 
tion, digestive  troubles,  increase  in  size  of  the  liver,  urobilinuria,  jaundice, 
haemorrhage,  etc.) ;  (3)  bronzed  colour  of  the  skin,  especially  of  the  face,  the 
genital  organs,  and  the  flexures  of  the  limbs.  The  pigmentary  patches  are 
rare  in  the  mucosae,  unlike  the  pigmentation  in  Addison's  disease. 

Pigmentary  hypertrophic  cirrhosis  is  hardly  ever  seen,  except  in  feeble 
patients  suffering  from  cachexia,  tuberculosis,  alcoholism,  malaria,  cancer, 
etc.  In  those  individuals  who  are  already  diseased  the  signs  of  cirrhosis 
and  the  bronzed  tint  develop  insidiously,  and  the  examination  of  the  urine 
reveals  the  presence  of  glucose.  The  loss  of  flesh  is  rapid,  diarrhoea  appears, 
and  fever  is  frequent,  the  temperature  varying  from  98°  to  100°  F.  The 
patient  becomes  cachectic,  and  death  generally  supervenes  a  few  months 
after  the  appearance  of  the  bronzed  tint  and  of  the  diabetes.  The  fatal 
termination  is  frequently  hastened  by  such  infectious  complications  as 
moist  gangrene,  extensive  erysipelas,  pneumonia,  broncho-pneumonia,  or 
miliary  tuberculosis. 

Such  is  the  common  clinical  picture.  Nevertheless,  all  the  symptoms 
are  not  constant.  Thus,  diabetes  may  be  absent,  as  in  the  case  of  my 
patient ;  the  bronzed  tint  of  the  skin  may  likewise  be  wanting.  The  name 
of  "  bronzed  diabetes  "  is  not,  therefore,  applicable  to  all  cases  of  pigmentary 
cachexia.  Hypertrophy  of  the  liver  is  not  constant,  and  the  organ  may  be 
atrophied.  The  liver  may,  indeed,  be  infiltrated  with  ochre  pigment,  while 
the  cirrhosis  is  very  slight.  Ascites  is  absent,  and  no  collateral  circulation 
develops.  Accordingly,  masked  forms  are  seen,  and  bronzed  cirrhosis  is 
often  but  a  chance  find  at  the  autopsy.  If  care  were  taken  to  submit 
all  livers  to  the  sulphide  of  ammonia  and  the  ferrocyanide  tests,  it  would 
be  found  that  pigment  giving  the  reactions  of  iron  was  relatively  frequent. 

Pathogenesis. — The  first  writers  on  this  subject  believed  that  bronzed 
cirrhosis  was  always  the  consequence  of  diabetes,  and  explained  the  for- 
mation of  the  pigment  by  the  defective  action  of  the  liver  in  diabetes.  In 
Marie's  opinion,  the  diabetes  is  secondary,  and  the  primary  phenomenon 
is  the  change  in  the  blood-corpuscles  and  the  conversion  of  their  haemo- 
globin into  iron  pigment.     This  pigment  accumulates  afterwards  in  the 


DISEASES  OF  THE  LIVER  907 

parencliymata  ;  in  the  liver  it  produces  cirrhosis  ;  in  the  pancreas  the 
changes  induce  diabetes.  Ausscher  and  Lapicque  have  shown  experimen- 
tally that,  if  a  dog's  blood  is  injected  in  the  peritoneum  of  another  dog,  and 
the  animal  is  killed  a  few  days  later,  the  liver  will  be  found  infiltrated  with 
iron  pigment.  I  was  able  to  lay  hold  of  the  formation  of  this  pigment  at 
the  expense  of  the  haemoglobin  in  the  following  case  :  A  woman  in  one  of  my 
wards  died  during  an  attack  of  hsemoglobinuria,  and  Widal  found  at  the 
post-mortem  examination  iron  pigment  in  the  cells  of  the  convoluted  tubules. 
In  my  case  of  pigmentary  cirrhosis,  diabetes,  alcoholism,  malaria,  and 
tuberculosis  were  absent,  but  the  patient  had  had  for  some  months  recurrent 
purpura,  with  subcutaneous  haemorrhages.  The  ochre  pigment  was  also 
seen  around  the  hsemorrhagic  foci,  but  in  patients  who  are  in  good  health 
it  is  quickly  absorbed.  And  the  same  fact  obtains  in  dogs  (used  for  experi- 
ment— Ausscher  and  Lapicque)  if  several  months  are  allowed  to  elapse 
before  the  animal  is  killed.  It  might  be  said  that  previous  visceral  changes 
are  essential  if  the  pigment  is  to  remain  fixed  in  the  organs.  This  explains 
the  fact  that  the  disease  is  hardly  ever  seen,  except  in  individuals  rendered 
cachectic  by  tuberculosis,  alcoholism,  cancer,  or  malaria.  The  treatment 
of  pigmentary  cachexia  is  purely  symptomatic,  for  we  know  of  no  means 
capable  of  preventing  the  formation  or  of  hastening  the  absorption  of  the 
iron  pigment. 

X.  HYPERTROPHIC  BILIARY  CIRRHOSIS— HANOT'S  DISEASE. 

We  have  seen  in  alcoholic  cirrhosis  that  the  morbid  process  first  attacks  the  portal 
and  hepatic  veins,  and  then  the  hepatic  cells.  In  hypertrophic  bihary  cirrhosis  the 
process  commences  in  the  hepatic  cells  and  the  biliary  canaliculi,  the  reaction  of  the 
vital  elements  preceding  or  accompanying  the  lesions  of  the  connective  tissue. 

Every  cirrhosis,  however,  in  which  the  biliary  apparatus  is  affected,  does  not 
deserve  a  place  in  the  category  of  so-called  biliary  cirrhosis.  Jaundice  may  appear  in 
atrophic  cirrhosis,  with  neo-formation  of  biliary  canaliculi,  and  is  an  integral  part  of 
biliary  cirrhosis  duo  to  gall-stones.  Jaundice  may  appear  in  alcoholic,  fatty,  pig- 
mentary, or  malarial  hypertrophic  cirrhosis,  proving  that  there  are  several  varieties  of 
hypertrophic  cirrhosis  with  jaundice. 

There  is,  however,  a  typo  of  hypertrophic  biliary  cirrhosis,  which  was  described  by 
Hanot  in  1876.  "  Chronic  jaundice  ;  considerable  hypertrophy  of  the  liver,  often  also 
of  the  spleen ;  absence  of  ascites  and  of  collateral  circulation  in  the  abdominal  wall ; 
symptoms  of  icterus  gravis,  as  the  most  common  termination,"  are  the  cardinal  features 
ascribed  by  Hanot  to  the  disease  that  rightly  bears  his  name.  For  my  description  I 
shall  select  a  typical  case  of  hypertropliic  biliary  cirrhosis. 

Anatomical  Pathology— Autopsy. — The  size  of  the  liver  is  considerable. 
The  weight  may  exceed  100  ounces.  The  shape  is  not  altered  ;  the  edge 
remains  sharp,  and  the  surface  is  smooth,  or  at  most  is  but  slightly  granular 
or  nodular — features  very  different  from  atrophic  cirrhosis,  in  which  the 
liver  is  atrophied  and  hobnailed. 


908  TEXT-BOOK  OF  MEDICINE 

Externally  tlie  hypertropliied  liver  is  of  an  olive-grey  colour,  especially 
in  the  projecting  parts.  On  section,  it  is  firm  and  resistant,  but  it  does 
not  creak  under  the  scalpel,  as  in  atrophic  cirrhosis.  It  is  of  a  dark  brown 
or  greenish  colour,  according  to  the  amount  of  bile  present.  The  surface 
of  the  section  is  overrun  by  wide  bands  of  connective  tissue,  and  studded  at 
intervals  with  projecting  granulations,  which  cannot  be  enucleated,  and 
are  therefore  very  different  from  the  granulations  of  the  atrophic  liver.  There 
is  no  amyloid  degeneration,  Glisson's  capsule  is  often  inflamed,  thickened, 
and  adherent  to  the  neighbouring  organs  (perihepatitis). 

The  bloodvessels  and  the  large  bile-ducts  of  the  hilum  are  normal.  The 
gall-bladder  shows  no  lesion.  It  may  be  small,  and  contain  only  a  little 
bile,  but  no  calculi.  The  glands  of  the  hilum  are  generally  not  swollen. 
The  hypertrophy  of  the  liver  is  due  to  several  causes  :  to  abundant  connective 
tissue  that  is  less  fibrous  and  retractile  than  that  of  atrophic  cirrhosis ;  to 
the  integrity  of  a  large  number  of  hepatic  cells  ;  to  the  frequent  hypertrophy 
of  the  cells  ;  and  to  the  formation  of  biliary  canaliculi. 

Histological  Examination. — 1.  Portal  Spaces. — In  specimens  stained 
with  picrocarmine  under  a  low  magnifying  power  the  cirrhotic  tissue 
appears  in  the  form  of  patches,  stars,  or  of  irregular  islets,  whence  the  name 
"  insular  cirrhosis."  These  islets  are  caused  by  the  tracts  which  penetrate 
into  the  fissures  between  the  hepatic  lobules.  The  tracts  incompletely 
surround  an  islet  or  a  group  of  islets,  and  skirt  the  lobules,  so  that  the 
latter  assume  the  form  of  an  indented  oval.  The  connective  bands  generally 
penetrate  the  lobule,  and  bend  back  or  terminate  in  a  swollen  end,  without 
reaching  as  far  as  the  central  vein  of  the  lobule. 

The  fibrous  tissue  is  not  dense  ;  it  has  few  fibres  and  little  elasticity.  It 
has  been  compared  with  the  neuroglia  of  disseminated  sclerosis  (Brissaud), 
and  does  not  resemble  the  fibrous  tissue  of  venous  cirrhosis. 

In  the  new  connective  tissue  blocking  the  portal  spaces  sections  of  the 
biliary  canals,  portal  veins,  and  capillaries  are  seen.  The  striking  fact  is 
the  size  and  number  of  the  biliary  canals,  of  which  several  may  be  counted 
in  each  portal  space.  The  number  of  embryonic  cells,  with  which  the  canals 
are  surrounded,  shows  that  they  are  a  centre  of  fibrous  formation.  They 
may  be  recognized  by  the  thickness  of  their  walls,  by  their  large  connective 
sheath,  by  their  deep  colour,  and  by  their  lumen,  which  is  lined  by  one  or 
two  rows  of  deeply  stained  cubical  cells.  The  thickness  and  the  staining  of 
the  biliary  canaliculi  distinguish  them  from  the  portal  veins,  the  walls  of 
which,  though  thicker  than  in  the  normal  condition,  are  only  half  as  thick 
as  the  walls  of  the  biliary  canals.  This  is  the  essential  difference  from 
atrophic  cirrhosis,  which  presents  inverse  lesions — that  is  to  say,  the  portal 
veins  are  thicker  and  more  deeply  stained  than  the  biliary  canals.  The 
portal  veins,  dilated  and  gorged  with  blood  in  atrophic  cirrhosis,  are  often 


DISEASES  OF  THE  LIVER  909 

empty  in  hypertrophic  biliary  cirrhosis.  In  a  word,  the  dominant  factor 
in  hypertrophic  biUary  cirrhosis  is  angiocholitis  and  periangiocholitis. 
The  dominating  factor  in  atrophic  cirrhosis  is  phlebitis  and  bivenous  peri- 
phlebitis. 

2.  Hepatic  Lobules. — We  have  just  seen  that  the  hepatic  lobules  are 
indented  and  furrowed  by  the  connective  tissue  arising  as  islets  in  the  portal 
spaces.  Sometimes  the  intralobular  connective  tissue  is  a  direct  out- 
growth of  the  perilobular  tissue  ;  sometimes  it  appears  to  be  independent  of 
it ;  but  whatever  source  it  may  arise  from,  the  cirrhosis  is  extra-  and  intra- 
lobular. 

Several  authors  admit  that  intralobular  cirrhosis  arises,  not  at  the 
expense  of  the  connective  tissue  of  the  lobule,  but  at  the  expense  of  the 
epithelial  elements  (epithelial  cirrhosis).  The  parenchyma  of  the  cells  is 
said  to  undergo  change,  and  to  give  birth  to  new  tissue  (parenchymatous 
inflammation).  The  cirrhosis  would  then  be  both  interstitial  and  parenchy- 
matous, and  would  come  under  the  heading  of  Epithelial  Cirrhosis.  Such 
is  not  the  present-day  opinion.  "  The  doctrine  of  epithelial  cirrhosis  has 
had  its  day  "  (Letulle).  At  any  rate,  in  hypertrophic  biliary  cirrhosis  the 
central  vein  of  the  lobule  is  never  cirrhotic.  According  as  the  lobule  is 
more  or  less  deformed,  the  topography  of  the  hepatic  lobule  is  modified, 
the  hepatic  vein  loses  its  central  position,  and  may  even  disappear.  When 
the  lobules  are  much  involved,  the  cells  are  dissociated  and  deformed,  but 
the  degeneration  and  the  atrophy  of  the  cells  so  frequent  in  atropliic  cir- 
rhosis are  exceptional  in  hypertrophic  cirrhosis.  One  of  the  most  promi- 
nent characters  of  this  hypertrophic  cirrhosis,  says  Hanot,  is  the  integrity 
of  most  of  the  hepatic  cells.  In  certain  lobules,  even  those  which  are 
attacked  by  fibrosis,  the  cells  preserve  their  columnar  disposition,  and  are 
not  crowded  together,  as  in  atrophic  cirrhosis,  but  each  cellular  ray  is 
separated  from  its  neighbour  by  an  empty  space,  and  these  spaces  radiate 
in  little  columns.  The  cells  preserve  their  normal  size  and  shape,  although 
some  are  hypertrophied.  They  stain  with  carmine,  and  are  rarely  infil- 
trated with  fat  or  bile  pigment. 

3.  Biliary  Network. — The  biliary  canals  visible  to  the  naked  eye  undergo 
no  notable  modification.  The  process  primarily  attacks  the  caualiculi  of 
the  portal  spaces,  and  causes  angiocholitis.  Furthermore,  in  the  hyper- 
plastic connective  tissue  we  see  a  large  number  of  nuich  finer,  elongated 
canaliculi,  which  ramify  and  form  meshes  by  their  anastomo.ses.  These 
dilated  canaliculi  sometimes  form  biliary  angiomata,  which  may  become 
cystic  (Sabourin).  Small  biliary  abscesses  have  also  been  seen  following 
suppurative  angiocholitis.  (Some  canaliculi  are  formed  by  a  wall  lined 
with  cubical  epithelium;  others  have  a  flattened  epithelium.  In  any  case 
they  are  not  pseudo-,  but  true,  canaliculi,  because  the  smallest  of  them  has  a 


910  TEXT-BOOK  OF  MEDICINE 

lumen.  In  some  specimens  they  may  be  seen  penetrating  the  hepatic 
lobules  in  the  spaces  between  the  little  columns  of  cells. 

The  marked  development  of  the  biliary  canaliculi  is  met  with  in  acute 
just  as  in  chronic  hepatitis  (Cornil),  but  in  no  case  is  it  as  marked  as  in 
hypertrophic  cirrhosis.  What  is  the  origin  of  these  biliary  canaliculi  ? 
Are  they  completely  moulded,  or  are  they,  while  scarcely  visible  in  the 
normal  condition,  produced  by  the  inflammation  of  the  tissues  around  them  ? 
This  network  of  canaliculi  is  not  found  in  a  healthy  liver,  but  it  can  be  pro- 
duced experimentally.  In  their  experiments  on  biliary  cirrhosis  caused 
by  the  ligature  of  the  common  bile-duct,  Charcot  and  Gombault  found  the 
development  of  a  rich  network  of  canaliculi  with  cubical  epitheUum,  and 
in  several  specimens  they  were  able  to  prove  the  union  of  the  extralobular 
with  the  intralobular  canaliculi.  They  thought  that  the  intralobular 
canaliculi  were  but  the  transformation  of  those  normally  present  in  the 
lobule.  How,  then,  is  the  presence  of  cubical  epithelium  in  the  new  canali- 
culi to  be  explained  ?  Kiener  and  KeLsch  have  answered  this  question, 
admitting  that  the  intralobular  biliary  canaliculi  and  their  cubical  epitheUum 
are  formed  at  the  expense  of  the  hepatic  cells,  "  the  hepatic  cells  returning 
to  the  embryonic  stage  after  having  been  previously  the  seat  of  nutritive 
irritation."  This  opinion  was  adopted  by  several  authors  (Charcot)  ;  the 
present  tendency  is  to  reject  it.  The  progressive  atrophy  of  the  epithelia, 
says  Letulle,  already  recognized  by  histologists,  but  incorrectly  interpreted, 
served  as  a  basis  for  the  doctrine  of  the  possible  return  of  the  epithelia  to 
the  embryonic  condition ;  but  well-observed  cases  have  thrown  it  in  the 
shade  (Brault).  "  The  frequency  of  biliary  canahcuU  in  all  hepatic  affections, 
and  their  direct  relations  with  the  biliary  canals  of  the  portal  spaces  and 
with  the  intralobular  canaliculi,  would  rather  lead  us  to  consider  them  as  old 
canaliculi  brought  out  either  by  the  retreat  of  the  hepatic  lobules  or  by  the 
Inflammation  of  the  connective  tissue  in  the  midst  of  which  they  are  found. 

4.  Bloodvessels. — In  describing  the  lesions  of  the  portal  spaces  I  said 
that  phlebitis  and  periphlebitis  may  be  met  with,  but  the  phlebitis  is  only 
slight,  and  does  not  form  the  principal  lesion,  as  in  atrophic  cirrhosis.  The 
integrity  of  the  portal  circulation  assuring  the  function  of  the  hepatic  ceU 
explains  why  hypertrophic  cirrhosis  may  last  for  years  without  compromising 
life.  Moreover,  the  newly-formed  fibrous  tissue  contains  a  vascular  network 
between  the  portal  vessels  and  the  capillaries  of  the  affected  lobule.  This 
network  is  said  to  be  not  of  new  formation.  "  It  would  rather  represent 
that  portion  of  the  hepatic  capillary  network  in  the  meshes  of  which  con- 
nective tissue  has  been  substituted  for  the  glandular  cells  "  (Ackermann). 

In  any  case,  wide  communications  exist  between  the  portal  and  central 
veins,  and  injections  into  the  portal  vein  do  not  meet  with  the  same  obstruc- 
tion as  in  atrophic  cirrhosis. 


J 


DISEASES  OF  THE  LIVER  911 

5.  Process. — I  have  discussed  the  different  changes  in  hypertrophic 
biliary  cirrhosis.  But  how  does  the  process  commence  ?  It  begins  in  the 
biliary  canaliculi  of  the  portal  spaces  (biliary  cirrhosis),  whereas  the  process 
in  Laennec's  cirrhosis  commences  in  the  portal  and  the  hepatic  veins  (bi- 
venous  cirrhosis).  As  the  inflammatory  signs  are  very  marked  in  the 
immediate  neighbourhood  of  the  biliary  canals  in  the  portal  spaces,  Hanot 
has  rightly  supposed  that  the  lesion  is  at  first  confined  to  these  canals 
(angiochohtis  and  periangiocholitis).  This  inflammatory  process  is  syste- 
matic, commencing  in  the  interlobular  ducts  almost  at  the  same  time 
througjiout  the  whole  liver,  and  spreading  in  the  manner  already  de- 
scribed. 

Perhaps,  too,  the  process  commences  in  the  hepatic  cells,  the  hyper- 
trophy and  overactivity  leading  to  a  kind  of  biliary  diabetes.  This  poly- 
cholia  would  then  cause  enlargement  of  the  intralobular  biHary  canaliculi, 
stagnation  of  the  bile  in  the  extralobular  canaliculi,  and  consecutive  angio- 
chohtis (Schachmann). 

The  theory  that  the  process  in  hypertrophic  cirrhosis  commences  in  the 
inflammation  of  the  biliary  canalicuH  is  confirmed  by  the  following  facts  : 
The  persistent  obhteration  of  the  common  bile-duct  by  a  calculus  or  by 
cancer  of  the  pan'^-reas,  and  the  experimental  ligature  of  this  canal  in 
animals  causes  fibrous  lesions,  closely  resembling  those  of  hypertrophic 
cirrhosis.  Evidently  there  are  difl^erences ;  thus,  experimental  biliary 
cirrhosis  is  not  hypertrophic,  or,  at  least,  the  hypertrophy  is  transient. 
Furthermore,  it  is  accompanied  by  rapid  change  in  the  hepatic  cells  and 
by  lesions  of  the  large  biliary  canals,  which  is  not  the  case  in  hypertrophic 
cirrhosis ;  but  it  allows  us  to  witness,  as  it  were,  in  the  very  act,  the  course 
and  formation  of  the  cirrhotic  tissue,  which  commences  in  the  biliary 
vessels,  and  then  spreads  to  the  connective  tissue.  This  theory  has  been 
questioned  on  the  ground  that  the  formation  of  the  biliary  network  which 
is  so  well  marked  in  hypertrophic  cirrhosis  also  exists  in  acute  atrophy  of 
the  Uver  and  in  all  foruLs  of  cirrhosis.  This  biliary  network  is  found  "  in 
the  midst  of  the  pathological  fibrous  tissue  of  the  gland,  no  matter  what 
is  the  origin  or  the  nature  of  the  morbid  process."  This  biliary  network, 
however,  though  it  has  been  found  in  several  affections  of  the  liver,  in  no 
wise  diminishes  the  value  of  the  initial  localization  of  hypertrophic  biliary 
cirrhosis  in  the  canaliculi  of  the  portal  spaces. 

G.  The  accessory  lesions  of  hy[)ertrophic  cirrhosis  are  hypertrophy  of 
the  spleen,  which  is  rarely  absent.  The  spleen  may  weigh  three  or  four 
times  its  normal  weight.  I  would,  further,  mention  })erihepatitis  and 
dilatation  of  the  right  side  of  the  heart,  with  tricuspid  insufficiency  (Potain). 

Symptoms. — Confirmed  hypertrophic  biliary  cirrhosis  is  characterized 
by  three  essential  symptoms  :  enlargement  of  the  liver,  persistent  jaundice, 


912  TEXT-BOOK  OF  MEDICINE 

and  hypertrophy  of  the  spleen.  The  troubles  of  the  onset  are  variable. 
Some  cases  begin  with  flatulence,  eructations,  loss  of  appetite,  a  feeling  of 
discomfort  in  the  epigastrium,  and  a  sensation  of  weight  in  the  right  hypo- 
chondrium.  The  disease  may  begin  with  congestion  of  the  liver,  accom- 
panied by  fever.  These  congestive  attacks  are  followed  by  jaundice,  and 
simulate  catarrhal  icterus.  When  they  are  accompanied  by  pain,  they 
simulate  hepatic  colic.  These  various  modes  of  commencement  are  only 
met  with  in  certain  cases.  As  a  rule,  jaundice  is  the  first  symptom,  fever, 
pain,  and  dyspeptic  troubles  being  absent.  No  matter  what  is  the  early 
character  of  the  disease,  jaundice  is  the  chief  symptom,  and  mugt  first 
demand  our  attention. 

The  jaundice  is  due  to  catarrh  of  the  biliary  canaliculi  and  to  the  resulting 
retention  of  the  bile.  It  may  be  slight  or  severe,  varying  from  a  pale 
yellow  to  the  olive  tint  generally  seen  at  an  advanced  stage  of  the  disease. 
It  lasts  for  months  and  years  without  ever  completely  disappearing,  because 
the  catarrh  of  the  bile-ducts  is  permanent.  The  retention  of  the  bile  causes 
the  urine  to  be  more  or  less  charged  with  pigment. 

As  the  catarrh  only  obliterates  a  portion  of  the  bile-ducts,  sufficient 
bile  continues  to  flow  into  the  intestine.  Accordingly,  the  faecal  matter  is 
not  colourless,  as  it  is  in  ordinary  catarrhal  jaundice,  where  the  common 
bile-duct  is  for  the  time  being  obliterated.  In  twenty-six  cases  of  hyper- 
trophic biliary  cirrhosis  absence  of  colour  in  the  faecal  matter  has  been 
noticed  only  twice,  and,  even  when  it  exists,  it  is  incomplete  or  transitory. 
In  order  to  be  complete,  obstruction  of  the  biliary  canals  or  an  arrest  in 
the  secretion  of  bile  would  be  necessary.  The  attacks  of  jaundice  are  in 
some  cases  preceded  by  hepatic  pain  and  fever.  The  jaundice  is  sometimes 
accompanied  by  pruritus  and  xanthelasma. 

The  examination  of  the  urine  reveals  more  than  the  presence  of  bihary 
pigments  ;  the  urea  is  less  than  in  normal  urine.  This  diminution  of  the 
urea  is  not  due  to  the  diminution  of  the  nitrogenous  foods,  for  patients 
continue  to  eat  well,  but  to  the  fact  that  the  liver  does  not  act  properly. 
The  urine  contains  neither  albumin  nor  sugar.  The  patient  can  take  a 
certain  quantity  of  sugar  without  glycosuria — a  proof  that  the  hepatic 
cells  are  but  Kttle  affected,  and  that  they  continue  to  convert  the  sugar  in 
the  food. 

Enlargement  of  the  liver  is  a  constant  symptom,  and  may  come  on 
gradually  or  in  successive  attacks.  It  may  be  subject  to  oscillations,  but 
it  is  persistent,  and  has  no  tendency  to  terminate  in  atrophy.  The  Hver 
finally  becomes  enormous,  but  it  retains  its  form,  and  its  edge  remains 
sharp.  It  is  hard  and  smooth  to  the  touch,  reaches  up  into  the  thoracic 
cavity  beyond  the  fifth  intercostal  space,  and  descends  into  the  abdomen 
as  far  as  the  umbilical  region,  and  its  left  lobe  projects  into  the  hypochon- 


DISEASES  OF  THE  LIVER  913 

drium  close  to  the  spleen.  This  hypertrophy  causes  bulging  of  the  lower 
intercostal  spaces. 

Examination  of  the  liver  does  not  cause  any  pain.  In  some  cases,  how- 
ever, the  hepatic  region  is  sensitive  on  account  of  the  perihepatitis  that 
often  accompanies  cirrhosis. 

The  spleen  is  almost  always  much  hj^ertrophied,  and  its  dimensions 
may  be  the  easier  appreciated,  as  it  attains  twice  or  three  times  its  normal 
size.  The  hypertrophy  of  the  liver  and  of  the  spleen  explains  the  bulging 
and  the  deformity  of  the  supra-umbilical  region. 

The  absence  of  ascites  and  of  a  collateral  circulation  are  negative  symp- 
toms of  great  value.  The  absence  of  ascites  is  not  surprising,  because  the  portal 
venous  system  is  intact.  When  ascites  exists,  it  usually  occurs  at  an  ad- 
vanced period  of  the  disease.  In  atrophic  cirrhosis  the  ascites  may  reach 
its  full  development  at  an  early  date. 

Duration — Termination. — Hypertrophic  cirrhosis  is  a  chronic  and  fatal 
disease,  lasting  from  three  to  ten  years.  Patients  may,  for  years,  present 
the  cardinal  symptoms  of  this  affection — viz.,  hypertrophy  of  the  liver 
and  spleen  with  chronic  jaundice — without  being  otherwise  incommoded. 
Many  preserve  their  appetite  and  strength  indefinitely.  Sometimes,  how- 
ever, especially  in  alcoholic  or  overworked  persons,  acute  phases  appear, 
and  are  characterized  by  fever,  with  hepatic  pain  and  increased  jaundice. 
After  a  time,  loss  of  flesh,  emaciation,  and  cachexia  (dryness  of  the  skin, 
anorexia,  diarrhoea,  and  cutaneous  eruptions)  supervene,  and  end  in  death. 
In  other  cases,  death  is  hastened  by  a  cholera-like  attack,  due,  no  doubt,  to 
secondary  infection  by  the  coli  bacillus.  Pulmonary  complications  some- 
times hasten  the  end.  Finally,  in  some  cases,  the  liver  being  without 
defence  and  the  door  being  open  to  toxines  and  micro-organisms,  the 
hepatic  cell  is  destroyed,  and  symptoms  of  icterus  gravis  suddenly  appear. 
They  include  multiple  haemorrhages,  nervous  troubles,  and  coma,  which 
rapidly  prove  fatal. 

Diagnosis. — As  long  as  the  liver  is  not  hypertrophied  and  permanent 
jaundice  does  not  develop,  the  diagnosis  is  impossible,  since  the  disease  rests 
on  these  two  fundamental  symptoms.  The  pains  associated  with  jaundice 
simulate  hepatic  colic,  and  the  attacks  of  jaundice,  with  dyspeptic  troubles, 
resemble  catarrhal  jaundice.  This  last  error  is  the  more  likely,  m  that 
catarrhal  jaundice  may  last  two  months  or  more,  the  liver  being  hypertro- 
phied. It  is  true  that  in  catarrhal  jaundice  decoloration  of  the  facal 
matter  is  the  rule.     It  is  the  exception  in  hypertrophic  cirrhosis. 

Later,  when  the  liver  has  increased  in  size  and  the  jaundice  has  become 
permanent,  the  diagnosis  Ls  even  more  diflicult. 

Primary  cancer  of  the  liver  resembles  hypertr()|)liic  cirrhosis  in  the 
enlargement  of  the  liver,  but  it  differs  from  the  latter  in  the  absence  of 

58 


914  TEXT-BOOK  OF  MEDICINE 

jaundice.  Secondary  cancer  is  often  accompanied  by  jaundice,  but  the 
tumour  is  uneven  and  nodular.  In  cancer  of  the  liver,  the  spleen  is  not 
hypertrophied,  and  in  a  few  months  the  disease  reaches  the  cachectic  stage. 
Melanotic  cancer  presents  this  peculiarity — that  the  hypertrophied  liver  is 
neither  deformed  nor  nodular  ;  but  the  other  distinctive  signs  persist,  and 
jaundice  is  generally  absent  (Straus). 

In  leucocythaemia,  the  liver  is  often  enlarged,  and  the  spleen  is  hyper- 
trophied, but  jaundice  is  wanting,  and  examination  of  the  blood  is  conclusive. 

Patients  suffering  from  malarial  cachexia  may  have  enlarged  livers 
and  spleens,  but  in  these  diseases  the  jaundice  is  much  less  pronounced.  The 
actual  troubles  have  been  preceded  by  attacks  of  malaria,  and  quinine  has 
an  influence  that  is  not  seen  in  hypertrophic  cirrhosis. 

Hypertrophic  cirrhosis  has  great  analogy  with  hydatid  cysts  of  the 
liver,  and  the  proof  is  that  exploratory  punctures  have  several  times  been 
made,  either  through  error  or  through  an  incomplete  diagnosis.  The 
hydatid  cyst  has  not  on  palpation  the  fibrous  hardness  of  the  hypertrophied 
liver.     The  spleen  is  normal,  and  jaundice  is  exceptional. 

The  amyloid  liver  may  be  as  large  as  the  hypertrophied  cirrhotic  liver. 
It  is  not  accompanied  by  jaundice,  and  it  is  related  to  causes  (syphilis, 
chronic  suppuration)  favouring  the  deposit  of  lardacein  in  the  system. 

In  bronzed  diabetes,  marked  hypertrophy  of  the  liver  may  be  observed, 
but  the  skin  of  the  patient  is  rather  bronzed  than  jaundiced.  The  spleen 
is  not  enlarged,  and  the  presence  of  sugar  in  the  urine  and  the  concomitant 
symptoms  give  the  differential  diagnosis. 

The  diagnosis  is  sometimes  difficult  between  hypertrophic  cirrhosis  and 
a  syphilitic  liver.  Syphilitic  hepatitis  runs  the  following  course  :  It  causes 
but  slight  pain,  and  is  characterized  by  vague  malaise  and  digestive  troubles. 
It  is  accompanied  by  diarrhoea  and  albuminuria,  but  hardly  ever  brings  on 
jaundice.  Locally  hypertrophy  of  the  liver  and  of  the  spleen,  without 
ascites  or  with  moderate  ascites,  is  generally  seen.  In  exceptional  cases 
palpation  shows  that  the  surface  is  uneven.  In  aU  cases  we  must  look 
for  symptoms  or  marks  of  syphilis ;  in  doubtful  cases  treatment  must  be 
exhibited  without  delay. 

The  difference  between  hypertrophic  and  atrophic  cirrhosis  is  such  that 
an  error  of  diagnosis  is  impossible.  In  the  former  the  liver  is  bulky ;  the 
spleen  is  much  enlarged ;  jaundice  is  constant ;  and  we  find  neither  ascites 
nor  collateral  circulation.  In  the  latter  the  liver  is  small ;  jaundice  is 
scarcely  ever  present;  and  ascites  and  the  complementary  circulation  are 
the  rule.  Between  these  well-defined  types,  however,  there  are  mixed 
forms,  presenting  some  difficulties  in  diagnosis. 

Splenomegalic  Form. — Hanot's  hypertrophic  cirrhosis  may  present 
varieties  differing  slightly  from  the  common  type.     In  certain  cases  the 


I 


DISEASES  OF  THE  LIVER  915 

spleen  assumes  unusual  proportions.  In  the  classical  cases  the  hypertrophy 
of  the  liver  greatly  exceeds  that  of  the  spleen.  On  examining  the  patient, 
it  is  the  size  of  the  liver  that  first  attracts  attention.  The  right  hypo- 
chondrium  bulges  more  than  the  left.  The  deformity  of  the  abdomen  is 
rather  hepatic  than  splenic.  Post-mortem  examination  shows  that  the  liver 
weighs  5  or  6  pounds,  while  the  spleen  weighs  on  an  average  2  pounds. 

In  some  cases  the  spleen  is  so  large  that  it  attracts  quite  as  much  atten- 
tion as  the  liver.  The  left  hypochondrium  bulges  as  much  as  the  right  one, 
and  the  spleen  descends  into  the  abdomen,  forming  a  tumour  of  considerable 
size.  To  obtain  an  idea  of  the  size  to  which  the  spleen  may  attain,  it  will  be 
sufl&cient  to  quote  a  few  cases  in  which  the  weights  of  the  two  organs  have 
been  noted : 

Liver,  70  ounces ;  spleen,  60  ounces  (Landrieux  and  Milian). 
Liver,  75        „         spleen,  60        „       (Guillain). 
Liver,  60        „         spleen,  70        „        (Smith). 

Gilbert  and  Fournier  have  described  this  form  under  the  name  of  "  hyper- 
splenomegalic  biliary  cirrhosis."  I  do  not  think  that  there  is  any  need  for 
this  variety  of  hypertrophic  biliary  cirrhosis,  because  the  other  symptoms, 
the  anatomical  characters,  the  setiological  conditions,  the  evolution  and 
the  termination,  are  common  to  these  varieties  of  biliary  cirrhosis.  It  is, 
nevertheless,  important  to  recognize  these  forms  with  great  splenic  enlarge- 
ment in  order  not  to  direct  the  diagnosis  unduly  towards  splenomegaly  of 
a  different  nature,  when  the  case  is  really  one  of  Hanot's  disease.  We  find, 
in  opposition  to  the  cases  in  which  the  spleen  is  very  much  enlarged,  cases 
in  which  its  size  is  scarcely  altered. 

.ffitiology — Treatment. — Hypertrophic  cirrhosis  is  a  disease  of  adult 
age.  Alcoholism  can  only  be  blamed  in  a  moderate  degree.  The  hypo- 
thesis of  infection  is  possible,  but  has  not  been  proved. 

The  treatment  is  practically  the  same  as  in  atrophic  cirrhosis  :  purgatives 
for  the  dyspeptic  troubles,  diuretics,  tonics,  Vichy  water,  Carlsbad  water, 
Tharasp  water,  milk  diet,  iodide  of  potassium,  and  hydrotherapy. 


XI.  MIXED  CIRRHOSIS. 

Description. — The  difference  between  atrophic  cirrhosis  and  hyper- 
trophic biliary  cirrhosis  is  so  great,  especially  when  extreme  types  are 
chosen,  that  certain  authors  consider  them  to  be  absolutely  distinct  species. 

In  order  to  span  the  distance  that  seems  to  sepaiate  these  two  forms  of 
cirrhosis,  it  will  suflicc  to  nioiitioii  Cliarcot's  propositions  : 

Atrophic  cirrhosis  ia  annular,  multilobular,  extralobular,  and  of 
venous  origin. 

58—2 


916  TEXT-BOOK  OF  MEDICINE 

Hypertrophic  cirrhosis  is  insular,  monolobular,  both  extra-  and 
intralobular,  and  of  biliary  origin. 

While  the  various  terms  of  these  propositions  may  not  be  absolutely 
true,  it  is  none  the  less  certain  that  the  process  in  these  two  forms  of  cirrhosis 
is  different.  In  atrophic  cirrhosis  the  lesion  commences  in  the  portal  and 
hepatic  veins  (bivenous  cirrhosis).  In  hypertrophic  cirrhosis  the  lesion 
commences  in  the  biliary  canals  and  the  hepatic  cells  (biliary  or  visceral 
cirrhosis).  In  the  former  the  fibrous  tissue  is  indurated  and  retractile, 
like  scar  tissue,  and  causes  atrophy  of  the  organ,  and  the  hepatic  cells  are 
frequently  affected  or  destroyed.  In  the  latter  the  cirrhotic  tissue  remains 
in  an  incomplete  fibroid  state,  and  has  not  the  same  importance,  while  the 
hepatic  cells  are  for  the  most  part  intact  or  hypertrophied. 

This  difference  in  appearance,  however,  does  not  mean  that  atrophic 
cirrhosis  and  hypertrophic  cirrhosis  are  absolutely  opposite.  It  is  true 
they  form  two  distinct  varieties  when  dealing  with  extreme  types,  but  on 
some  occasions  we  find  ourselves  face  to  face  with  mixed  or  intermediate 
forms  which  serve  to  bridge  the  extreme  types. 

To  these  mixed  or  intermediate  cases  I  have  given  the  name  of  mixed 
cirrhosis.  Clinically  and  anatomically  they  belong  partly  to  atrophic 
and  partly  to  hypertrophic  cirrhosis.  Gruiter  has  collected  several  cases, 
and  a  fair  number  of  cases  have  been  since  observed. 

Clinically,  mixed  cirrhoses  are  apt  to  mislead  us.  We  have  been  so 
accustomed  to  the  hard-and-fast  division  of  atrophic  venous  cirrhosis  and 
hypertrophic  biliary  cirrhosis  that,  when  icterus  appears  during  the  course 
of  cirrhosis  thought  to  be  atrophic,  or  ascites  appears  in  a  cirrhosis  thought 
to  be  hypertrophic,  the  diagnosis  becomes  doubtful,  and  we  are  loath  to 
admit  that  a  case  of  cirrhosis  has  broken  the  barriers  imposed  by  too  limited 
a  classification. 

And  yet  cases  of  mixed  cirrhosis  are  not  rare.  They  show  at  the  same 
time  the  symptoms  and  the  lesions  of  atrophic  and  of  hypertrophic  cirrhosis. 
To  enable  the  reader  to  form  a  better  judgment  I  will  give  a  resume  of  three 
cases : 

Case  1. — An  alcoholic,  non-syphilitic  patient  was  taken  ill  with  cirrhosis.  He  had 
ascites  and  complementary  abdominal  circulation,  as  in  atrophic  cirrhosis,  and  icterus, 
as  in  hypertrophic  cirrhosis.  At  the  post-mortem  examination  the  liver  was  small  and 
granular,  and  the  histological  examination  showed  lesions  of  atrophic  (perilobular 
fibrous  sclerosis),  and  also  of  hypertrophic  cirrhosis  (rich  biUary  network,  invasion  of 
the  lobule  by  embryonic  cells). 

Case  2. — An  alcohohc,  non-syphihtic  patient  was  taken  ill  with  cirrhosis.  The  liver 
was  enlarged,  and  the  jaundice  was  persistent,  as  in  hypertrophic  cirrhosis  ;  well- 
developed  collateral  circulation  and  considerable  ascites,  as  in  atroishic  cirrhosis,  were 
foimd. 

Case  3. — An  alcoholic  patient  was  seized  with  cirrhosis.  The  disease  commenced 
with    persistent    jaundice,    as   in    hypertrophic    cirrhosis.     Considerable    ascites  then 


DISEASES  OF  THE  LIVER  917 

supervened,  as  in  atrophic  cirrhosis.  At  the  post-mortem  examination  a  slightly- 
atrophied  Uver  was  found,  and  the  microscopic  examination  showed  an  extra-  and  intra- 
lobular fibrosis  and  a  marked  biliary  network  at  the  same  time. 

Cases  of  mixed  cirrhosis  will  become  more  numerous,  according  as  they 
are  sought  for.  The  conclusions  which  I  think  we  may  draw  from  a  study 
of  these  cases  are  that  venous  atrophic  cirrhosis  and  hypertrophic  biliary 
cirrhosis  form  varieties  that  are  the  more  distinct,  the  more  extreme  the 
types  described  are,  and  that  it  is  greatly  to  the  credit  of  the  Paris  school 
to  have  shed  light  on  the  chaos  of  chronic  hepatitis.  The  spirit  of  systema- 
tization  and  of  classification  must,  however,  not  be  pushed  too  far.  Clinical 
medicine  accommodates  itself  but  ill  with  too  clearly  defined  a  selection  of 
morbid  species,  and  the  lesion  is  here,  as  always,  in  agreement  with  the  clinical 
conditions.  Between  the  extreme  types  described  in  the  preceding  sections 
there  is  room  for  intermediate  forms,  and  it  seems  to  me  that  the  name 
"  mixed  cirrhosis  "  should  be  appUed  to  them. 


XII.  TUBERCULOSIS  OF  THE  LIVER. 

Writers  in  the  first  half  of  the  last  century  considered  tuberculosis  of  the  liver  as  an 
exception.  In  the  opinion  of  Andral  and  Cruveilhier,  fatty  degeneration  was  the  usual 
lesion  of  this  organ  in  phthisical  patients." 

Thaon,  in  1872,  stated  that,  in  eight  cases  out  of  ten,  careful  observations  would 
reveal  nodules  in  the  fiver  of  tubercular  patients  ;  but,  later,  Julius  Arnold  went  so  far 
as  to  state  that  the  nodules  were  found  in  all  cases  of  tuberculosis.  The  truth  is  that, 
while  the  hepatic  tubercle  is  frequent  in  all  varieties  of  tuberculosis,  it  is  the  rule  in 
childi'en,  and  during  the  course  of  acute  alidominal  tuberculosis.  The  nodule  is  its  most 
frequent  form,  but  the  lesion  may  run  its  normal  course,  and  give  rise  to  caseous  masses, 
cavities  (Sergent,  Jacobson),  and  abscesses. 

Steatosis  and  tubercles  are  not  the  only  lesicms  seen  in  the  fiver  of  phthisical  patients  ; 
fibrosis  may  also  occur  in  it,  as  in  the  lung.  The  history  of  tubercular  cirrhosis 
of  the  fiver  has  been  elucidat<*d  during  the  past  few  years,  and  furnishes  an  interesting 
contribution  to  the  general  history  of  cirrhosis  of  infectious  origin. 

In  addition  to  the  fatty  hypertrophic  cirrhosis  of  Hutinel  and  Sabourin  (1881),  the 
works  of  Hanot,  Lauth,  and  Gilbert  have  taught  us  that  there  are  two  other  varieties 
of  tubercular  cirrhosis — the  one  furrowed  and  comparable  with  the  condition  found  in 
pyphifitic  patients,  and  the  other  closely  resembling  common  alcoholic  cirrhosis. 

In  phthisical  patients  with  cachexia  amyloid  degeneration  of  the  liver  may  be  found, 
and  in  plithisical  patients  with  diseased  hearts  the  so-called  cardiac  fiver  may  bo 
noticed. 

These  changes  are  not  peculiar  to  tubercular  patients,  and  have  been  described 
elsewhere.  The  experimenter,  as  well  as  the  pathologist  and  the  clinical  physician, 
has  derived  benefit  from  the  study  of  tuberculosis  of  tlio  liver.  It  must  not  bo  forgotten 
that  the  experimental  hepatic  tubercle  has  furnished  most  valuable  enlightenment  on 
the  much-disputed  histogenesis  of  the  tubercle. 

Pathological  Anatomy.— The  tubercular  nodule  is  the  most  cliarac- 
teri.stic  lesion.  'I'lic  liv(u-  is  (congested,  and  the  nodules  are  widely  dis- 
seminated in  the  lobules  and  in  tlie  porto-biliary  spaces.    They  form  little 


918  TEXT-BOOK  OF  MEDICINE 

round  grey  and  semitransparent  spots,  that  often  require  a  lens  in  order 
to  be  seen.  According  to  Brissaud  and  Toupet,  the  topography  of  the 
tubercle,  which  varies  in  each  case,  is  subject  to  certain  laws.  In  the  same 
liver  the  nodule  is  said  to  be  always  systematized  in  the  subdivisions  of  the 
same  order  of  Glisson's  capsule.  The  sublobular  portal  space  is  said  to  be 
the  most  frequent  seat  of  the  lesion.  In  time  the  tubercles  may  increase 
in  size  and  become  caseous.  The  cavity  is  an  exceptional  lesion  in  the  liver 
of  tubercular  patients.  When  it  exists,  it  is  always  peribiliary,  and  is 
the  result  of  tubercular  angiocholitis.  The  walls  of  the  biliary  canal  in 
which  it  is  inserted  are  studded  with  fine  granules.  By  virtue  of  this  localiza- 
tion of  the  hepatic  cavities  around  the  biliary  canals,  Chauifard  supposes 
that  other  associated  germs  of  intestinal  origin  assist  Koch's  bacillus.  It 
is  very  difficult  to  stain  Koch's  bacilli  in  tuberculosis  of  the  liver,  no  doubt 
because  of  the  special  qualities  of  the  chemical  action  in  the  liver. 

Fat  is  found  in  almost  every  tubercular  liver.  Fatty  degeneration  of 
the  liver  may  be  either  systematic  or  general.  Around  the  hepatic  tubercles 
there  may  often  be  seen  a  small  zone  of  fatty  degeneration,  which  forms,  "  as 
it  were,  a  layer  concentric  to  the  central  epithelioid  and  embryonic  zones  " 
(Hanot  and  Lauth). 

Under  the  name  of  nodular  fatty  evolution  in  tubercular  patients 
Sabourin  has  described  a  lesion,  arising  systematically  around  the  porto- 
bUiary  spaces  as  a  centre,  and  sparing  the  parenchyma  around  the  central 
veins.  Whether  the  steatosis  is  local  or  general,  the  fat  always  infiltrates 
the  cellular  elements.  The  nuclei  still  retain  their  affinity  for  taking  stains. 
According  to  Hanot  and  Lauth,  it  is  simple  infiltration,  and  not  degeneration. 
The  process  of  steatosis  and  fibrosis  may  combine  so  as  to  produce  the  lesion 
known  as  fatty  hypertrophic  cirrhosis,  the  aetiology  of  which,  according  to 
many  writers,  depends  on  both  alcoholism  and  tuberculosis. 

The  liver  is  enlarged,  its  edges  are  thickened,  and  its  weight  may  be 
100  ounces.  It  is  of  a  yellow-ochre  colour,  and  the  cut  surface  is  smooth 
and  fatty.  Small  rosy  patches  in  the  porto-biliary  spaces  are  formed  of  new 
connective  tissue.  Under  the  microscope  we  find  porto-biliary  cirrhosis, 
which  is  both  insular  and  diffuse.  The  connective  tissue  thus  developed 
around  the  blood  and  biliary  vessels  has  characters  difEerentiating 
it  from  other  cirrhoses.  It  does  not  bring  about  fibrosis.  It  is  studded 
with  tubercular  follicles,  which  sometimes  penetrate  the  adjacent  parts  of 
the  lobule,  and  it  sends  into  the  lobule  fine  pencilled  bands  that  separate 
and  envelop  the  hepatic  cells,  so  as  to  form  a  true  monocellular  cirrhosis. 
Here,  again,  the  hepatic  cells  are  surcharged  with  fat,  and  are  not  in  a  con- 
dition of  degeneration. 

Amongst  the  other  types  of  tubercular  cirrhosis  the  most  interesting 
is  the  variety  described  by  Hanot  and  Lanta.     The  liver  is  lobulated  and 


DISEASES  OF  THE  LIVER  91d 

furrowed  by  fibrous  bands,  that  cause  it  to  resemble  the  liver  produced  by 
tight-lacing.  The  cirrhosis  is  porto-bUiarj^  with  numerous  biliary  canaliculi. 
There  is  a  periportal  steatosis,  with  fine  intercellular  connective  radiations, 
and  numerous  tubercular  granulations  disseminated  in  the  hepatic  paren- 
chyma. 

There  is  a  rare  form  of  hepatic  tuberculosis,  characterized  by  nodular 
hepatitis  without  fatty  degeneration,  and  analogous  to  that  described  by 
Kelsch  and  Kiener  in  the  malarial  liver.  This  hepatitis  is  either  isolated  or 
associated  with  hepatic  cirrhosis.  The  various  lesions,  which  I  have 
separated  for  purposes  of  description,  are  often  isolated  or  at  times 
differently  associated  in  the  livers  of  tubercular  patients. 

Experiments  and  Pathogenesis. — The  entrance-gate  of  the  tubercle 
bacillus  into  the  liver  of  human  beings  is  very  variable.  The  bacillus  may 
enter  by  the  portal  veins  or  by  the  arterial  vessels,  by  the  peritoneum,  and 
by  the  biliary  passages.  In  the  foetus  it  may,  in  exceptional  cases,  follow 
the  umbilical  vein  (Sabouraud).  The  hepatic  tubercle  has  been  reproduced 
experimentally  in  animals  by  varying  the  afferent  channel.  The  injection 
of  tubercular  matter  into  the  peritoneum  of  a  guinea-pig  causes  death  in 
two  to  six  weeks.  The  liver  and  spleen  are  filled  with  tubercles,  and  the 
retroperitoneal  and  subcutaneous  glands  are  swollen  and  caseous  (Straus 
and  Gamaleia).  In  man  tuberculosis  of  the  liver  is  often  combined  in  like 
manner  with  tubercular  peritonitis. 

The  inoculation  of  a  pure  culture  of  tuberculosis  into  the  mesenteric  veins 
of  a  rabbit  (Gilbert  and  Lion)  causes  the  death  of  the  animal  in  three  to  five 
weeks.  The  liver  and  the  spleen  are  the  only  organs  crammed  with  tuber- 
cular nodules.  The  tubercles  appear  on  the  seventh  day  around  the  peri- 
portal capillaries.  Their  evolution  follows  the  multiplication  of  the  bacilli 
in  the  vessels, 

A  virulent  cultiire  of  human  tuberculosis  injected  into  the  general 
circulation  by  the  marginal  vein  in  a  ral)bit's  ear  produces  rapid  miliary 
tuberculosis  (Koch,  Straus  and  Gamaleia).  The  bacilli  in  this  case  reach 
the  liver  by  the  hepatic  artery,  and  so  cause  tuberculosis. 

Cornil  and  Yersin,  using  the  same  method,  only  found  acute  septica3mia, 
with  swelling  of  the  liver  and  the  spleen,  which  were  crammed  with  bacilli, 
though  no  tubercles  were  present.  The  reason  was  that  they  had  employed 
the  cultures  from  avian  and  not  human  tuberculosis.  Hanot  and  Gilbert 
were  able  to  o])serve  tubercular  fiijrosis  of  the  liver  in  a  guinea-pig.  The 
fibrosis  was  perilobular,  and  the  fibrous  bands  penetrated  the  lobule.  They 
only  saw  in  this  a  tu])orcular  lesion,  giving  rise  to  fibrosis.  In  a  guinea-pig 
inoculated  with  avian  tul)erculosis  the  same  writers  \v<>r('  able  to  produce  a 
tubercular  furrowed  liver. 

Finally,  Pillct  has  recently  shown  that  cultures  of  Ir.unnn  tuljorculoais 


920  TEXT-BOOK  OF  MEDICINE 

inoculated  in  a  guinea-pig  or  in  a  dog  may  cause  large  degenerative  lesions 
in  the  liver  from  coagulation  necrosis.  The  hepatic  cells  swell,  their  proto- 
plasm liquefies,  and  their  nucleus  loses  its  affinity  for  colouring  matter. 

Experimental  tubercular  hepatitis  has  contributed,  as  we  have  said,  to 
the  elucidation  of  the  histogenesis  of  the  tubercle  in  general.  Cornil  and 
Yersin  made  intravenous  injections  of  avian  cultures  in  rabbits,  and  were 
able  to  observe  the  course  of  the  lesion  in  the  liver.  About  the  fifth  or 
sixth  day  after  inoculation  the  bacilli  simply  cause  small  fibrinous  clots  in 
the  capillaries,  where  they  end  near  the  portal  spaces.  A  zone  of  leuco- 
cytes soon  envelops  the  fibrinous  thrombus  within  the  vessel.  The  leuco- 
cytes, no  doubt  under  the  influence  of  the  substances  secreted  by  the  bacilli, 
are  converted  into  epithelioid  or  giant  cells.  The  process  has  not  time  to 
proceed  farther,  as  death  supervenes  about  the  end  of  the  third  week. 
Metchnikoff,  and  Gilbert  and  Girode  consider  that  the  principal  part  in  the 
formation  of  the  nodules  and  of  the  giant  cells  is  played  by  the  endothelial 
cells  of  the  vessels  and  by  the  large  mononuclear  leucocytes.  One  of  the 
proofs  of  the  activity  of  these  elements  is  the  presence  of  glycogen  in  the 
protoplasm. 

The  hepatic  cells  do  not,  as  Baumgarten  maintained,  take  part  in  the 
initial  constitution  of  the  tubercle.  The  hepatic  tubercle  may  consist  in 
a  simple  agglomeration  of  round  cells,  like  the  infective  nodules  of  typhoid 
fever  or  smallpox.  Experiments  as  well  as  pathological  anatomy  prove, 
therefore,  that  the  tubercle  bacillus  produces  in  the  liver  the  fatty  degenera- 
tion of  the  cell  and  the  fibrosis,  as  well  as  the  tubercle.  How  does  it  produce 
these  different  lesions  ?  Does  it  do  so  by  direct  action,  or  by  means  of  the 
toxines  which  it  secretes  ?  According  to  Hanot  and  Lauth,  the  bacilli 
act  through  their  secretions,  which  are  said  to  be  sclerogenous  for  the  con- 
nective tissue  and  fat-producing  for  the  hepatic  cell.  The  experiments 
carried  out  with  Koch's  tuberculin  have  not  confirmed  this  alluring  hypothesis 
(Chauffard). 

It  is,  perhaps,  more  probable  to  consider,  with  Hanot  and  Gilbert,  that 
the  difference  of  the  lesions  is  due  to  an  abnormal  individual  resistance 
against  the  tubercle  bacillus,  or  to  an  infection  of  the  organism  by  bacilli 
which,  in  the  very  extensive  scale  of  virulence  that  the  bacillus  of  Koch 
must  possess,  occupy  no  very  high  place  as  regard  species. 

Koch's  bacillus  is,  perhaps,  not  the  only  factor  at  work.  Alcoholism  has 
been  considered  as  a  contributory  cause  in  the  first  researches  published  on 
fatty  hypertrophic  cirrhosis.  Whilst  Sabourin  wrongly  adopted  alcohol  as 
the  only  cause,  Hutinel  explained  the  fibrosis  by  alcoholism,  and  the  fatty 
condition  of  the  liver  by  tuberculosis.  According  to  Hanot,  alcoholism  plays 
only  a  secondary  part,  and  recent  observations  made  by  Hutinel  on  young 
children  free  from  the  suspicion  of  alcoholism  are  in  favour  of  this  opinion. 


DISEASES  OF  THE  LIVER  921 

The  researches  of  Hanot  and  Letienne  have  proved  that  biliary  infections 
play  a  secondary  part. 

Symptoms. — Clinically,  hepatic  tuberculosis  is,  as  a  rule,  silent  in  its 
progress,  whether  we  have  to  deal  with  tubercular  granules,  peribiliary 
cavities,  or  nodular  foci.  The  symptomatology  in  these  cases  points  to  the 
general  disease — tuberculosis — rather  than  to  the  hepatic  localization.  If, 
however,  we  make  a  practice  of  examining  the  liver  in  tubercular  patients, 
certain  signs  will  show  that  the  organ  is  affected.  The  slightly  hypertrophied 
liver,  extending  two  or  three  fingers'  breadth  below  the  edge  of  the  false 
ribs,  may  be  somewhat  painful  on  pressure.  The  spleen  is  also  somewhat 
enlarged.  Slight  jaundice,  some  decoloration  of  the  faeces,  scanty  and 
brick-coloured  urine,  urobilinuria,  and  alimentary  glycosuria,  show  that 
the  liver  is  diseased.  As  for  the  anatomical  type,  it  is  sometimes  impos- 
sible to  decide  without  taking  these  symptoms  into  account,  and  confusion 
between  a  fatty  and  an  amyloid  liver  is  still  possible.  Tubercular  cirrhosis, 
however,  has  a  much  clearer  clinical  indi\aduality,  which  should  be  well 
known,  so  that  errors  of  diagnosis  may  be  avoided. 

During  the  past  few  years  two  types  have  been  described^atty  hyper- 
trophic cirrhosis  of  the  Hutinel-Sabourin  type  and  tubercular  cirrhosis  of 
the  Hanot-Lauth  type. 

In  fatty  hypertrophic  cirrhosis  a  premonitory  period  and  a  stationary 
stage  may  be  distinguished.  In  the  premonitory  period  the  patient  is  an 
alcoholic  who  shows  all  the  symptoms  of  gastro-intestinal  alcoholism — viz., 
phlegm,  anorexia,  vomiting,  slight  swelling  of  the  liver,  and  scanty  urine, 
loaded  with  urates.  On  these  symptoms  there  are  grafted  those  of  pul- 
monary tuberculosis,  which  most  frequently  become  predominant.  After 
some  months,  a  chill,  a  fresh  outburst  of  tuberculosis,  or  some  alcoholic 
excess,  causes  the  latent  cirrhosis  to  throw  off  its  mask.  The  digestive 
troubles,  then,  become  marked,  the  anorexia  is  complete,  the  skin  assumes 
a  yellowish  tint,  and  the  urine  becomes  scanty,  with  but  little  urea,  though, 
on  the  other  hand,  urobilin,  sugar,  and  sometimes  albumin,  are  present. 

The  faecal  matter  is  sometimes  colourless  ;  the  lower  limbs  become 
(jedematous ;  attacks  of  haemorrhage  (especially  epistaxis  and  haematemesis) 
may  appear ;  and  the  patient  falls  into  a  state  of  profound  asthenia.  To 
these  syin})tonis  of  auto-intoxication  there  are  added  a  subcontinuous 
febrile  condition  and  an  aggravation  of  the  pulmonary  tuberculosis,  which 
may  prevent  the  lesion  being  recognized.  Ascites  is,  in  general,  negligible, 
and  the  subcutaneous  veins  are  not  much  dilated.  The  key  to  the  diag- 
nosis lies  in  the  examination  of  the  liver,  which  is  considerably  increased 
in  size,  and  extends  below  the  false  riijs  by  four  or  five  fingers'  breadth.  It 
is  hard,  smooth,  and  painful  on  the  slightest  pressure.  The  spleen  is  like- 
wise   enlarged.     This    stationary    stage,    characterized    by    painful    liyper- 


922  TEXT-BOOK  OF  MEDICINE 

trophy  of  the  liver,  with  hepatic  insufficiency,  is  generally  complete  in  five 
or  six  weeks. 

Although  alcoholism  is  frequent  in  the  premonitory  period,  it  is  not 
indispensable  to  the  development  of  fatty  hypertrophic  cirrhosis,  as  shown 
by  the  recent  observations  of  Laure  and  Honorat,  and  of  Hutinel,  in 
children.  Tubercular  cirrhosis  of  the  Hanot-Lauth  type,  which  anatomi- 
cally is  allied  to  alcoholic  cirrhosis  by  the  topography  of  the  fibrosis,  may 
show  itself  clinically  by  the  cardinal  symptom  of  Laennec's  cirrhosis — 
ascites.  The  abdominal  effusion  and  the  collateral  circulation  may  be 
sufficiently  marked  to  make  the  diagnosis  between  the  two  affections  most 
difficult. 

The  appearance  of  abdominal  pains,  tenderness  of  the  liver  on  pressure, 
marked  jaundice,  and  rapid  cachexia,  are  especially  observed  in  tubercular 
cirrhosis.  Advanced  signs  of  pulmonary  tuberculosis  or  of  tubercular 
peritonitis  are  most  important  in  diagnosis.  Tubercular  peritonitis  often 
completes  this  form  of  cirrhosis,  and  in  a  number  of  cases,  clinically  labelled 
as  tubercular  peritonitis  of  an  ascitic  form,  the  effusion  is  due  rather  to  a 
cirrhotic  lesion  than  to  peritonitis.  Clinical  medicine  has,  therefore,  gained 
by  the  careful  anatomical  study  of  the  liver  in  tubercular  patients  during 
recent  years,  and  we  see  that  the  methodical  examination  of  this  organ  in 
tubercular  patients  will  furnish  valuable  indications  as  to  prognosis  and 
diagnosis. 

XIII.  CANCER  OF  THE  LIVER  AND  BILE-DUCTS. 

Pathological  Anatomy — etiology. — Cancer  of  the  liver  maybe  primary 
or  secondary.  Primary  cancer  is  very  rare,  since  it  forms  only  the  eighth 
part  of  the  cancerous  tumours  of  this  organ,  but  secondary  cancer  is  fre- 
quent. It  may,  indeed,  be  said  that  secondary  growths  are  most  common 
in  the  liver.  Cancer  of  the  stomach,  intestines,  rectum,  lungs,  uterus,  bones, 
skin,  or  choroid,  may  lead  to  secondary  growths  in  the  liver,  including 
columnar- celled  epitheUoma,  encephaloid,  scirrhous,  hsematoid,  colloid,  and 
melanotic  carcinoma,  according  to  the  rule  that  a  secondary  cancer  is  always 
of  the  same  kind  as  the  primary  growth.  The  encephaloid  form  and  the 
cylindrical  epithelioma  are  the  most  frequent. 

L  Secondary  Cancer. — I  have  just  said  that  columnar-celled  epithelioma 
is  one  of  the  most  common  malignant  tumours  of  the  liver.  The  reason  is 
that  this  variety  has  as  its  seat  of  origin  the  stomach,  the  intestine,  and  the 
bile-ducts,  the  mucosae  of  which  are  provided  with  columnar  epithelium, 
and  has,  as  a  means  of  transport,  the  portal  veins  leading  from  these  organs 
to  the  liver.  Histologically,  the  columnar  epithelioma  differs  from  encepha' 
loid  and  colloid  carcinoma  by  reason  of  its  tube-like  or  irregular  cavities. 


DISEASES  OF  THE  LIVER  923 

lined  with  columnar  cells,  and  seated  in  the  midst  of  a  fibrous,  embryonic, 
or  mucous  stroma ;  but  to  the  naked  eye  "  this  epithelioma  presents  abso- 
lutely the  same  disposition,  the  same  dissemination,  and  the  same  aspect 
as  encephaloid  carcinoma." 

These  secondary  cancers,  instead  of  forming  one  single  mass,  like  massive 
primary  cancer,  form  islets  that  are  more  or  less  spherical,  mammillated, 
varying  in  size  from  a  millet-seed  to  the  head  of  a  foetus,  and  disseminated 
throughout  the  entire  organ.  On  scraping  the  cut  section,  the  islets  yield 
a  milky  juice,  and  their,  yellowish- white  colour  stands  out  against  the 
brown-red  background  of  the  parenchyma.  The  nodules  which  protrude 
on  the  surface  of  the  liver  are  often  umbilicated,  from  the  degeneration  and 
softening  of  their  central  portion.  The  softening  may  be  so  complete  as 
to  convert  the  cancerous  tumour  into  a  cyst,  which,  in  its  turn,  becomes  the 
seat  of  haemorrhages.  These  cancers  acquire  enormous  proportions,  some 
weighing  as  much  as  20  pounds.  Their  development  is  sometimes  very 
rapid,  and  they  may  arise  from  a  cancerous  ulcer  of  the  stomach  hardly  as 
large  as  a  florin.  Melanotic  sarcoma  also  grows  to  a  large  size.  It  is 
usually  secondary  to  a  primary  growth  in  the  choroid.  It  is  not  nodular, 
like  the  encephaloid  cancer,  and  the  hepatic  tissue  is  infiltrated  with  black 
pigment. 

A  study  of  the  cancerous  lesions  under  the  microscope  will  show  that 
all  the  elements  of  the  hepatic  lobule  (cells,  vessels,  biliary  canals,  and  con- 
nective tissue)  are  invaded  by  the  cancer.  If  we  study  the  hepatic  zone 
next  to  the  cancer,  which  serves,  so  to  say,  as  the  transition  tissue,  we  find 
that  the  hepatic  cells  are  deformed,  spindle-shaped,  hypertrophied,  and 
swollen  by  accumulations  of  protoplasm.  The  interlobular  connective 
tissue  loses  its  fibrous  appearance,  and  becomes  infiltrated  with  embryonic 
nuclei.  The  ramifications  of  the  portal  vein  and  of  the  hepatic  artery 
which  surround  the  lobule  become  thickened,  and  their  walls  are  infiltrated 
with  cancer  cells.  The  endothelium  of  the  vessels  is,  in  its  turn,  invaded, 
and  cancerous  vegetations  project  into  the  lumen  of  the  vessel.  The  biliary 
canaliculi  are  invaded  in  a  similar  manner ;  their  calibre  is  increased,  and 
their  walls  are  infiltrated  with  cancer  cells.  The  same  process  mav  attack 
the  larger  branches  of  the  portal  vein,  causing  ulceration  of  the  walls.  "  It 
would  be  incorrect  to  say  that  the  growth  near  the  vein  has  perforated  the 
wall  so  as  to  open  the  vein,  for  it  is  the  carcinomatous  nodule  in  the  walls 
of  the  vein  that  has  become  ulcerated  "  (Cornil  and  llanvier).  The  question 
is :  Which  tissue  of  the  liver  is  first  attacked  by  the  cancer  ?  Is  it  the  glandular 
(Rokitansky,  Lancereaux),  or  the  connective  tissue  (Virchow,  Vulpian)  ? 
Both  opinions  are  admissible,  though  the  epithelial  origin  now  seems  to  be 
])n)V(>(l.  It  is,  however,  certain  that  the  portal  vessels  and  the  biliary  ducts 
play  a  considerable  part  in  the  transportation  and  dissemination  of  cancer. 


924  TEXT-BOOK  OF  MEDICINE 

2.  Primary  Cancer. — Primary  cancer  is  much  rarer  than  secondary 
cancer.  In  some  cases  it  has  the  nodular  form  of  secondary  cancer,  but  it 
most  frequently  deserves  the  name  of  massive  cancer,  because  it  forms 
a  uniform  mass.  When  the  growth  does  not  reach  the  surface  of  the  organ, 
the  cancer  is  said  to  be  almond-like.  The  liver  in  massive  cancer  is  not 
nodular  and  deformed  externally,  as  in  secondary  cancer,  and  its  surface 
and  form  remain  normal ;  but  the  hypertrophy,  especially  in  the  right  lobe, 
is  such  that  it  may  weigh  from  15  to  18  pounds. 

On  section,  the  liver  is  transformed  into  a  soft  or  lardaceous  mass, 
yielding  a  small  amount  of  cancerous  juice  on  scraping.  The  surface  of  the 
section  is  greyish  or  yellowish,  and  the  centre  of  the  cancer  is  hardly  ever 
softened,  whilst  softening  is  frequent  in  the  nodules  of  secondary  cancer. 
In  some  cases  a  few  nodules  are  found  around  the  main  growth. 

The  extrahepatic  bile-ducts  and  the  large  arterial  and  venous  trunks 
are  healthy.  Perihepatitis,  which  is  frequent  in  secondary  cancer,  with 
its  superficial  nodules,  is  rare  in  massive  cancer.  Here,  as  in  secondary 
cancer,  cancerous  degeneration  is  found  in  the  glands  of  the  hilum  as  well 
as  in  the  gastro-hepatic,  peripancreatic,  prevertebral,  and  mediastinal 
glands,  into  which  the  lymphatics  of  the  liver  empty.  Specific  emboli  may 
follow  the  course  of  the  hepatic  veins  and  sow  cancer  in  the  lungs. 

At  first  sight  massive  cancer  has  most  frequently  the  look  of  encepha- 
loid  cancer,  with  or  without  hsomorrhagic  foci.  Histological  examination 
shows  that  it  is  a  variety  of  epithelial  cancer.  Prirhary  cancer  of  the  liver 
assumes  two  principal  forms — alveolar  epithelioma  and  trabecular  epithe- 
lioma. These  two  forms  may  combine  and  take  on  the  trabeculo-alveolar 
form,  but  in  the  great  majority  of  cases  the  alveolar  epithelioma  is  the 
type  of  massive  or  nodular  primary  cancer,  whilst  the  trabecular  epithelioma 
is  the  type  of  primary  cancer  with  cirrhosis. 

3.  Adenoma  and  Cirrhosis. — When  describing  alcoholic  venous  cir- 
rhosis of  the  liver,  I  said  that  discrete  or  confluent  and  small  or  large  adeno- 
matous growths  may  be  met  with  in  cirrhotic  livers.  These  growths  do 
not  project  in  a  section  of  the  liver ;  they  have  a  putty-like  consistency 
and  a  yellowish-grey  colour,  sometimes  tinted  by  haemorrhage.  A  stream 
of  water  may  enucleate  them  from  the  surrounding  capsule. 

According  to  some  writers,  the  association  of  cirrhosis  with  adenoma 
of  the  liver  may  be  explained  in  the  following  manner  :  Interstitial  hepatitis 
opens  the  scene,  and  produces  cellular  irritation  and  parenchymatous 
hepatitis,  which  may  end  in  the  formation  of  epithelial  tumours  or  adeno- 
mata. From  this  point  of  view  the  adenoma  would  so  far  be  a  benign 
tumour,  like  adenomata  of  the  breast.  The  adenoma,  however,  may, 
according  to  some  writers,  be  transformed  into  carcinoma — that  is  to  say, 
into  a  malignant  tumour.     The  proofs  of  this  transformation  are  said  to  be 


DISEASES  OF  THE  LIVER  925 

drawn,  not  from  the  structure  of  the  tumour,  for  the  structure  of  a 
tumour  does  not  suffice  to  indicate  its  malignancy ;  they  are  drawn  from 
the  general  invasion  of  the  glands  of  the  hilum  and  "  the  neoformation 
of  a  tissue  made  up  of  hepatic  cells  in  the  interior  of  the  portal  vessels — an 
indication  that  the  adenoma  becomes  infective."  Adenoma  of  the  liver  is 
said  to  have  this  character  in  common  with  certain  adenomata  of  the  breast, 
which,  after  being  harmless  for  a  long  time,  assume  the  characters  of 
malignant  tumours.  According  to  Brissaud,  the  series  of  transformations 
is  even  more  complete.  The  venous  cirrhosis  is  the  cause  of  the  adenoma, 
and  the  adenoma  is  transformed  into  carcinoma — in  other  words,  cirrhosis, 
adenoma,  and  carcinoma  are  successive  links  in  the  same  pathological 
chain. 

Gilbert  interprets  the  association  of  adenoma  and  of  cancer  in  another 
manner.  According  to  him,  there  is  no  question  of  transformation,  for 
adenoma  and  cancer  are  one.  "  Adenoma,  as  described  by  Kelsch  and 
Kiener  and  by  Sabourin,  forms,  according  to  my  opinion,  a  particular 
variety  of  hepatic  carcinosis,  and  cannot  therefore  undergo  cancerous 
transformation." 

This  is  also  the  opinion  of  Hanot :  "  Adenoma  is  a  variety  of  epithe- 
lioma. It  is  a  trabecular  epithelionaa,  also  called  adeno-carcinoma,  and  it 
might  be  called  cylindroma,  tubular  epithelioma,  or  acinous  epithelioma." 
As  I  have  previously  remarked,  in  the  great  majority  of  cases  alveolar 
epithelioma  is  the  type  of  massive  or  nodular  primary  cancer,  whilst  trabe- 
cular epithelioma  is  the  type  of  primary  cancer  with  cirrhosis.  Hanot  and 
Gilbert  write  :  "  The  relations  of  trabecular  epithelioma  and  of  cirrhosis 
have  been  differently  understood  by  writers.  Lancereaux  supposes  that 
the  cirrhosis  results  from  development  of  the  neoplastic  nodules  in  the 
liver.  Sabourin,  on  the  other  hand,  places  cirrhosis  first  in  chronological 
order,  and  looks  upon  adenoma  as  a  complication  of  cirrhosis.  We  cannot 
accept  either  of  these  explanations.  Lancereaux's  explanatioji,  which 
might  be  maintained  if  it  were  always  a  question  of  the  coexistence  of  neo- 
plastic nodules  disseminated  throughout  the  liver,  together  with  cirrhosis, 
cannot  account  for  cases  in  which  only  a  few  neoplastic  nodules  coexist 
with  cirrhosis.  Sabourin's  explanation  falls  to  the  ground  when  confronted 
with  the  fact  that  adenoma  may  exist  without  cirrhosis.  We  admit,  with 
Kelsch  and  Kiener,  the  simultaneous  development  of  cirrhosis  and  adenoma, 
and  we  believe  that  these  two  processes  result  from  the  action  of  the  same 
irritating  agent  on  the  connective  tissue  and  on  the  hepatic  epithelium,  that 
tlie  cirrhosis  may  evolve  by  itself,  and  also  that,  in  exceptional  cases, 
trabecular  epithelioma  may  develop  sc])arately."  This  simultaneous  process 
of  cirrhosis  and  adenoma  was  very  evident  in  one  of  my  cases.  The  in- 
vasion of  the  lymphatics  and  of  the  glands  is  rapid  in  alveolar  epithelioma, 


926  TEXT-BOOK  OF  MEDICINE 

whereas  trabecular  epithelioma  invades  the  veins  and  respects  the  lym- 
phatics. 

4.  Ascites  and  Jaundice. — The  compression  of  the  portal  vessels  by  the 
cancerous  tumour  causes  ascites  ;  the  compression  of  the  bile-ducts  in  the 
hilum  of  the  liver  causes  jaundice. 

Adhesions  are  established  between  the  cancerous  liver  and  the  neigh- 
bouring organs,  and  are  frequently  invaded  by  the  growth. 

The  causes  of  hepatic  cancer  are  as  obscure  as  the  causes  of  cancer  in 
general.  Hereditary  predisposition  plays  a  great  part,  and  though  cancer 
of  the  liver  is  a  disease  of  advanced  age,  it  is,  nevertheless,  seen  rather  often 
in  adults,  and  even  in  children. 

Symptoms. — Secondary  cancer  of  the  liver  sometimes  shows  itself  as 
a  late  epiphenomenon  in  advanced  stages  of  cancer  of  the  stomach,  intestine, 
or  rectum,  and  the  patient  succumbs  before  the  hepatic  lesion  has  given  rise 
to  special  symptoms.  Sometimes,  on  the  contrary,  cancer  of  the  stomach, 
gall-bladder,  or  intestine,  has  only  shown  indefinite  symptoms,  when  the 
hepatic  cancer  declares  itself,  and  spreads  with  such  rapidity  that  it  claims  the 
entire  attention.  Finally,  there  are  cases — rare,  it  is  true — in  which  hepatic 
cancer  is  primary.  In  these  various  conditions  what  symptoms  and  signs 
indicate  cancer  of  the  liver  ? 

Let  us  deal  first  with  secondary  cancer.  It  often  commences  with  a 
latent  stage,  and  some  patients  have  advanced  cancer  (hypertrophy  and 
nodules  in  the  liver,  cachexia)  without  having  experienced  manifest  symp- 
toms. Amongst  the  symptoms  digestive  troubles  appear  first,  and  we  find 
dryness  of  the  mouth,  loss  of  appetite,  anorexia,  ballooning  of  the  belly,  and 
foetid  stools.  So  far  there  is  nothing  significant.  The  patient  complains 
of  heaviness  or  dull  pain  in  the  right  hypochondrium.  Acute  pains  are 
absent,  unless  perihepatitis  is  present.  Jaundice  is  frequent,  and  has  been 
noticed  in  thirty-nine  cases  out  of  ninety-one  (Frerichs).  It  varies  from  a 
slight  tinge  to  deep  and  permanent  coloration.  It  is  due  to  multiple 
causes  :  catarrh  or  compression  of  the  bile-ducts.  Ascites  is  frequent,  but 
not  as  abundant  as  in  cirrhosis.  It  is  due  to  divers  causes  :  cancerous  masses 
obstructing  the  large  trunks  of  the  portal  vein,  partial  peritonitis  near  the 
liver,  or  the  cancerous  nodules  which  invade  the  peritoneum  and  the 
omentum.     In  the  latter  case  the  ascitic  liquid  is  often  blood-stained. 

Melsena  is  fairly  common  when  the  cancer  attacks  the  gall-bladder  and 
bile-ducts  (Hanot).  Dilatation  of  the  subcutaneous  abdominal  veins  is 
often  noticed. 

The  liver  is  enlarged  in  four-fifths  of  the  cases  (Lebert),  and  may  weigh 
15  or  16  pounds.  It  reaches  below  the  false  ribs,  and  stands  out  in  relief 
under  the  abdominal  wall,  extending  below  the  umbilical  region,  and  en- 
croaching on  the  left  flank.     When  the  growth  is  formed  of  large  nodules, 


DISEASES  OF  THE  LIVER  927 

as  is  usually  tlie  case,  the  upper  surface  of  the  liver  is  hard,  uneven,  and 
nodular.  Its  sharp  edge,  instead  of  being  smooth  and  thin,  grows  soft  and 
irregular.  In  some  cases  the  growth  of  the  cancer  is  so  rapid  that  con- 
siderable increase  is  noticed  from  one  week  to  another.  The  spleen  is  never 
hypertrophied.     This  negative  sign  is  most  valuable. 

As  the  disease  progresses  the  general  symptoms  become  more  marked. 
Emaciation,  loss  of  strength,  anaemic  colour  of  the  skin,  gradual  diminution 
of  the  red  blood-corpuscles,  and  peripheral  oedema,  are  the  signs  of  cancerous 
cachexia,  and  the  patient  dies — in  a  couple  of  months  if  the  course  of  the 
cancer  is  acute,  and  in  six  or  eight  months  if  the  course  is  chronic.  Death 
is  due  to  cachexia  or  to  complications,  such  as  subacute  peritonitis,  cerebral 
troubles  and  multiple  haemorrhages,  icterus  gravis,  lowering  of  the  tempera- 
ture, or  rupture  of  a  blood-cyst  found  in  the  interior  of  a  cancerous 
nodule. 

Primary  cancer  of  the  liver  in  its  massive  form  presents  a  somewhat 
different  picture.  Anorexia,  nausea,  and  meteorism  open  the  scene,  as  in 
secondary  cancer.  Pain  in  the  right  hypochondrium  is  common,  but 
ascites,  dilatation  of  the  subcutaneous  abdominal  veins,  and  jaundice  are 
almost  always  absent.  The  chief  sign  is  hypertrophy  of  the  liver,  which  is 
usually  considerable  ;  but  the  liver  is  smooth  and  hard,  with  a  sharp  edge, 
that  shows  neither  the  indentations  nor  the  deformities  found  in  secondary 
cancer.  Another  very  important  symptom  is  acholia,  or  hypocholia.  The 
liver  makes  but  little  bile,  because  many  cells  are  replaced  by  the  neoplasm. 
The  faecal  matter  is  almost  colourless,  and  very  offensive.  The  intestinal 
coils  are  distended  by  gas.  The  same  cause — i.e.,  the  changes  in  the  liver 
producing  acholia — opposes  the  production  of  jaundice.  "  Jaundice  in 
these  conditions  is  almost  unrealizable,  even  though  the  excretory  bile-ducts 
are  blocked  "  (Gilbert).  Though  the  acholia  (acholia  by  secretion)  may  not 
be  absolutely  special  to  massive  cancer  of  the  liver,  it  has  none  the  less  a 
great  value.  It  realizes  the  type  of  acholia  from  secretory  trouble,  in 
which  decoloration  of  the  faecal  matter  coincides  with  the  absence  of 
jaundice,  and  is  very  different  from  false  acholia  or  acholia  caused  by  ex- 
cretory trouble,  such  as  obstruction  of  the  common  bile-duct,  in  which 
case  decoloration  of  the  faecal  matter  is  accompanied  by  an  icteric  tint  of 
the  skin  and  of  the  urine.  The  urine  is  scanty,  and  never  contains  albumin, 
it  is  very  poor  in  urea,  on  account  of  the  lesions  in  the  liver  and  of  the 
inanition  (Robin). 

Cachectic  oedema,  obliterating  phlebitis  and  diarrhoea,  are  observed  in 
all  forms  of  cancer.  During  the  course  of  hepatic  cancer  fever  is  at  times 
a  symptom  of  great  iniportance.  It  may  be  remittent  (Monneret)  or 
intermittent,  with  evening  exacerbations.  It  is  due  to  periliepatitis  or  to 
true  attacks  of  hepatitis.     Febrile  cancer  ends  very  rapidly  in  death. 


928  TEXT-BOOK  OF  MEDICINE 

Diagnosis. — The  diagnosis  of  cancer  of  the  liver  is  especially  difl&cult 
when  the  cancer  is  primary  and  massive,  because  it  has  several  signs  in 
common  with  the  amyloid  liver,  with  certain  forms  of  hypertrophic  cirrhosis, 
and  with  hydatid  cysts. 

Amyloid  degeneration  of  the  liver  causes  smooth  hypertrophy  of  the 
liver,  with  absence  of  jaundice  and  ascites,  just  like  massive  cancer ;  but  it 
differs  from  cancer  in  the  hypertrophy  of  the  spleen,  in  the  presence  of 
albuminuria  and  in  the  pathological  conditions  (scrofula  or  prolonged 
suppuration)  which  cause  lardaceous  disease. 

Hypertrophic  biliary  cirrhosis,  Uke  massive  cancer,  causes  enormous 
smooth  hypertrophy  of  the  liver,  without  ascites  and  without  dilatation  of 
the  abdominal  veins  ;  but  it  differs  from  cancer  by  its  slow  course,  poly- 
cholia,  and  early  persistent  jaundice. 

Hydatid  cysts  of  the  liver,  like  massive  cancer,  cause  a  large  smooth 
tumour,  with  absence  of  ascites  and  icterus  ;  but  they  differ  from  cancer 
in  the  following  points  :  In  hydatid  cyst  the  liver  is  not  uniformly  enlarged, 
but  is  swollen  at  one  point,  and  gives  a  feeling  of  resistance  or  almost 
of  fluctuation,  and  not  a  feeling  of  wood-like  hardness.  The  cyst  is  for  a 
long  time  compatible  with  good  health.  The  diagnosis  is  very  difficult  in 
a  case  of  alveolar  cyst,  and  tapping  is  often  the  only  means  of  diagnosis. 

The  diagnosis  is  sometimes  difiicult  between  cancer  and  syphilis  of  the 
liver,  because  we  find  in  either  case  an  enlarged  lobulated  fiver,  jaundice, 
ascites,  oedema,  and  cachexia.  The  only  distinctive  sign  is  that  in  cancer 
the  compfications  are  rapid,  whereas  they  are  slow  in  syphilis. 

The  prognosis  is  absolutely  fatal,  and  the  treatment  is  purely  pallia- 
tive. It  consists  in  maintaining  the  patient's  strength  and  in  treating  the 
symptoms  as  they  arise. 

Cancer  of  the  Biliary  Passages. 

Cancer  of  the  gall-bladder  and  bile-ducts  is  almost  always  primary. 

Primary  cancer  of  the  gall-bladder  may  be  columnar-celled,  encephaloid, 
colloid,  or  scirrhous.  The  mucous  surface  of  the  bladder  is  villous  at  the 
points  invaded  by  the  new  growth.  The  cavity  of  the  bladder  is  generally 
enlarged,  and  the  walls,  especially  the  tunica  musculosa,  are  hypertrophied. 

The  bile  contained  in  the  bladder  is  sometimes  colourless,  sometimes 
brown  and  thick.  Gall-stones  are  usually  found  (fourteen  times  in  fifteen 
cases),  and  it  is  probable  that  the  appearance  of  the  cancer  precedes  the 
formation  of  the  calculi. 

The  tumour  commences  in  the  bladder,  and  then  invades  the  cystic  and 
common  ducts,  narrowing  their  calibre.  The  neighbouring  lymphatic 
glands  are  attacked,  and  the  duodenum,  the  colon,  and  the  stomach  are  the 
seat  of  adhesions,  often  infiltrated  with  growth.     The  liver  is  almost  always 


DISEASES  OF  THE  LIVER  929 

invaded,  and  in  certain  cases  the  primary  growth  in  the  gall-bladder  is  small, 
while  the  liver  is  crammed  with  secondary  growths. 

The  cancer  may  primarily  invade  the  large  bile-ducts,  and  Claisse  has 
compiled  the  following  statistics  :  Primary  cancer  of  the  large  bile-ducts  is 
often  situated  at  the  duodenal  end  of  the  common  duct.  The  lesion  may, 
however,  occur  in  other  spots.  In  Claisse's  two  cases  the  cancerous  nodule 
attacked  the  hepatic  duct  and  the  middle  portion  of  the  common  duct.  In 
Griffon  and  Aitigue's  case  the  cancerous  nodule  was  not  far  from  the  end 
of  the  common  duct,  but  did  not  involve  the  ampulla  of  Vater.  Hebb, 
Birsch-Hirschfeld,  and  Kraus  have  noted  the  localization  of  cancer  in  the 
middle  portion  of  the  common  duct.  In  Rabe's  case  the  cancer  was  seated 
in  the  middle  portion  of  the  common  duct,  and  the  gall-bladder  was  involved. 
In  the  two  cases  of  Naunyn  and  Schuppel  the  cancer  was  situated  in  the 
hepatic  duct  or  at  the  union  of  the  hepatic  and  cystic  ducts.  Such  was 
the  case  in  one  of  Jourdan's  patients.  In  Debove's  case  the  cancer  was 
situated  between  the  cystic  duct  and  Vater's  ampulla.  In  my  own  case  the 
cancer  was  found  at  the  union  of  the  cystic  and  common  ducts. 

Cancer  of  the  common  bile-duct  generally  causes  permanent  jaundice, 
and  the  diagnosis  is  very  difficult,  as  we  shall  see  in  Section  XXI.  When  the 
infection  involves  the  Hver,  the  symptoms  are  blended  with  those  of  hepatic 
cancer.  Melsena  almost  always  points  to  the  presence  of  cancer  of  the 
bihary  passages  (Hanot). 

XIV.  SYPHILIS. 

In  this  section  I  shall  describe  secondary  and  tertiary  troubles  and 
hereditary  syphilis. 

1.  Secondary  Troubles — Jaundice. 

Benign  Jaundice. — Jaundice  appears  within  a  few  months  of  infection. 
The  colour  of  the  skin  is  sometimes  light,  sometimes  deep,  yellow, 
and  the  faeces  may  or  may  not  be  colourless.  The  jaundice  may  appear  as 
an  isolated  symptom,  but  it  more  often  is  accompanied  by  digestive  troubles, 
diarrhoea,  and  especially  by  general  symptoms — fever,  lassitude,  malaise, 
headache — which  belong  to  this  stage  of  syphilis.  The  pathogenesis  of 
the  condition  is  imperfectly  known.  It  is  probably  due  to  catarrh  of  the 
bile-ducts,  analogous  to  the  secondary  syphilitic  catarrh  of  the  mucosnc  of 
the  pharynx,  larynx,  or  bronchi. 

Icterus  Gravis. — Icterus  gravis  may  appear  during  the  secondary  stage 
of  sy])hilis.  Contrary  to  the  opinion  of  Mauriac,  who  believed  in  simple 
coincidences,  the  observations  of  Lei)ert,  (lubler,  Lacombc,  Senator,  Ro(jue 
and  Devic,  and  Talamon,  show  that  icterus  gravis  is  a  direct  manifestation 

59 


930  TEXT-BOOK  OF  MEDICINE 

of  the  syphilitic  infection.  It  is  chiefly  seen  in  women.  In  Talamon's  case 
the  histological  examination  showed  acute  diffuse  hepatitis,  characterized 
by  embryonic  infiltration  of  the  whole  connective  tissue  of  the  organ,  with 
more  or  less  profound  destruction  of  the  hepatic  cells.  The  lesions  are 
those  of  acute  yeUow  atrophy,  without  any  specific  character.  Early  hepatic 
syphilis,  then,  may  be  compared  with  early  renal  syphihs,  in  which  the 
anatomical  lesions  are  those  of  ordinary  toxic  nephritis.  Between  the  benign 
and  maKgnant  varieties  of  early  syphilitic  icterus  there  are  intermediate 
forms,  as  one  of  Senator's  cases  seems  to  show. 

As  it  is  important  not  to  confound  syphilitic  icterus  with  common 
catarrhal  icterus,  we  must  always  look  for  some  syphihtic  manifestation  on 
the  mucosae  or  the  skin.  The  spots  of  the  macular  roseola  may  be  hidden 
by  the  jaundice,  but  the  papular,  squamous,  or  lenticular  syphihdes  are 
perfectly  recognizable.  The  syphihdes  of  the  throat,  mouth,  vulva,  or 
anus,  the  crusts  of  the  scalp,  and  adenitis  in  the  groin,  are  signs  which  may 
help  us  in  the  diagnosis,  and  must  be  carefully  sought  after.  The  patho- 
genic cause  of  the  jaundice  being  recognized,  it  is  necessary  to  order  imme- 
diate treatment  with  mercury. 

2.  Tertiary  Troubles — Syphilitic  Liver. 

Pathological  Anatomy. — In  hepatic  syphihs,  perihepatitis  is  more  pro- 
nounced than  in  any  other  form  of  chronic  hepatitis.  It  fonns  solid  and 
resistant  adhesions  between  the  liver  and  the  diaphragm.  The  false  mem- 
branes may  surround  the  liver,  compressing  the  veins  and  ducts  in  the 
hilum,  and  causing  ascites  and  jaundice. 

Syphilis  of  the  liver  shows  itself  in  the  form  of  fibrosis  or  of  gummata. 
The  two  kinds  of  lesions  are  generally  associated  (sclero-gummatous  hepa- 
titis), though  one  of  them  may  predominate.  We  can,  then,  describe 
(1)  fibrous  hepatitis  ;  (2)  gummatous  nodular  hepatitis. 

1.  Diffuse  fibrous  hepatitis  has  some  characters  in  common  with  ordinary 
cirrhosis.  The  liver  is  hypertrophied  or  atrophied,  nodular,  dark  brown, 
and  lobulated  rather  than  granular,  whilst  it  is  granular  rather  than  lobu- 
lated  in  atrophic  cirrhosis.  In  typical  cases  the  lesion  has  the  follo^ving 
characters  :  the  edges  of  the  Uver  are  anfractuous  and  irregular  ;  the  surface 
is  nodular,  and  furrowed  by  deep  fibrous  cicatrices,  whence  the  name  of 
tight-laced  liver.  The  fibrous  tissue,  which  forms  bands,  encloses  small 
indurated  or  caseous  gummata.  Adhesions  are  formed  between  the  liver 
and  the  neighbouring  organs  (kidney,  colon,  or  diaphragm).  In  some  cases 
atrophy  of  one  lobe  and  hypertrophy  of  the  other  are  noticed.  Under  the 
microscope  the  syphihtic  liver  shows  a  mixture  of  common  and  of  hyper- 
trophic cirrhosis.  The  cirrhotic  tissue  surrounds  the  lobules,  and  penetrates 
into  them.     The  hepatic  arterioles  are  affected  by  endarteritis,  and  are 


DISEASES  OF  THE  LIVER  931 

doubtless  the  origin  of  the  sclero-gummatous  process.  These  arterial  lesions 
are  ahnost  peculiar  to  syphilitic  cirrhosis,  and  portal  phlebitis  is  of  secondary- 
import. 

2.  Gummatous  nodular  hepatitis  is  characterized  by  the  presence  of 
gummata  on  the  surface  or  in  the  parenchyma  of  the  Uver.  The  tumours 
rarely  exceed  the  size  of  a  pea  or  of  a  small  nut.  They  are  generally  spherical, 
and  often  grouped  in  islets,  each  enclosing  several  gummata.  During  the 
first  period  of  their  growth  the  gummata  are  greyish  and  resistant,  but  later 
their  centre  becomes  opaque  and  softens.  The  fibrous  tissue  then  invades 
the  little  tumour,  and  the  gummata  contract,  and  those  present  on  the 
surface  of  the  liver  under  Glisson's  capsule  often  terminate  in  star-shaped 
cicatrices  with  puckered  edges.  On  making  a  section  of  a  gumma  three 
distinct  zones  are  seen.  The  central  part  is  opaque  and  caseous,  and  often 
divided  into  Islets.  Around  this  central  mass  is  a  fibrous  covering,  com- 
posed of  connective  tissue,  that  varies  in  appearance  according  to  the  age 
of  the  gumma.  The  most  external  zone  is  formed  of  fibrous  tissue,  which 
infiltrates  between  the  neighbouring  hepatic  lobules. 

To  these  lesions  must  be  added  amyloid  degeneration,  which  attacks  the 
liver  as  a  secondary  lesion  in  the  same  manner  as  it  attacks  the  spleen  and 
the  kidneys.  Hanot  found  hypertrophic  hepatitis  with  splenomegaly  and 
chronic  jaundice  in  three  cases — an  anatomical  syndrome  which  belongs 
to  hypertrophic  cirrhosis.  In  the  lobule  he  found  dilated  capillaries,  the 
walls  of  which  were  infiltrated  with  nuclei,  and  filled  with  white  corpuscles  ; 
displaced  rows  with  atrophied,  hypertrophied,  or  disaggregated  cells ; 
numerous  embryonic  nodules  in  the  portal  spaces — lesions,  in  short,  conmion 
to  every  infected  liver.  Hanot  in  his  specimens,  however,  did  not  find 
telangiectatic  cirrhosis,  catarrhal  angiocholitis,  or  newly-formed  biliary 
canaliculi. 

Description. — The  tertiary  lesions  are  generally  late,  but  they  may 
appear  as  early  as  the  third  or  fourth  year  after  infection.  Their  onset  is 
usually  obscure,  and  is  not  accompanied  by  acute  pain,  fever,  or  marked 
symptoms.  Only  slight  digestive  troubles  may  be  found.  Later,  the 
symptoms  are  more  evident.  The  appetite  is  bad,  the  digestion  is  at  fault, 
the  loss  of  flesh  progresses,  and  diarrhoea,  oedema  of  the  feet  and  legs,  and 
absolute  loss  of  strength  appear.  The  patient  has  a  yellowish  colour,  but 
true  jaundice  is  rarely  seen.  Ascites  and  collateral  circulation  are  often 
absent,  or  only  appear  at  a  late  period.  In  some  cases  hepatic  syphilis 
is  most  insidious,  and  ascites  is  the  first  symptom.  It  is  due  to  several 
causes — either  compression  of  the  portal  vein  by  the  glands  in  the  hilum  or 
by  adhesions,  or  to  compression  of  the  hepatic  veins  at  their  entrance  into 
the  vena  cava  (liarth). 

Examination  cf  the  liver  furnishes  indefinite  information.     The  liver 

59—2 


932  TEXT-BOOK  OF  MEDICINE 

may  be  li}^ertropliied  or  atrophied.  It  is  nodular  and  uneven.  Hanot 
has  applied  the  name  of  "  syphihtic  hypertrophic  hepatitis  with  chronic 
jaundice  "  to  a  special  form  of  tertiary  hepatic  syphilis,  which  he  considers  a 
morbid  entity.  As  it  is  accompanied  by  splenomegaly,  it  somewhat  re- 
sembles certain  forms  of  malarial  hepatitis  and  Hanot's  disease.  It  is 
distinguished  from  the  latter  by  the  syphilitic  aetiology,  by  the  absence  of 
paroxysmal  attacks,  and  by  the  more  rapid  march  of  events  when  treatment 
has  been  taken  in  hand  too  late.  Furthermore,  the  spleen  and  the  liver  are 
never  as  large  as  in  Hanot's  disease.  Finally,  leucocytosis,  which  is  the 
rule  in  the  latter  affection,  has  not  been  noted  in  the  former. 

Hepatic  syphilis  runs  a  very  slow  course.  It  may  take  years.  As  long 
as  the  liver  performs  its  functions  sufficiently,  and  as  long  as  the  other 
viscera  are  free,  there  is  no  danger;  but  the  risks  arise  when  amyloid  or  fatty 
degeneration  causes  hepatic  insufficiency,  or  when  the  kidneys  are  attacked, 
and  urinary  insufficiency  results. 

3.  Hereditary  Syphilis.    * 

Hereditary  syphilis  of  the  liver  in  the  new-born  child  (early  hereditary)  and 
that  at  a  more  advanced  age  (late  hereditary)  must  be  described  separately. 

Description. — Syphilis  of  the  liver  during  intra-uterine  life  hampers  the 
venous  circulation.  The  pressure  in  the  umbilical  vein  increases,  and  extra- 
foetal  ascites  or  hydramnios  is  produced.  The  size  of  the  mother's  abdomen 
may  be  enormous  (48  inches  at  the  umbilicus).  The  movements  of  the 
foetus  cannot  be  felt  distinctly,  and  the  uterus  forms  a  huge  sac,  in  which 
a  fluid  thrill  may  be  felt.  At  the  same  time,  especially  in  acute  hydramnios, 
where  the  abdominal  girth  has  not  been  able  to  increase  gradually,  compres- 
sion of  the  abdominal  organs  and  of  the  ureters,  increasing  dyspnoea,  vomit- 
ing, cyanosis,  and  lumbo-abdominal  pains  show  themselves  (Chauffard). 
The  foetus  dies  in  the  proportion  of  23  per  cent.  (Bar).  The  accouchement 
is  often  premature,  and  takes  place  under  the  worst  conditions. 

In  the  new-born  child  syphilis  is  but  the  continuation  of  the  intra- 
uterine disease.  In  some  cases  the  child  is  born  with  syphilitic  cachexia 
(extreme  wasting,  palmar  and  plantar  pemphigus),  and  death  supervenes 
in  a  few  hours.  In  other  cases  the  new-born  child  appears  to  be  in  good 
health,  and  syphilis  of  the  liver,  like  all  the  other  forms  of  early  hereditary 
syphilis,  appears  during  the  first  months  of  life.  Syphilis  of  the  liver  is 
generally  accompanied  by  coryza,  mucous  and  cutaneous  syphilides,  fissures 
of  the  umbilicus,  anus,  or  lips,  eruptions  on  the  skin,  etc.  The  hepatic  or 
hepato-splenic  lesion  may  be  so  pronounced  that  a  spleno-hepatic  form  of 
heredo-syphilis  has  been  described.  The  skin  is  bistre-coloured  or  yellowish  ; 
the  digestive  troubles  are  constant ;  the  loss  of  flesh  is  rapid  ;_and  the  liver 
is  enlarged,  smooth,  and  tender  on  pressure.     The  belly  is  enlarged  and 


DISEASES  OF  THE  LIVER  933 

streaked  with  veins.  Tympanites  is  sometimes  accompanied  by  ascites. 
The  spleen  is  enlarged  and  painful.  The  prognosis  is  very  grave,  but 
recovery  may  occur. 

The  diagnosis  of  hepatic  syphiHs  is  easier  in  the  new-born  child  than 
in  the  adult,  because  the  customary  symptoms  of  early  heredo-syphilis  are 
usually  present. 

Pathological  Anatomy. — The  description  of  the  syphilitic  liver  in  the 
adult  differs  from  that  applicable  in  the  foetus  or  in  the  new-born  child. 
This  anatomical  difference  is  the  result  of  variation  in  the  mode  of  infection. 
In  the  adult  the  lesion  is  disseminated  in  the  liver,  following  the  hepatic 
arterioles,  which  are  attacked  ynth.  arteritis  and  peri-arteritis,  and  ending 
by  a  more  or  less  slow  process  in  sclero-gummatous  tissue.  In  the  foetus, 
on  the  contrary,  the  liver  immediately  receives  a  portion  of  the  blood  from 
the  placenta,  and  is  infected  as  a  whole.  "  It  sustains  the  first  attacks 
of  the  infection,  and  thus  reacts  more  surely  to  congenital  syphilis " 
(ChaufEard).  We  find  in  a  syphilitic  child  stillborn  or  dying  soon  after 
its  birth  from  hepatic  syphilis  the  following  lesions  :  The  liver  has  pre- 
served its  form  and  its  smooth  appearance,  because  there  is  as  yet  no  fibrosis. 
The  organ  is  larger  than  in  the  normal  condition,  hard,  and  elastic.  The 
habitual  red-brown  tint  has  given  place  to  a  grey-yellowish  colour,  like  flint, 
and  on  section  of  the  parenchyma  we  see  little  whitish  granulations  (micro- 
scopic gummata)  like  grains  of  semolina  (Gubler).  The  lesions  are  usually 
found  in  the  left  lobe  and  the  sharp  edge  of  the  liver. 

This  syphilitic  hepatitis  is  a  young  cirrhosis.  The  embryonic  tissue  is 
not  yet  fibrous,  but,  histologically,  diffuse  and  nodular  lesions  are  noticed. 
Hutinel  and  Hudelo  have  shown  that  this  periportal  cirrhosis  at  its  com- 
mencement follows  the  vessels,  and  with  them  penetrates  the  hepatic  lobules, 
where  it  becomes  diffuse.  The  perihepatitis  is  not  as  marked  as  in  the 
adult,  and  the  ascites  is  often  blood-stained. 

Late  Hereditary  Syphilis. — I  must  specially  mention  the  late  form  of 
hereditary  syphilis.  The  gummatous,  amyloid,  and  cirrhotic  lesions  in 
the  liver  may  be  the  result  of  hereditary  syphilis  appearing  in  childhood 
and  adolescence  or  adult  life.  Fournier  has  collected  twenty-five  cases. 
When  the  lesion  is  cirrhotic,  the  liver  is  generally  enlarged,  indurated,  and 
deformed.  Jaundice  is  rare,  but  ascites  is  constant,  and  sometimes  it  is 
the  symptom  whit-h  gives  the  alarm.  This  syphilitic  cirrhosis  is  often 
associated  with  hypertrophy  of  the  spleen  and  with  renal  lesions  acc-ompanied 
by  albuminuria. 

We  can  understand  the  difhculties  of  diagnosis  in  syphilitic  cirrhosis 
if  a  proper  clue  is  not  given  by  the  antecedents  and  by  the  reminders. 
We  may  look  upon  the  case  as  one  of  common  cirrhosis — a  disea.se  usually 
incurable — when  we  are  really  face  to  face  with  syphilitic  mischief,  which 


934  TEXT-BOOK  OF  MEDICINE 

often  recovers.  Too  much  attention  cannot,  therefore,  be  given  to  the 
pathogenic  diagnosis,  and  too  much  care  cannot  be  devoted  to  the  tracing 
of  acquired  or  hereditary  syphihs,  which  may  assist  in  finding  the  cause  of 
the  disease. 

The  course  of  the  disease  may  help  in  diagnosis.  Syphihtic  cirrhosis 
most  resembles  Laennec's  atrophic  cirrhosis.  Ascites,  oedema  of  the  lower 
limbs,  meteorism,  and  collateral  circulation  exist  in  both  cases.  In  syphi- 
litic cirrhosis  the  liver  is  more  enlarged,  and  the  ascites  and  the  other 
symptoms  develop,  as  a  rule,  much  later. 

In  hereditary  syphilis  it  is  very  necessary  to  recognize  the  stigmata 
which  may  help  in  diagnosis.  They  include  dental  changes,  diffuse  kera- 
titis, natiform  cranium,  bosses  on  the  forehead,  nasal  deformities  with  or 
without  ozsena,  swelling  and  incurvation  of  the  tibia,  cicatrices  on  the  skin, 
sarcocele,  and  glandular  enlargement. 

The  treatment  is  that  of  tertiary  syphilis.  Injections  of  biniodide  of 
mercury,  with  or  without  iodide  of  potassium,  must  be  employed  as  soon 
as  the  cause  of  the  disease  is  known  or  suspected. 


XV.  HYDATID  CYSTS  OF  THE  LIVER. 

Evolution  of  the  Hydatids. — The  mature  cyst  is  formed  of  an  envelope 
containing  clear  watery  liquid,  i.i  which  float  daughter  cysts,  echinococci, 
and  booklets.     We  must  now  study  the  life-history  of  the  hydatid  in  detail. 

There  is  a  little  ribbon-like  worm,  called  Tcenia  nana  (dwarf),  or  Tcenia 
echinococcus,  measuring  4  millimetres  in  length,  reaching  its  complete  develop- 
ment in  the  intestine  of  the  dog.  This  little  worm  is  composed  of  a  head  like 
that  of  the  echinococcus  and  of  three  segments.  The  head  is  armed  with 
a  double  row  of  strong  booklets  and  with  four  suckers.  The  last  of  these 
segments  contains  a  branching  ovary,  a  lateral  genital  orifice,  and  several 
thousand  embryos,  or  eggs.  These  segments  are  excreted  in  the  dog's 
dejecta,  and  break  up,  liberating  the  eggs.  The  eggs  attach  themselves 
to  vegetables  or  plants,  and  may  be  swallowed  by  man  or  by  a  herbivorous 
animal,  with  the  following  result :  The  egg  introduced  into  the  digestive 
passages  has  a  very  thick  wall,  which  softens,  setting  free  the  embryo, 
The  hexacanthic  embryo,  provided  with  sharp  spicules,  perforates  the 
tissues,  and  is  probably  carried  by  the  blood  of  the  portal  vein  to  the  liver, 
in  which  it  is  usually  arrested.  It  loses  its  booklets,  and  secretes  from  its 
posterior  portion  an  envelope,  in  Avhich  it  becomes  encysted,  forming  the 
hydatid  pocket,  composed  of  an  internal  layer,  which  is  but  the  transfor- 
mation of  the  embryo  (germinative  membrane),  and  of  an  external  layer, 
which  is  the  product  of  the  secretion.  A  clear  and  transparent  liquid 
accumulates  in  the  cavity. 


DISEASES  OF  THE  LIVER  935 

At  a  later  stage  the  cyst  surrounds  itself  with  a  new  wall  or  pericystic 
layer.  This  is  a  borrowed  wall,  which  forms  no  part  of  the  cyst,  and  which 
is  due  to  the  irritation  of  the  neighbouring  hepatic  connective  tissue.  Let 
us  next  consider  the  cyst  at  this  advanced  period  of  its  evolution. 

As  I  have  said,  the  pericystic  layer  does  not  form  an  integral  portion  of 
the  cyst,  but  is  a  connective  fibroid  membrane,  produced  by  the  irritant 
action  of  the  parasitic  vesicle.  This  membrane  may  be  I  inch  in  thick- 
ness. It  is  covered  with  a  nutrient  network  of  vessels  derived  from  the 
hepatic  artery  and  the  portal  vein.  It  is  in  this  layer  that  the  phenomena 
of  calcification  and  suppuration  take  place.  This  fibrous  envelope  is 
intimately  connected  with  the  parenchyma  of  the  liver,  but  it  can  be 
separated  from  the  cyst.  The  isolated  cyst  appears  in  the  form  of  a  soft 
whitish  and  trembling  spheroidal  mass.  I  have  already  explained  the 
formation  of  the  two  membranes  which  make  up  the  wall  of  the  cyst,  and  I 
shall  now  follow  them  in  their  growth. 

The  external  membrane  of  the  cyst  has  a  thickness  of  from  1  to  3  milU- 
metres,  and  looks  like  half-cooked  albumin.  It  is  opaline,  semitransparent, 
and  formed  of  several  stratified,  non-vascular,  amorphous  layers.  These 
layers  have  been  compared  to  the  leaves  of  unequal  thickness  formed  by 
the  edges  of  an  album.  When  cut,  they  curl  up  like  elastic  membranes, 
though  the  microscope  shows  no  trace  of  any  figured  element.  As  this 
formation  is  absolutely  peculiar  to  hydatid  cysts,  it  is  impossible  to  make 
a  mistake,  and  the  diagnosis  is  fixed  when  a  shred  is  found  in  a  pathological 
liquid.  Above  this  membrane  we  find  a  granular,  raspberry-like,. germi- 
native  membrane  (Giraldes),  which  gives  birth  to  vesicles  and  to  echinococci. 

The  vesicles  begin  as  sessile  buds,  which  become  pedunculated  and 
filled  with  liquid.  They  enlarge,  become  detached,  and  fall  into  the  interior 
of  the  cyst  (daughter  vesicles).  The  daughter  vesicles  in  the  primary  cyst 
are  more  or  less  bulky,  and  some  of  them  contain  a  third  or  fourth  genera- 
tion. Their  structure  is  identical  with  the  parent  cyst.  As  long  as  the 
germinative  membrane  of  the  hydatid  cyst  produces  vesicles  and  not 
echinococci,  the  cyst  is  said  to  be  acephalocystic.  When  the  germinative 
vesicle  produces  echinococci,  the  cyst  is  said  to  be  fertile.  This  fertility 
may  be  shown  by  the  iodophilic  reaction.  With  iodized  gum  (Loeper) 
the  germinative  membrane,  the  heads  of  the  echinococci,  and  the  hydatids 
are  seen  to  be  filled  with  glycogen  when  they  are  aUve  ;  tliey  have  none 
when  they  are  dead. 

The  echinococcus  (e;^u'09.  hedgeliog  ;  KOKKo^i,  grain)  at  first  resembles 
a  whitish  granulation,  which  protrudes  on  the  internal  surface  of  the  cyst, 
and  becomes  pedunculated.  It  is  formed  of  a  head  with  four  suckers  and 
a  double  crown  of  twenty  to  thirty  booklets.  The  head  is  separated  from 
the  body  by  a  neck.    The  body  Is  rounded,  and  ends  in  a  process,  fixing 


936 


TEXT-BOOK  OF  MEDICINE 


Fig.  56. 

(a)  Adult  Tcenia  nana,  or  echinococciis.  The  head  is  provided  with  a  double 
crown  of  hooklets  and  four  suckers.  The  last  segment  contains  an  ovary,  with  a 
lateral  genital  pore. 

(b)  Egg  ;  the  granular  shell  encloses  the  hexacanthic  embryo. 

(c)  The  ingested  hexacanthic  embryo,  perforating  the  tissues  by  means  of  its  hooklets. 

(d)  Hydatid  cyst,  formed  by  the  distension  of  the  embryo,  fixed  and  encysted  in  the 
liver. 

(e)  Under  the  pericystic  stratified  membrane,  the  true  wall,  or  proligerous  membrane, 
gives  birth  to  sessile  buds,  which  form  secondary  vesicles,  or  daughter  cysts. 

(/)  Vesicle,  without  echinococcus,  such  as  the  acephalocystic  cyst  produces. 
{g)  Vesicle,  with  an  echinococcus  and  a  granddaughter  cyst. 
(h)  Hydatid,  producing  scolex,  each  of  which  has  the  head  of  an  echinococcus. 
(i)   Hydatid  full  of  piled-up  echinococci. 

(j)  Freeing  of  the  echinococci  by  the  bursting  of  a  hydatid  daughter  cyst. 
{k)  Free  scolex  in  the  mother  hydatid. 

(I)   Scolex  of  echinococcus,  with  its  four  suckers  and  its  crown  of  hooklets. 
(m)  Separate  hooklets. 

(n)  The  echinococcus,  still  pedunculated  and  adherent  to  the  fertile  wall ;  the  tube 
is  evaginated. 

(o)  The  same,  with  the  tube  invaginated. 


DISEASES  OF  THE  LIVER  937 

the  animal  to  the  germinative  membrane.  When  this  process  breaks,  the 
animal  falls  into  the  Uquid  of  the  cyst.  The  liquid  is  transparent,  like 
spring-water,  whence  the  name  of  these  cysts  {v8dTL<i,  from  vScop,  water). 
The  quantity  of  the  Uquid  varies  from  a  few  ounces  to  several  pints.  Under 
the  microscope  booklets  are  visible.  They  contain  chloride  of  sodium,  but 
no  albumin.  The  presence  of  albumin  in  the  liquid  indicates,  according 
to  Gubler,  the  death  of  the  hydatids. 

The  presence  of  glycogen  indicates  activity  on  the  part  of  the  hydatid. 
"  The  iodine  reaction  in  the  scolices  of  the  aspirated  fluid  in  the  internal 
layer  of  the  young  hydatids,  or  in  the  germinal  membrane  of  the  cyst, 
shows  that  the  hydatid  is  active,  even  though  the  fluid  is  turbid  and  the 
vesicles  are  withered"  (Loeper). 

Pathological  Anatomy. — The  pathological  anatomy  of  the  cysts  in 
the  liver  is  in  part  concerned  with  the  evolution  of  the  cyst  and  with  its 
various  modes  of  termination,  such  as  perforation,  rupture,  fistulse,  and 
divers  transformations.  The  pathological  anatomy  will,  therefore,  be  given 
during  the  course  of  the  description. 

I  must,  however,  mention  hypertrophy  of  the  liver  due  to  compensatory 
hyperplasia.  I  have  already  discussed  this  question  under  the  Enlarged 
Cirrhotic  Liver  of  Alcoholic  Patients,  and  the  same  question,  slightly 
modified,  presents  itself  in  dealing  with  hydatid  cysts  of  the  liver.  Several 
writers  have  studied  this  vicarious  hypertrophy  which  attacks  the  cystic 
lobe,  but  more  especially  the  unaffected  lobe,  and  I  know  of  no  more  com- 
plete example  than  the  one  related  by  Chauffard, 

In  this  case  the  patient  died,  and  the  liver,  which  contained  a  hydatid  cyst,  weighed 
230  ounces  before  and  90  ounces  after  evacuation  of  the  cyst — that  is  to  say,  about 
35  ounces  more  than  a  normal  hver.  The  left  lobe  weighed  40  ounces.  The  compen- 
satory hyperplasia  had,  indeed,  outstripped  the  object,  and  it  was  really  hepatic  tissue 
of  good  quaUty  which  had  thus  been  regenerated.  In  spite  of  the  presence  of  an 
enormous  hydatid  cyst,  the  normal  action  of  the  liver  was  more  than  assured.  As  a 
matter  of  fact,  says  ChaufTard,  in  all  this  hyperplastic  tissue  there  was  an  absence  of 
cirrhotic  lesions,  the  hepatic  cells  being  well  preserved,  and  their  protoj  lasm,  with  the 
nucleus,  having  a  normal  aspect.  The  trabecular  ordination  was,  liowever,  modified, 
and  the  hepatic  parenchyma  recalled  a  fietal  liver  at  the  seventh  month  of  intra- 
uterine life.  "  There  was  the  image  of  an  almost  full  cellular  parenchyma."  The 
hepatic  cell.s  were  grouped  in  small  radial  colunms,  let  into  the  connective  tissue  around 
the  portal  spaces,  "  like  the  radiating  veins  of  a  palm-leaf  around  their  pedicle."  Such 
is  the  compensatory  hyperplasia  found  in  a  Uver  containing  a  hydatid  cyst  ;  it  may  be 
likened  to  the  hyperplasia  in  the  enlarged  alcoholic  liver,  in  the  malarial  liver,  and  in  the 
tul)orcular  liver,  where  it  forms  foci  of  nodular  hyperplasia. 

Symptoms.— During  the  first  period  of  its  evolution,  sometimes  for 
montlis,  as  long  as  the  cyst  has  not  reached  a  fair  size,  the  parasite  does  not 
reveal  its  presence  by  any  marked  symptom,  and  even  when  it  has  become 
large,  some  patients  only  complain  of  enlargement  of  the  abdomen.     And 


938  TEXT-BOOK  OF  MEDICINE 

yet  before  tlie  cyst  provokes  serious  troubles,  we  may  find  symptoms 
which  are  frequently  unrecognized,  but  which  I  consider  very  important, 
because  they  give  the  diagnosis  at  a  period  when  the  hydatid  tumour  is 
but  slightly  apparent.  These  symptoms  are  pain  in  the  right  shoulder, 
the  appearance  of  urticaria,  distaste  for  fatty  food,  and  the  development 
of  pleurisy  on  the  right  side. 

Pain  in  the  right  shoulder,  so  frequent  in  some  affections  of  the  liver,  is 
almost  constant  in  the  case  of  hydatid  cyst,  especially  when  the  cyst 
approaches  the  upper  surface  of  the  Hver. 

Urticaria  is  a  curious  symptom.  I  am  not  speaking  of  urticaria  after 
aspiratory  puncture,  but  I  allude  to  nettle-like  eruptions  appearing  during 
the  evolution  of  the  hydatid  cyst,  of  which  I  have  been  able  to  collect  five 
cases.* 

I  have  several  times  noticed  another  early  symptom — distaste  for  fatty  substances. 
In  one  patient  this  distaste  was  present  for  two  years,  and  was  so  great  that  he  had 
repeatedly  ordered  less  butter  and  fat  to  be  used  in  the  kitchen.  I  have  quoted  similar 
cases  elsewhere.f  A  woman  suffering  from  a  hydatid  cyst  had  from  the  first  a  dis- 
taste for  fatty  foods.  After  meals  she  suffered  from  regurgitations,  and,  without  any 
attack  of  nausea,  her  mouth  became  filled  with  the  fatty  portions  of  her  food.  In 
another  patient  this  regurgitation  of  fatty  matter  was  so  marked  at  the  outset  of  the 
disease  that  she  rejected  the  fat  immediately  after  meals.  The  expectoration  had  on 
paper  the  look  of  spots  of  oil,  and  she  compared  her  saliva  to  what  is  commonly  called 
"  the  eyes  on  the  soup."  The  symptom  existed  for  several  weeks,  to  the  exclusion  of 
any  other  digestive  trouble,  and  then  disappeared  with  the  progress  of  the  disease. 

Secondary  pleurisy,  either  dry  or  with  effusion,  which  sometimes  accom- 
panies tumours  of  the  abdominal  organs  (kidneys,  spleen,  or  liver),  is  equally 
likely  in  hydatid  cysts  of  the  liver.  It  has  been  noticed  by  several  writers, 
and  I  have  collected  six  cases.  When  the  cyst  is  large,  and  especially  when 
it  is  seated  on  the  convex  surface  of  the  liver,  we  can  understand  how  the 
inflammatory  process  spreads  gradually  from  the  peritoneum  to  the  pleura  ; 
but  there  are  cases  in  which  the  cyst  is  deeply  seated  and  of  small  size,  when 
pleurisy  appears  as  a  forerunner. 

Boulay  and  I  saw  a  patient  suffering  from  a  cyst  of  the  liver,  in  whom  the  other 
symptoms  had  been  preceded  by  three  slight  attacks  of  pleurisy  on  the  right  side. 

It  is  not  impossible  for  the  inflammatory  process  to  be  carried  to  the 
pleura  by  the  lymphatics  (Schweiger-Seidel,  Recklinghausen),  since  the 
serous  cavities  of  the  pleura  and  of  the  perivoneum  communicate  by  means 
of  lymphatic  vessels  and  spaces.  Further,  if  the  inflammatory  process  in 
some  cases  is  able  to  spread  from  the  peritoneum  to  the  pleura,  the  converse 
is  true,  as  cases  of  pleurisy  of  the  diaphragm,  followed  by  peritonitis,  show. 

*  Dieulafoy,  "  Les  Kystes  hydatiques  et  leur  Traitement"  (Gaz.  Hehdom.,  1877, 
No.  30). 

f  Dieulafoy,  "  Traite  de  I'Aspiration,"  p.  67. 


DISEASES  OF  THE  LIVER  939 

The  development  of  pleurisy  seems  sometimes  to  hasten  the  growth 
of  the  cyst  (Verneuil).  A  patient  has  a  small  cyst.  In  the  meantime  he 
gets  pleurisy,  and  the  cyst  {pars  minoris  resistentice)  undergoes  an  increase 
in  size. 

Epistaxis,  dragging  and  heaviness  in  the  pit  of  the  stomach  and  in  the 
hypochondrium,  are  svmptoms  belonging  to  the  early  stage  in  the  growth 
of  the  hydatid  cyst. 

When  the  cyst  becomes  large,  it  follows  two  principal  directions.  It 
sometimes  projects  on  the  convex  surface  of  the  liver,  and  pushes  up  the 
diaphragm,  but  does  not  depress  the  liver  much.  It  protrudes  into  the 
thoracic  cavity,  and  simulates  an  effusion  into  the  right  pleura.  Sometimes 
it  forms  an  abdominal  tumour.  The  enlargement  of  the  organ  is  not 
uniform,  as  it  is  in  hypertrophy.  We  find  a  more  or  less  limited  tumour, 
which  often  protrudes  into  the  epigastric  region,  or  in  other  cases  raises  the 
false  ribs  and  dilates  the  last  intercostal  spaces  on  the  right  side.  Some- 
times the  tumour  appears  in  the  right  hypochondrium,  assumes  an  elon- 
gated or  bilobed  form,  encroaches  on  the  linea  alba,  after  the  manner  of  a 
pedunculated  tumour,  and  reaches  the  left  hypochondrium.  The  plates 
in  Frerichs'  work  show,  even  if  the  situation  of  the  tumour  only  be  con- 
sidered, how  cysts  of  the  liver  hajve  been  mistaken  for  tumours  of  the 
peritoneum,  spleen,  or  ovary.  Palpation  and  percussion  give  the  limits 
of  the  tumour,  which  is  smooth,  uniform,  and  resistant,  and  which  some- 
times gives  the  sensation  of  fluctuation.  Unless  there  is  some  complication 
(perihepatitis),  the  hydatid  cyst  develops  without  pain. 

The  hydatid  thrill  (Boinet),  which  is  said  to  be  due  to  the  elasticity  of 
the  walls  of  the  cyst,  or  to  collision  of  the  hydatids  when  percussion  is  per- 
formed, is  very  rare.  Ascites  and  jaundice  are  generally  absent,  unless 
there  are  complications,  such  as  compression  of  the  portal  vein  or  of  the  bile- 
ducts,  or  the  development  of  catarrhal  jaundice. 

The  veins  of  the  abdomen  are  slightly  dilated,  and  the  collateral  circula- 
tion is  only  seen  in  compression  of  the  portal  vein. 

Course — Duration — Termination. — Left  to  itself,  the  hydatid  cyst  of 
the  liver  may  grow  during  a  period  of  two  to  six  years  without  causing 
serious  mischief,  but  at  a  more  or  less  distant  date  cachexia  appears.  In 
this  case  the  general  condition  of  the  patient  becomes  bad,  the  appetite  is 
lost,  digestion  is  painful,  the  loss  of  flesh  is  considerable,  and  there  are 
attacks  of  haemorrhage,  epistaxis,  or  metrorrhagia.  This  hydatid  cachexia 
may  appear  early,  as  I  have  several  times  observed.  It  may  be  said  that 
the  patients  become  intoxicated  by  the  hydatids. 

The  dyspna^a  makes  constant  progress  if  the  cyst  pushes  up  the  dia- 
phragm and  interferes  with  the  function  of  the  lungs.  Some  patients 
experience  pain  in  the  abdomen,  the  loins,  or  the  thorax.     They  are  unable 


940  TEXT-BOOK  OF  MEDICINE 

to  find  a  comfortable  position  in  bed,  and  sufEer  from  distressing  insomnia. 
In  many  cases  the  cyst  suppurates,  and  causes  perforation.  Even  the 
general  symptoms  have  become  marked.  The  causes  of  suppuration 
in  hydatid  cysts  have  been  elucidated  by  Chauffard  and  Widal.  Their 
conclusions  are  as  follows  : 

The  liquid  in  the  hydatid  is  aseptic,  but  it  is  a  medium  favourable  to 
the  growth  of  pyogenic  microbes.  The  absolute  impermeability  of  the 
hydatid  membrane  to  micro-organisms  protects  the  cyst  from  infection, 
the  membrane  filtering  the  organisms.  The  hydatid  membrane,  however, 
allows  soluble  substances,  such  as  sublimate,  iodide  of  potassium,  and 
pyocyanine,  to  dialyze  into  the  vesicle.  The  agents  of  suppuration  can, 
therefore,  only  penetrate  into  the  interior  of  the  cyst  by  effraction  when  a 
path  has  been  opened  by  pericystic  lesions.  It  is  through  this  vascular 
pericystic  pocket  that  the  pyogenic  invasion  occurs.  Pericystitis  causes 
necrobiosis  of  the  subjacent  hydatid  membrane,  and  the  enemy  enters  the 
fortress.  The  cyst  becomes  infected.  The  pyogenic  agents  may  get  into 
the  pericystic  pocket  through  the  biliary  passages  (ascending  angiocholitis) 
or  through  the  bloodvessels  and  the  lymphatics.  The  pyogenic  agents  are 
probably  those  of  ordinary  suppuration,  but  it  is  remarkable  that  in  some 
cases  the  pus  is  sterile. 

Gaseous  Cysts— Pyopneumohydatid. 

In  some  cases  gas  forms  in  the  suppurating  cyst.  It  is  generated  in  situ, 
and  is  due  to  the  suppuration.    The  following  case  occurred  at  the  Hotel-Dieu : 

A  woman  had  complained  for  some  time  of  acute  pain  in  the  right  hypochondrium. 
In  the  right  diaphragmatic  region  there  was  an  oblong  bulging,  with  oedema  and 
collateral  circulation.  Percussion  gave  a  tympanitic  note.  Below  the  bulging,  the 
liver  dullness  descended  as  low  as  the  umbilicus.  The  evening  temperature  was  104°  F., 
and  the  dyspnoea  was  severe. 

At  the  base  of  the  chest,  on  the  right  side  and  behind,  percussion  gave  a  tympanitic 
note,  with  bruit  d'airain,  and  auscultation  yielded  metallic  breathing.  No  succussion 
splash.  What  was  the  diagnosis  ?  The  signs  found  were  those  of  a  gas-containing 
cavity,  occupying,  behind  and  on  the  right,  the  base  of  the  thorax,  and  in  front  the 
hepato -gastric  plane.  Pneumothorax  appeared  to  be  the  lesion,  but  it  was  necessary 
to  ascertain  the  relation  of  the  collection  to  the  diaphragm.  Was  the  collection  above 
or  below  the  diaphragm  ? 

The  patient  did  not  cough,  and  there  was  no  sputum.  Tubercular  pneumothorax 
was  not  admissible,  more  especiallj"  because  it  would  not  explain  the  bulging  in  the 
gastro-hepatic  region.     The  mischief  was  below  the  diaphragm. 

There  was  no  history  of  gastric  or  duodenal  ulcer,  which  might  have  perforated  and 
given  rise  to  subphrenic  pyopneumothorax.  Subphrenic  empyema  consecutive  to 
appendicitis  was  out  of  the  question,  because  the  patient  had  shown  no  symptoms  of 
appendicitis,  and,  as  I  have  shoAvn  under  Appendicular  Pleurisy,  appendicitis,  which 
often  causes  putrid  effusion  with  gas  in  the  thorax,  does  not  provoke  the  formation  of 
gas  in  subphrenic  abscesses.  The  patient  finally  said  that,  some  twenty  years  before, 
Le  Dentu  had  punctured  a  hydatid  cyst,  and  drawn  oflf  turbid  fluid. 


DISEASES  OF  THE  LIVER  941 

Mauclaire  opened  the  abdomen,  and  exjDosed  the  hydatid  cyst  in  the  liver.  The 
tumour  was  situated  in  the  upper  part  of  the  right  lobe  ;  it  had  pushed  down  the  liver, 
and  had  extended  towards  the  thorax.  As  soon  as  the  thickened  fibrous  wall  was 
opened  freely,  foul-smelling  gas,  pus,  and  fragments  of  dead  hydatids  escaped.  Some 
pus  was  removed  in  sterile  pipettes  for  examination. 

The  autopsy  showed  that  the  cyst  had  no  connection  with  the  intestinal  tract ;  the 
gas  must,  therefore,  have  formed  in  situ  from  fermentation  in  the  i)us.  Bacteriological 
examination  of  the  pus  showed  the  reason.  The  formation  of  the  gas  was  due  to  a 
streptococcus  and  various  anaerobic  germs. 

Halle  and  Bacaloglu  found  aerobic  and  anaerobic  organisms  in  the  pus 
from  a  suppurating  hydatid  cyst  of  the  liver.  The  pus  contained  the 
streptococcus  and  the  Bacillus  coli  in  small  numbers,  and  a  great  abun- 
dance of  anaerobic  microbes  {Staphylococcus  farvulus  and  BacUlics  fragilis). 
Gas  was  not  present,  the  suppuration  being  foetid,  but  not  putrid. 

In  a  similar  case  to  the  one  I  have  described,  Gilbert  and  Weil  found  the 
Bacillus  coli  as  the  only  organism  present.  In  Lippmann's  case  the  pus 
contained  various  anaerobic  micro-organisms.  Deve  has  described  two 
cases  of  gas  formation  in  suppurating  hydatids  of  the  Uver. 

Let  us  next  consider  the  results  of  suppuration  in  the  cyst,  which  may 
be  due  to  injury  or  some  intercurrent  disease. 

1.  Opening  of  the  Cyst  into  the  Air-Passages. — Cysts  of  the  convex 
face  of  the  liver  have  a  special  tendency  to  open  into  the  air-passages.  The 
walls  of  the  cyst  become  inflamed,  the  hydatids  die,  the  Uquid  becomes 
purulent,  and  adhesions  are  formed  between  the  cyst  and  the  diaphragm, 
between  the  diaphragm  and  the  pleura. 

This  inflammatory  process  is  generally  ushered  in  by  rigors,  fever,  pains 
in  the  region  of  the  liver,  and  on  auscultation  the  rub  of  dry  pleurisy  is 
sometimes  heard.  The  rupture  of  the  cyst  may  take  place  under  various 
conditions.  If  the  layers  of  the  pleura  are  adherent  (this  is  most  often  the 
case),  the  cyst  opens  into  the  bronchi,  and  the  pus  is  coughed  up.  The 
vomica  is  preceded  and  accompanied  by  sharp  pain,  attacks  of  coughing, 
attempts  at  vomitiiig,  and  fits  of  suffocation.  The  patient  brings  up  streams 
of  sero- purulent,  fcetid  liquid,  which  is  sometimes  mixed  with  blood,  and 
in  which  shreds  of  hydatid  membranes  are  found.  The  presence  of  bile  in 
the  vomica  is  of  evil  omen.  During  the  following  days  the  li([uid  con- 
tinues to  come  out  by  the  broncho-liepatic  fistula,  and  in  the  end  a  cure  may 
be  effected,  though  it  is  far  more  common  for  the  patients  to  be  carried 
off  by  some  complication  (pulmonary  gangrene,  hjcmoptysis),  or  to  succumb 
from  the  results  of  interminable  suppuration.  Auscultation  of  the  thoracic 
region  generally  yields  the  signs  of  partial  pneumothorax.  When  the 
adhesions  have  not  united  the  two  layers  of  the  pleura,  the  cyst  empties 
itself  into  the  pleural  cavity,  and  causes  grave  mischief. 

In  some  cases  the  hydatid  cyst  empties  into  the  bronchi  through  a  narrow 


942  TEXT-BOOK  OF  MEDICINE 

fistula.  The  pus  is  then  brought  up  in  small  quantities.  It  is  usually  foul- 
smelhng  and  blood-stained.  The  narrowness  of  the  opening  allows  neither 
hydatids  nor  membranes  to  pass.  The  diagnosis  is,  then,  difficult,  and  the 
prognosis  is  grave. 

2.  Opening  of  the  Cyst  into  the  Digestive  Tract.— Here,  as  in  the  pre- 
ceding form,  the  opening  of  the  cyst  is  preceded  by  an  inflammatory  pro- 
cess, which  causes  suppuration  in  the  cyst  on  the  one  hand,  and  adhesions 
between  the  cyst  and  the  neighbouring  organs  on  the  other.  This  process 
may  be  latent,  though  it  is  more  often  accompanied  by  fever,  pain,  and 
symptoms  of  peritonitis.  Rupture  of  the  cyst  into  the  intestine  generally 
takes  place  in  the  colon,  and  the  pain  is  exceedingly  severe  at  the  moment 
of  perforation.  If  the  opening  of  communication  is  large  enough,  the 
liquid  and  the  membranes  are  emptied  into  the  intestine,  and  are  passed 
fer  anum.  The  hepatic  tumour  grows  smaller,  the  discharge  continues  for 
some  time,  and  a  cure  may  take  place  (twenty-seven  times  in  thirty-two  cases 
— Letourneur).  If  the  orifice  is  insufficient,  a  kind  of  chronic  diarrhoea  is 
the  result,  and  the  indefinite  suppuration  wears  out  the  patient.  Rupture 
of  the  cyst  into  the  stomach  is  extremely  rare,  and  is  generally  followed 
by  death.  Rupture  into  the  duodenum  is  unfavourable.  The  cyst  is  got 
rid  of  both  by  the  stomach  and  by  the  intestine. 

3.  Opening  of  the  Cyst  into  the  Peritoneum. — Rupture  of  the  cyst 
into  the  peritoneum  is  not  always  spontaneous.  It  is, sometimes  the  result 
of  traumatism,  and  causes  fatal  peritonitis  if  the  cyst  is  infected.  If  the 
liquid  of  the  cyst  is  aseptic,  peritonitis  may  be  absent,  and  recovery  has 
been  noted  in  eleven  out  of  thirteen  cases  (Finsen).  The  mixture  of  bile 
with  the  discharged  hydatid  liquid  is  not  serious,  provided  the  bile  is  not 
infected.  An  eruption  of  urticaria  has  often  been  noticed  after  rupture  of 
the  cyst.  To  this  curious  symptom  I  shall  refer  later.  In  some  cases  the 
vesicles  discharged  into  the  peritoneum  have  continued  to  live  and  to 
proliferate. 

4.  Relation  of  the  Cyst  to  the  Bile-Duets. — Ulceration  of  the  bile-ducts 
close  to  the  cyst  and  passage  of  the  bile  into  the  cyst  may  be  favourable, 
because  the  bile  may  kill  the  hydatids  and  bring  about  recovery.  The  cyst 
may  open  into  the  gall-bladder  or  into  the  common,  hepatic,  cystic,  or  intra- 
hepatic ducts.  Rupture  of  the  cyst  into  the  common  duct  is  serious.  If 
the  hydatid  is  not  large,  it  may  pass  through  the  duct,  causing  hepatic 
colic,  and  cure  is  possible.  If  the  membranes  block  the  duct  and  give  rise 
to  chronic  obstructive  jaundice,  dilatation  of  the  ducts  on  the  proximal 
side  of  the  obstruction  and  acute  purulent  angiocholitis  follow. 

5.  I  shall  quote,  as  quite  an  exception,  the  opening  of  the  cyst  into  the 
pericardium  or  the  vena  cava,  ulceration  of  the  abdominal  wall,  and  opening 
of  the  cyst  in  the  neighbourhood  of  the  umbilicus,  or  in  an  intercostal  space. 


DISEASES  OF  THE  LIVER  943 

6.  Spontaneous  Cure. — Some  cysts  (33  per  cent.)  recover  spontaneously, 
without  reaching  a  large  size — for  example,  those  discovered  by  chance 
post  mortem.  The  cure  is  brought  about  by  the  death  of  the  echinococci. 
When  the  hydatid  dies  (no  matter  what  is  the  cause  of  death),  the  liquid 
loses  its  transparency,  becomes  albuminous,  and  is  absorbed.  The  booklets, 
salts  of  lime,  epithelial  cells,  and  crystals  of  hsematoidin  of  a  biliary  origin 
form  a  small  degenerated  caseous  mass.  The  pocket  of  the  cyst  becomes 
fibrous,  contracted,  and  infiltrated  with  calcareous  salts,  and  the  cyst  thus 
transformed  becomes  inoffensive. 

Diagnosis. — A  smooth,  painless,  resistant  bulging,  which  develops 
slowly  in  the  liver  without  fever,  jaundice,  and  ascites,  can  only  be  a  hydatid 
cyst.  The  diagnosis  is  not  always  so  simple.  Some  pedunculated  hydatid 
cysts  protrude  into  the  left  hypochondrium,  and  simulate  a  cyst  of  the 
spleen.  Others  descend  into  the  iliac  fossa,  and  simulate  a  cyst  of  the 
ovary.  Others  protrude  towards  the  diaphragm,  push  it  back,  encroach 
on  the  thoracic  cavity,  and  at  first  sight  simulate  effusion  into  the  pleura. 
These  possible  causes  of  error  must  be  remembered  in  order  to  avoid  mis- 
takes. The  enlarged  liver  of  leucocythaemia  and  of  malaria  is  characterized 
by  general  and  uniform  swelling,  which  does  not  resemble  the  more  or  less 
limited  tumour  of  the  cyst.  Besides,  the  setiological  conditions  and  the 
concomitant  symptoms  would  suffice  to  remove  all  doubts.  Hypertrophic 
cirrhosis,  with  uniform  enlargement  of  the  liver  and  chronic  icterus,  cannot 
be  taken  for  a  hydatid  cyst ;  but  the  opposite  mistake  has  been  made 
because  certain  cysts  of  the  liver,  accompanied  by  jaundice,  may  closely 
resemble  hypertrophic  cirrhosis.  There  is,  however,  the  difference  that 
in  hypertrophic  cirrhosis  the  spleen  is  likewise  hypertrophied,  and  the 
jaundice  is  contemporaneous  with  the  onset  of  the  disease. 

Secondary  cancer  of  the  liver  is  distinguished  by  its  rapid  gro^vth,  and 
by  the  indurated  bosses  of  the  tumour.  Primary  massive  cancer  does  not 
cause  bosses,  but  offers  a  ligneous  hardness  to  the  touch,  and  the  general 
malnutrition  of  the  patient  is  not  to  be  compared  with  the  excellent  health 
of  an  individual  with  a  hydatid  cyst.  Cysts  of  the  kidneys  may  project 
into  the  hypochondrium  so  as  to  simulate  a  cyst  of  the  liver.  In  some  very 
rare  cases  the  hydatid  cyst,  opening  into  the  peritoneum,  has  been  mistaken 
for  ascites. 

The  diagnosis  between  pleural  effusion  and  a  cyst  on  the  convex  face  of 
the  liver  is  often  very  difficult,  and  a  cyst  has  often  been  punctured  under 
the  impression  that  the  pleural  cavity  was  being  penetrated.  Percussion, 
auscultation,  the  form  and  limits  of  the  dullness,  give  imperfect  information. 
The  history  of  the  illness  must  be  investigated,  and  the  deformity  of  the 
thorax  must  be  carefully  studied.  As  a  matter  of  fact,  cysts  of  the  liver  do 
not  generally  simulate  large  effusions  into  the  pleura  (4  or  5  pints),  in 


944  TEXT-BOOK  OF  MEDICINE 

which  the  dullness  reaches  to  the  upper  level  of  the  thorax.  They  simulate^ 
rather,  the  average  effusions  of  2  or  3  pints,  which  cause  dullness,  with  its 
upper  limit  at  the  spine  of  the  scapula.  These  average  effusions  do  not 
cause  enlargement  of  the  hypochondrium  or  bulging  and  enlargement  of 
the  intercostal  spaces,  such  as  are  common  in  hydatid  cysts. 

In  hydatid  cysts  of  the  liver  or  of  the  spleen,  and  also  in  all  tumours  of 
the  hypochondrium,  I  would  advise  the  following  mode  of  exploration  :  The 
patient  is  first  examined  lying  on  a  couch  ;  he,  then,  stands  stripped,  in  the 
upright  position,  with  the  arms  extended.  Examination  from  the  front  and 
the  back  and  comparison  of  the  healthy  and  diseased  sides  show  any 
deformity  on  the  diseased  side. 

Eosinophilia. — Loeper  has  published  some  interesting  work  on  this 
point.  Leucocytosis  is  generally  slight  or  absent.  The  number  of  poly- 
nuclear  cells  is  practically  normal,  but  the  eosinophiles  are  usually  present 
in  increased  proportions.  This  observation  shows  that  the  hydatid  has  an 
affinity  for  the  eosinophile.  If  we  examine  the  liver,  we  find  in  the  con- 
nective tissue  and  in  the  intercellular  spaces  many  eosinophile  cells.  The 
number  is  most  marked  in  the  neighbourhood  of  the  cyst,  and  the 
eosinophiles  abound  in  the  fibrous  shell,  through  which  they  pass,  in- 
sinuating themselves  in  the  interstices  of  the  cyst- wall,  and  falHng  into  the 
cavity. 

Eosinophilia  is  the  most  marked  blood  reaction.  .  In  many  cases  it 
indicates  activity  on  the  part  of  the  cyst,  because  it  disappears  after  opera- 
tion. As  it  is  not  constant,  it  cannot  be  said  to  have  an  absolute  value.  It 
is  not  only  absent  in  dead  cysts,  but  also  in  some  living  cysts  of  large  size. 
These  negative  results  lessen  the  importance  of  eosinophilia.  Eosino- 
philia, even  though  marked,  is  not  always  pathognomonic  of  hydatid  cyst. 
Certain  tumours  of  the  spleen  and  certain  lesions  of  the  pleura  or  lung  may 
be  accompanied  by  an  increase  in  the  eosinophiles.  Examination  of  the 
blood,  therefore,  yields  presumptive,  but  not  positive,  evidence. 

When  suppuration  occurs  in  the  cyst,  we  find  more  or  less  marked 
polynu clear  leucocytosis. 

The  prognosis  of  hydatid  cysts  of  the  liver  is  very  serious,  on  account 
of  mishaps  of  rupture  of  the  cyst,  infection,  or  opening  into  the  thorax, 
peritoneum,  or  bile-ducts.  We  shall  see,  nevertheless,  that  the  treatment 
may  remove  these  grave  dangers,  and  make  the  prognosis  favourable. 

Treatment. — There  is  no  medical  treatment.  In  hydatid  cysts  of  the 
liver  surgical  intervention  is  imperative.  The  old-fashioned  treatment 
comprised  numerous  operations — electro-puncture ;  simple  puncture  without 
injection,  and  with  injection  of  iodine,  alcohol,  etc.  ;  incision  of  the  cyst, 
after  previous  adhesions.  I  have  seen  all  these  operations  employed,  and 
though  some  cases  were  successful,  there  were  very  many  fatal  results. 


DISEASES  OF  THE  LIVER  945 

Aseptic  methods  were,  then,  unknown.  I,  therefore,  tried  to  devise  an  opera- 
tion which  would  prevent  the  terrible  results  of  purulent  infection.  In  this 
way  I  began  my  researches  on  aspiration.  I  still  remember  the  first  hydatid 
cyst  treated  by  aspiration.  I  was  assistant  to  Axenfeld,  and  the  patient 
was  in  Clubler's  ward  at  the  Beaujeon  Hospital.  I  made  one  puncture 
with  a  No.  2  needle,  and  the  patient  recovered. 

Since  my  first  publications*  in  1870  the  treatment  of  cysts  of  the  liver 
by  aspiration  has  been  much  practised,  and  though  this  operation  does  not 
succeed  in  all  cases,  experience  has  proved  that  in  some  unilocular,  non- 
suppurating  cysts  puncture  by  means  of  the  aspirator  is  harmless,  and  is 
sometimes  followed  by  cure. 

Description  of  the  Operation.— The  choice  of  the  aspirator  is  a  matter 
of  indifference.  The  important  point  is  the  choice  of  the  needle.  I  use  a 
No.  2  needle,  which  measures  only  1^  millimetres  in  diameter,  and  I  put 
aside  the  trocar,  which  offers  no  advantages.  The  needle  having  been 
sterilized,  and  all  aseptic  precautions  having  been  taken,  the  preliminary 
vacuum  is  made  in  the  aspirator.  The  patient  is  placed  on  his  back,  and 
the  operator  introduces  the  needle  at  the  most  prominent  part  of  the 
tumour.  The  corresponding  cock  of  the  aspirator  is  then  opened,  and 
the  liquid  from  the  cyst  flows  into  the  bottle,  and  as  the  cyst  is  emptied 
care  is  taken  to  push  the  needle  a  little  deeper,  because  the  level  of  the 
liquid  in  the  tumour  is  being  gradually  lowered.  If  during  the  course  of  the 
operation  the  flow  of  the  liquid  stops  suddenly,  or  if  a  piece  of  hydatid 
membrane  is  thought  to  obliterate  the  needle,  the  needle  is  left  in  situ,  and  a 
new  puncture  is  made.  Care  must,  however,  be  taken  not  to  knead  the 
tumour,  so  as  to  favour  the  outflow  of  the  liquid.  Care  must  also  be  taken 
not  to  percuss  the  tumour  or  to  make  the  patient  sit  up,  in  order  to  ascer- 
tain the  dimiimtion  or  the  disappearance  of  the  liquid.  These  manoeuvres 
are  wrong.  They  may  favour  the  issue  of  a  few  drops  of  liquid,  and  become 
the  cause  of  complications.     These  details  are  of  importance. 

After  the  cyst  is  emptied,  the  needle  is  withdrawn,  care  being  taken  to 
leave  it  during  the  withdrawal  in  communication  with  the  aspirator,  as  by 
this  means  the  needle  cannot  leave  a  single  drop  of  liquid  in  the  peritoneum. 
After  the  operation,  a  bandage,  previously  applied,  is  gradually  tightened.  The 
patient  must  remain  still  on  his  back  for  some  hours.  He  may  get  up  the 
day  after  the  operation. 

The  operation  thus  performed  is  merely  a  harmless  needle-prick,  demand- 
ing neither  special  dexterity  nor  surgical  knowledge.  In  some  cases  of 
unilocular  non-suppurating  cysts  cure  is  obtained  by  one  aspiration.  It  will 
be  asked  what  becomes  of  the  pocket  of  the  cyst.  It  is  probable  that,  in 
part,  it  undergoes  fatty  degeneration,  as  in  spontaneous  cure.  This  happy 
♦  Dieulafoy,  Oaz.  des  Hup.,  1870,  and  "  Traitc  do  rAspinitiim,"  1873,  p.  .31. 

60 


946  TEXT-BOOK  OF  MEDICINE 

termination  is  the  more  frequent,  the  earlier  the  cyst  is  attacked.  Later, 
the  cystic  pocket,  as  it  grows  older,  becomes  vascular  and  thickened,  and 
the  chances  of  success  diminish. 

After-Effects  of  the  Operation— Urticaria.— The  after-efEects  are  so 
slight  that  recovery  is  practically  immediate.  Certain  urgent  symptoms 
may,  however,  show  themselves,  and  it  is  necessary  to  remember  them.  We 
see  patients  who  a  few  hours  after  the  operation  suffer  from  dyspnoea, 
nausea,  and  sometimes  hiccough,  vomiting,  or  fever,  and  we  naturally  fear 
the  onset  of  acute  peritonitis.  Itching,  however,  soon  supervenes  in  different 
parts  of  the  body,  and  an  attack  of  urticaria  appears. 

When  I  published  my  first  remarks  on  urticaria  after  puncture  of  cysts  of 
the  liver,  the  fact  had  passed  unnoticed  in  France,  but  cases  soon  multiplied  ;* 
I  have  collected  about  fifty.  It  is  only  right  to  say  that  this  fact  did  not 
pass  unnoticed  in  Denmark,  and  Finsen,  when  reporting  several  examples 
of  urticaria  following  rupture  of  hydatid  cysts  into  the  peritoneum,  points 
out  that  puncture  of  the  cyst  may  lead  to  the  same  result.  The  urticaria 
shows  itself  in  somewhat  different  forms.  Sometimes  it  is  not  accompanied 
by  any  other  symptom  save  slight  itching  that  lasts  a  day  or  two.  At 
other  times  the  urticaria  is  preceded  and  accompanied  by  the  general 
symptoms  above  mentioned.  In  some  cases  the  urticaria  invades  the 
mucous  membranes  of  the  mouth  or  of  the  pharynx.  The  fever,  nausea,  and 
vomiting  generally  become  severe,  and  last  two  or  three  days.  Sometimes 
the  urticaria  affects  certain  portions  of  the  body.  I  have  seen  a  case  in 
which  it  was  limited  to  the  right  side. 

These  symptoms  closely  resemble  those  of  mussel-poisoning.  In  both 
cases  it  is  a  question  of  intoxication.  The  hydatid  fluid  is  toxic,  and  may 
contain  substances  that  belong  to  the  class  of  ptomaines  analogous  to  the 
mytilotoxin  of  poisonous  mussels.  According  to  Viron,  the  hydatid  liquid 
contains  an  albuminoid  substance  something  like  toxalbumin. 

Aseptic  hydatid  liquid,  when  injected  under  the  skin  with  a  Pravaz 
syringe,  may  produce  urticaria.  The  toxicity  of  the  hydatid  liquid  is  thus 
clearly  established,  and  explains  the  nettle-Hke  eruptions  which  may  super- 
vene during  the  growth  of  the  cyst,  and  which  I  have  pointed  out  as  re- 
vealing signs.  It  perhaps  explains  the  early  hydatid  cachexia  of  certain 
patients  in  whom  the  general  symptoms  are  more  pronounced  than  the 
local  troubles.  In  some  cases  puncture  of  a  hydatid  cyst  of  the  hver  has 
caused  fatal  complications. 

*  Dieulafoy,  Gaz.  des  Hop.,  1870;  "Traite  de  I'Aspiration  des  Liquides  Morbides," 
1873.  Hayem  et  Ferrand,  Soc.  Med.  des  Hop.,  1874.  Bussard,  Gaz.  des  Hop.,  1875. 
Feytaud,  Th.  de  Paris,  1875.  Raynaud,  Verneuil,  Legroux,  Soc.  Anat.,  1875.  Archam- 
bault,  Union  Med.,  1876.  Lereboullet,  Gaz.  Held.,  1876.  Bradbury,  British  Medical 
Journal,  1874.     Neisser,  "  Die  Echinococcenkrankheit,"  Berlin,  1877. 


DISEASES  OF  THE  LIVER  947 

Moissenet  :  A  man  suflfering  from  hydatid  cyst  of  the  Hver  was  operated  upon,  the 
pimcture  being  made  with  a  capillary  trocar  and  the  discharge  of  the  hquid  being  stopped 
at  30  ounces.  Five  minutes  later,  says  Moissenet,  the  patient  was  seized  with  syncope. 
Two  hours  afterwards  there  was  a  severe  rigor,  with  pallor  of  the  face,  pinched  nose, 
hollow  eyes,  and  hiccough,  nausea,  copious  green  vomiting,  and  yet  there  was  no  pain 
on  pressing  the  belly.  The  symptoms  became  worse  and  worse  :  the  pulse  stood  at  125  ; 
the  extremities  grew  cold  ;  the  facies  became  more  marked  ;  and  the  patient  succumbed 
during  the  night.  The  post-mortem  revealed  a  hydatid  cyst,  as  large  as  an  adult  head, 
containing  clear  liquid  and  daughter  vesicles. 

Martineau  :  Aspiratory  puncture  was  performed  on  a  patient  suffering  from  hydatid 
cyst  of  the  Uver.  A  colourless  Uqmd  flowed  from  the  cannula  ;  after  a  few  grammes  had 
passed,  the  discharge  ceased,  and  did  not  appear  again,  in  spite  of  a  change  of  place  of 
the  cannula.  On  withdrawal  ]\Iartineau  foimd  that  it  was  obstructed  by  hydatid  debris. 
A  few  minutes  afterwards  the  patient  was  taken  ill  with  intense  dyspnoea  and  vomiting. 
Respiration  stopped,  the  pulse  became  imperceptible,  and  the  patient  fell  into  a  state  of 
syncope,  dying  in  twenty-four  hours.  At  the  post-mortem  examination  mucus  ob- 
structed the  bronchi.  Old  pleural  adhesions,  pericarditis,  and  old  mitral  endocarditis 
were  found,  as  well  as  two  hydatid  cysts  in  the  hver,  one  of  which  showed  the  puncture. 
There  was  nothing  in  the  peritoneum. 

Bryant :  In  a  man  suffering  from  hydatid  cj'st  of  the  Uver  a  trocar,  not  larger  than 
a  silver  probe,  was  inserted  to  a  depth  of  about  3J  inches  to  the  right  of  the  median  line. 
Nine  ounces  of  a  clear  non-albuminous  hquid  were  withdrawn  to  diminish  the  tension. 
A  few  seconds  afterwards  the  patient  became  hvid,  lost  consciousness,  and  after  vomiting 
two  or  three  times,  had  an  epileptiform  fit.  At  the  same  moment  the  pulse  stopped. 
Artificial  respiration,  the  galvanic  battery,  and  nitrite  of  amyl  were  tried,  but  the 
patient  died  in  five  minutes.  The  post-mortem  examination  was  performed  by  Hilton 
Fagge.  The  peritoneum  contained  i  pint  of  blood-tinged  liquid.  A  hydatid  cyst  as 
large  as  a  man's  head  occupied  the  posterior  portion  of  the  right  lobe  of  the  liver.  There 
were  no  other  visceral  changes. 

Chauffard  :  In  order  to  confirm  the  diagnosis  of  a  hydatid  cyst  of  the  Uver  an 
aspiratory  pimcture  was  made.  A  httle  liquid  had  just  been  withdrawn,  when  the 
patient  was  taken  with  sudden  itching,  loss  of  consciousness,  and  an  epileptiform  fit, 
with  foaming  at  the  mouth,  and  emission  of  urine  and  fsecal  matter.  A  few  moments 
afterwards  there  was  another  epileptiform  fit,  with  clonic  movements,  restlessness, 
and  expectoration  of  whitish  froth.  In  a  few  minutes  the  patient  fell  back  exhausted. 
The  skin  had  a  cyanotic  tint,  the  pulse  grew  weaker  and  weaker,  collapse  was  imminent, 
the  face  was  bathed  in  sweat,  and  at  last  fatal  asphyxia  supervened.  The  post-mortem 
examination  revealed  neither  peritonitis  nor  fluid  in  the  peritoneum.  It  was  evidently 
a  case  of  superacute  hydatid  intoxication. 

We  must  try  to  explain  these  fatal  complications  occurring  after  punc- 
ture of  hydatid  cysts  in  the  liver.  One  fact  is  certain — namely,  that  the 
passage  of  a  few  drops  of  hydatid  liquid  into  the  peritoneal  cavity  may  cause 
benign  or  fatal  intoxication.  The  most  benign  comphcation  is  urticaria. 
The  grave  and  fatal  complications  have  just  been  described.  They  all  are 
due  to  the  passage  of  the  toxic  liquid  into  the  peritoneum.  The  treatment 
of  hydatid  cyst  by  puncture  is  not  to  be  feared.  Mishaps  result  from  small 
punctures,  which  withdraw  only  a  very  small  (quantity  of  the  li([uid,  because 
the  cystic  liquid  under  pressure  makes  a  way  for  itself  througli  the  little 
opening  left  by  the  needle,  is  absorbed  by  the  peritoneum,  and  gives  rise 
to  intoxication.     As  a  general  rule  small  punctures,  and  also  incomplete  or 

CO— 2 


948  TEXT-BOOK  OF  MEDICINE 

exploratory  punctures,  must  be  avoided.  This  mode  of  investigation  must 
never  be  employed  to  clear  up  the  diagnosis  of  cysts  of  the  liver.  No 
matter  how  fine  the  aspiratory  needle,  we  must  not  forget  that  it  may  leave 
an  open  channel  for  liquid  which  under  pressure  is  ready  to  pass  into  the 
peritoneum. 

Summary. — I  have  gradually  given  up  the  treatment  of  the  cyst  by  aspira- 
tory puncture  for  laparotomy.  In  cysts  of  the  anterior  surface  of  the  liver 
median  or  lateral  laparotomy  should  be  performed.  The  postero -inferior 
cysts  should  be  attacked  by  the  lumbar  incision.  In  subphrenic  cysts  the 
inferior  edge  of  the  thorax  should  be  resected  (Lannelongue).  Finally,  if 
the  cyst  reaches  up  into  the  thoracic  cavity,  it  should  be  attacked  through 
the  pleura,  with  or  without  costal  resection  (Segond). 

XVI.  ALVEOLAR  HYDATID  CYST  OF  THE  LIVER. 

Pathological  Anatomy. — The  alveolar  hydatid  cyst,  also  called  multi- 
locular  echinococcus,  is  so  rare  that  Carriere  was  only  able  to  collect  eighteen 
cases  in  his  interesting  thesis.  The  subsequent  cases  have  been  collected 
by  Vierordt  in  1886,  and  by  Posselt  in  1899.  In  this  variety  the  hydatids 
are  not  collected  in  one  mother  vesicle,  but  are  scattered  through  the 
parenchyma  of  the  liver,  forming  more  or  less  large  groups.  At  the  post- 
mortem examination  the  liver  is  found  to  be  uneveij  and  nodular.  Over 
the  hydatid  tumours  adhesive  peritonitis  is  often  found.  The  largest  group 
is  generally  seated  in  the  posterior  part  of  the  right  lobe.  A  section  shows 
that  this  cystic  mass  is  composed  of  a  thick  shell  and  of  a  cavity  containing 
purulent  fluid  and  caseous  debris  that  represent  the  parts  of  the  cyst  in  a 
condition  of  retrogression. 

The  shell  or  envelope  of  the  tumour  is  composed  of  a  fibrous  stroma, 
forming  a  number  of  pockets  of  various  dimensions.  These  pockets  con- 
tain little  gelatinous  and  colloid  bodies  which  are  really  hydatids.  The 
vesicles  of  a  multilocular  hydatid  have  the  same  structure  as  the  unilocular 
hydatid  already  described.  Many  of  them  are  sterile,  but  some  of  them 
contain  echinococci.  These  vesicles  are  in  considerable  quantity,  and  are  of 
variable  size.  Some  are  not  visible  to  the  naked  eye  ;  others  are  as  large  as 
a  hazel-nut.  When  the  hydatids  are  confluent,  the  alveoli  communicate 
with  one  another,  and  the  tumour  has  the  appearance  of  certain  cancers. 
The  hydatid  bulges  into  the  interior  of  the  vessels,  finally  causing  oblit- 
eration. The  branches  of  the  portal  vein  and  of  the  hepatic  artery 
(Ranvier),  the  bile-ducts  (Frerichs),  and  the  lymphatics  (Virchow)  are  thus 
obliterated. 

Many  hypotheses  have  been  formulated  to  explain  the  special  disposi- 
tion of  the  multilocular  echinococcus.     While  some  think  that  it  is  a  case 


DISEASES  OF  THE  LIVEK  949 

of  exogenous  proliferation  of  the  mother  hydatid,  which  is  said  to  give  birth 
to  daughter  hydatids  and  to  echinococci  from  its  external  wall  instead  of 
producing  them  from  its  internal  one,  others  hold  that  they  arise  from  a 
taenia  different  from  the  Twnia  eckinococcus. 

etiology. — The  alveolar  echinococcus  rarely  develops  before  the 
twentieth  year.  Close  contact  with  domestic  animals,  and  especially  with 
the  ox  (Posselt),  is  the  chief  cause  of  the  affection.  It  is  found  in  Southern 
Germany  (Bavaria,  Wiirtemberg),  in  the  North  of  Switzerland,  and  has 
just  invaded  the  Tyrol  (Posselt).  France  (Carriere's  patient  was  a  Bavarian) 
has  now  been  invaded.  Railliet  and  Morot  pointed  out  cases  in  animals 
in  1898.  So  far  only  two  cases  are  known  in  man — viz.,  that  of  Bruyant 
(alveolar  cyst  of  the  liver),  and  that  of  Renon  (alveolar  cyst  of  the  lung  and 
pleura). 

Symptoms. — The  alveolar  hydatid  cyst  develops  slowly,  and  its  onset 
passes  unnoticed  for  some  while.  Later  the  symptoms  are  peculiar,  in  that 
no  one  is  pathognomonic.  Thus,  the  liver  presents  nodules  and  bosses,  as 
in  cancer.  Ascites  is  often  present  (seven  cases  out  of  thirteen,  Frerichs) 
as  in  atrophic  cirrhosis ;  but  the  cyst  is  more  often  accompanied  by  chronic 
jaundice  (fifteen  cases  out  of  eighteen,  Carriere),  as  in  hypertrophic  cir- 
rhosis. The  general  health  remains  good ;  the  appetite  is  excellent ;  the 
fffices  are  colourless  from  the  onset  of  the  jaundice  ;  and  the  spleen  is  often 
hypertrophied.  This  diversity  in  the  symptoms  makes  the  difficulty  in 
diagnosis  obvious. 

The  course  of  the  disease  is  very  slow.  Haemorrhage  and  oedema  are 
frequent  at  an  advanced  period.  Death  occurs  in  eight  to  eleven  years 
after  the  onset  of  the  disease. 


XVII.  FATTY  AND  AMYLOID  DEGENERATION  OF  THE 

LIVER. 

1.  Fatty  Degeneration. — In  the  physiological  condition,  especially  after 
meals,  the  liver  contains  a  considerable  quantity  of  fat.  The  hepatic  cell 
can,  indeed,  manufacture  fat  from  proteids,  as  is  proved  by  the  fat  found 
in  dogs,  fed  on  an  exclusive  meat  diet.  The  fat  derived  from  digestion  is 
stored  in  part  in  the  hepatic  cell,  especially  in  the  cells  at  the  periphery 
of  the  lobule,  where  it  awaits  its  ulterior  elaboration.  This  accumulation 
of  fat  in  the  liver  is  even  more  abundant  during  pregnancy  and  lactation, 
on  account  of  the  nutrition  of  the  foetus  and  the  secretion  of  the  milk  ;  but 
in  this  case  the  fat  is  found  in  the  central  cells,  close  to  the  hepatic  vein. 
In  these  different  cases  the  fat  contained  in  the  liver  is  derived  from  outside 
and  infiltrates  the  hepatic  cell  for  the  time  being  by  pushing  aside  its  proto- 
plasm, but  the  cell  loses  neither  its  autonomy  nor  its  functions — in  a  word, 


950  TEXT-BOOK  OF  MEDICINE 

there  is  fatty  infiltration,  but  no  degeneration.  Not  only  does  the  liver 
elaborate  fat,  but  it  is  also  an  organ  for  the  excretion  of  fatty  matter.  In 
pathological  conditions,  there  is  fatty  degeneration — that  is  to  say,  the  fat 
is  formed  at  the  expense  of  the  protoplasm  of  the  cell.  In  consequence  of 
chemical  processes  not  fuUy  understood,  the  hepatic  cell  loses  its  structure 
and  properties,  and  becomes  transformed  into  fatty  tissue.  It  should  be 
noted  that  these  two  varieties — infiltration  and  degeneration — often  occur 
together. 

Steatosis  of  the  liver  is  produced  by  acute  and  chronic  intoxications, 
phosphorus-poisoning  being  the  most  typical.  Alcohol  is  a  fat-producing 
poison.  Arsenic  and  morphia  (morphia  habit)  give  the  same  result.  Stea- 
tosis is  sometimes  caused  by  the  organisms  of  the  infectious  diseases  and 
their  toxines :  puerperal  fever  (Widal),  typhoid  fever  (Legry),  cholera 
(Hanot  and  Gilbert),  and  pneumonic  infection  (Pilliet).  The  toxines,  no 
doubt,  play  the  most  important  part  in  steatosis  of  the  liver,  associated  with 
the  infectious  diseases.  This  hypothesis  is  proved  in  experiments  where 
only  toxines  are  present — viz.,  injection  of  cultures  of  the  diphtheria  bacillus 
(Roux  and  Yersin). 

I  have  just  reviewed  the  different  intoxications  which  may  cause  stea- 
tosis of  the  liver,  but  there  are  circumstances  in  which  it  is  associated  with 
other  pre-existing  lesions  (alcohoHsm,  tuberculosis,  and  syphilis).  Finally, 
in  some  cases  the  fatty  degeneration  is  the  consequence  of  an  anterior  pro- 
cess, such  as  cirrhosis,  cardiac  liver,  or  chronic  jaundice. 

Post  mortem  the  following  characteristics  are  met  with :  the  liver  is 
fatty,  enlarged,  and  of  a  dead-leaf  colour.  Its  tissue  is  soft,  and  on  section 
fatty  droplets  exude.  The  proportion  of  the  fatty  elements  is  notably 
modified,  and  the  liver  contains  20  to  25  per  cent,  instead  of  4  to  5  per 
cent.  The  bile  is  light  in  colour,  on  account  of  the  changes  in  the  proto- 
plasm, which  probably  helps  to  make  the  bile  pigment.  The  histological 
examination  shows  that  the  hepatic  cell  has  lost  its  polyhedral  form, 
becoming  spheroidal.  The  nucleus  of  the  cell  is  pushed  aside  to  the  periphery, 
the  protoplasm  has  more  or  less  disappeared,  and  the  cell  seems  to  be 
converted  into  a  fatty  mass. 

The  symptoms  of  hepatic  steatosis  are  so  obscure  that  the  diagnosis  can 
only  be  made  from  the  aetiology.  The  Hver  is  enlarged,  and  is  not  painful. 
Ascites,  jaundice,  and  collateral  circulation  are  absent.  When  the  steatosis 
takes  a  rapid  course,  the  symptoms  of  icterus  gravis  may  result. 

2.  Amyloid  Degeneration. — The  amyloid  liver  is  also  called  lardaceous, 
or  waxy.  The  name  "  amyloid  "  is  bad.  It  was  employed  by  Virchow, 
who,  relying  on  the  iodine  reaction,  supposed  the  presence  of  an  amyloid 
substance.  The  substance  that  infiltrates  the  cell,  is  of  an  albuminous 
nature,  though  it  differs  in  several  respects  from  true  albumin. 


DISEASES  OF  THE  LIVER  951 

The  causes  of  amyloid  degeneration  are  those  of  fatty  degeneration.  It 
is  always  a  secondary  process,  and  we  may  note,  as  having  a  special  action 
in  its  production,  chronic  tuberculosis,  especially  of  the  bones,  prolonged 
suppuration,  syphilis,  malaria,  and  leucocythaemia. 

The  amyloid  liver  is  enlarged.  Glisson's  capsule  is  smooth,  vitreous,  and 
but  rarely  thickened.  On  section,  the  liver  is  fairly  resistant,  lardaceous, 
and,  as  it  were,  infiltrated  by  a  highly  refracting  colloid  substance.  It  is 
easy  to  see  the  amyloid  infiltration  by  means  of  tincture  of  iodine.  If  the 
surface  is  moistened  with  tincture  of  iodine,  the  stained  part  assumes  a 
mahogany-red  tint,  which  turns  into  blue  and  violet.  If  the  test  is  made 
with  methyl-aniline  violet,  the  affected  parts  are  stained  red-violet  and 
the  healthy  parts  blue-violet  (Cornil).  Under  the  microscope  we  see  that 
the  degeneration  affects  the  cell  and  the  vessels,  especiallv  the  hepatic 
artery.  The  biliary  passages  remain  intact.  Amyloid  degeneration  of  the 
liver  is  often  associated  with  other  lesions  (steatosis,  syphilis). 

The  symptoms  of  the  amyloid  liver  are  as  obscure  as  those  of  the  fatty 
liver,  and  the  disease  might  be  latent  in  its  course  were  it  not  for  the  enor- 
mous enlargement  of  the  organ.  Furthermore,  amyloid  degeneration  of 
the  Uver  is  often  associated  with  amyloid  disease  of  the  spleen,  kidneys, 
and  intestine,  in  which  case  other  symptoms  appear  (diarrhoea, 
albuminuria). 

The  treatment  must  be  based  on  the  aetiology  of  the  amyloid  degenera- 
tion. Tonics,  constitutional  remedies,  and  a  long  sojourn  at  the  seaside 
should  be  advised  for  tubercular  patients  and  those  worn  out  by  long  suppu- 
ration. Iodide  of  potassium  and  mercurial  preparations  should  be  prescribed 
for  syphilitics. 

XVIII.  ABSCESS  OF  THE  LIVER. 

Acute  hepatitis,  which  often  terminates  in  suppuration,  and  gives  rise 
to  the  tropical  abscess,  is  rare  in  our  climate,  but  common  in  hot  countries. 
This  form  of  suppurative  hepatitis  will  be  the  principal  subject  of  this 
section.  Aside  from  suppuration  caused  by  hepatitis  in  warm  countries, 
other  forms  of  suppuration  leading  to  abscess  may  occur.  The  study  of 
these  forms  must  only  figure  in  this  section  as  an  indication,  and  I  shall 
merely  sketch  the  ]>rinci])al  varieties  l)efore  discussing  acute  hepatitis. 

1.  Metastatic  Abscesses  of  the  Liver. — These  abscesses  arise  from  any 
cause  of  purulent  infection,  such  as  traumatism,  head  injuries,  surgii^al 
operations,  smallpox,  puerperal  infection,  or  medical  septica'mia  (endo- 
carditis, infective  aortitis,  or  suppurative  ])neumonia).  The  abscesses  are 
miliary  and  commence  with  an  ecchymotic  tint  of  the  hepatic  lobule.  The 
bloodvessels  of  the  lobule  are  congested  with  red  and  white  corpuscles. 


952  TEXT-BOOK  OF  MEDICINE 

The  latter,  having  passed  out  of  the  bloodvessels,  infiltrate  the  lobule  ;  the 
hepatic  cell  becomes  granular  and  atrophied,  and  the  small  abscess  is  formed. 
These  little  islets  of  suppuration  grow  larger,  unite  with  the  neighbouring 
islets,  and  attain  the  size  of  a  pea  or  a  hazel-nut.  The  branches  of  the 
portal  vein  around  them  show  secondary  periphlebitis,  phlebitis,  and 
thrombosis.  The  phlebitis,  in  its  turn,  causes  extension  of  the  abscesses 
to  the  neighbouring  parts. 

How  is  the  formation  of  these  abscesses  to  be  explained  ?  The  old 
theory  of  capillary  embolism  (Virchow)  has  been  replaced  by  that  of  microbic 
infection.  The  pyogenic  microbes  enter  the  general  venous  system  and 
are  carried  to  the  liver  by  the  hepatic  artery.  These  pyogenic  agents, 
which  are  almost  always  the  streptococci  and  the  staphylococci,  are  arrested 
in  the  radiate  capillaries  of  the  hepatic  lobules,  where  the  circulation  has 
become  sluggish.  Their  presence  and  their  toxine  produce  lesions  in  the 
vascular  endothelium,  obliteration  of  the  capillaries,  invasion  of  leucocytes, 
formation  of  a  clot,  suppuration,  and  miliary  abscess. 

Hepatic  pyaemia  is  ushered  in  by  rigors,  marked  rise  in  temperature,  and 
profuse  sweating.  The  liver  becomes  enlarged  and  painful,  the  skin  is 
yellowish  and  earthy,  and  the  urine  contains  bile  pigment. 

2.  Pylephlebitis. — The  abscesses  do  nat  begin  in  the  general  venous 
system,  but  in  the  portal  system.  Purulent  inflammation  of  the  portal 
vein  (pylephlebitis)  may  follow  ulceration  of  the  intestine  (dysentery),  or 
an  abscess  in  the  spleen  and  the  phlebitis  extends  as  far  as  the  bloodvessels 
of  the  liver.  Various  micro-organisms,  especially  the  coli  bacillus,  must 
be  in  evidence.  At  several  points  in  the  liver  httle  abscesses  are  situated 
along  the  course  of  the  inflamed  veins.  The  vein  is  attacked  by  phlebitis 
and  periphlebitis,  and  surrounded  by  embryonic  tissue.  In  certain  places 
the  walls  of  the  vein  are  destroyed.  Such  is  the  course  of  the  abscesses 
caused  by  pylephlebitis,  but  in  many  cases  pylephlebitis  is  not  necessary, 
and  the  arrival  of  the  pathogenic  microbes  in  the  liver  may  cause  suppurative 
inflammation  of  the  vein,  which  produces  inflammation  of  the  liver  tissue 
and  abscesses  in  the  surrounding  region.  Abscesses  of  the  liver  consequent 
on  appendicitis  (appendicular  liver)  will  be  discussed  later. 

3.  Can  embolism  of  the  portal  vein  caused  by  thrombosis  of  the 
mesenteric  vein  or  of  the  other  portal  tributaries  cause  abscesses  of  the 
liver  ?  It  gives  rise  to  an  infarct  of  the  embolized  region,  with  consequent 
anaemia  and  granulo-fatty  degeneration ;  but  this  infarct  is  not  followed 
by  suppuration.  An  exception  must  be  made  with  regard  to  portal 
embolisms  loaded  with  micro-organisms,  such  as  the  coli  bacillus  (septic 
embolism). 

Widal  has  shown  that  the  pyaemic  abscesses  of  the  liver  in  puerperal 
infection  begin  round  the  hepatic  veins.     The   process    commences  with 


DISEASES  OF  THE  LIVER  953 

endophlebitis,  leading  to  periphlebitis  and  abscess.     The  periportal  tissue 
is  generally  free. 

4.  Biliary  Abscesses. — Several  causes  (gall-stones,  obstruction  of  the 
common  duct,  etc.)  may  lead  to  inflammation  and  enlargement  of  the  bile- 
ducts.  The  dilated  ducts  are  at  times  as  large  as  the  finger  and  filled  with 
muco-pus.  At  first  sight  the  condition  might  be  taken  for  abscesses,  but 
on  closer  inspection  it  will  be  seen  that  it  is  caused  by  dilatations  of  the  bile- 
ducts,  which  are  often  surrounded  by  new  connective  tissue.  In  certain 
cases,  however,  the  walls  of  the  ducts  are  destroyed,  and  the  angiocholitis 
is  followed  by  abscess  of  the  liver.  This  question  is  discussed  under  Angio- 
choHtis  and  Gall-stones.  We  have  seen  how  the  secondary  infections  begin 
and  cause  these  biliary  abscesses. 

Acute  Suppurative  Hepatitis — Large  Abscesses  of  the  Liver. 

etiology. — Acute  suppurative  hepatitis  is  rare  in  France,  and  very 
frequent  in  hot  countries  (India,  Algeria,  Senegal,  Bengal,  Cochin-China, 
Martinique).  Dysenteric  infection  is  the  chief  cause.  Several  conditions 
may  present  themselves  :  In  the  first  series,  dysentery  precedes  the  abscess  ; 
in  the  second  series  dysentery  and  abscess  march  side  by  side.  Finally,  in 
the  third  series,  the  hepatitis  or  tropical  abscess,  as  Murchison  called  it, 
appears  to  be  independent  of  dysentery.  This  independence  is  most  fre- 
quently only  apparent.  In  any  case,  it  may  be  said  that  the  amoeba  of 
dysentery  produces  hepatitis,  abscess  of  the  liver,  and  dysentery,  separately 
or  simultaneously. 

Abscess  of  the  liver  is  found  in  countries  where  dysentery  is  found,  and 
both  diseases  have  the  same  origin.  There  are,  however,  cases  of  suppu- 
rative hepatitis  in  hot  countries,  and  of  abscess  of  the  liver  which  have  an 
origin  apparently  independent  of  dysentery.  The  intimate  nature  of  these 
various  abscesses  is  unknown  to  us,  but  it  may  be  said  that  they  have  nothing 
in  common  with  malaria. 

Tropical  dysentery  is  not  the  only  form  which  may  cause  abscesses  of  the 
liver,  Boinet  has  described  large  abscesses  of  the  liver  of  dysenteric  origin 
in  France. 

What  does  bacteriology  teach  us  ?  In  non-dysenteric  abscesses  bac- 
teriology has  revealed  the  presence  and  also  the  absence  of  staphylococci. 
As  far  as  dysenteric  abscesses  are  concerned,  they  are  chiefly  due  to  amoebic 
dysentery.  The  pus  of  tropical  abscesses  of  the  liver  is  often  aseptic,  or 
of  slight  virulence,  even  though  it  is  exceedingly  foetid.  This  feeble  viru- 
lence is  the  more  remarkable  "  because  such  is  far  from  being  the  case  in 
angiocholitic  pus,  which  is  essentially  septic  and  infective  "  (Chauffard). 

Description. — Acute  hepatitis  does  not  always  commence  in  the  same 
manner.     It  is  sometimes  preceded  by  hepatic  congestion,  which  does  not 


954  TEXT-BOOK  OF  MEDICINE 

end  in  suppuration.  The  congestion  shows  itself  by  "  pain  in  the  side," 
with  or  without  fever ;  the  liver  is  enlarged,  and  vomiting  and  diarrhoea 
appear.  A  few  days  later  recovery  supervenes,  but  the  patient  is  liable  to 
recurrence  or  to  abscess  if  he  does  not  leave  the  country. 

Acute  hepatitis  often  commences  with  a  severe  rigor  and  sharp  pain  in 
the  hypochondrium  and  the  right  shoulder.  The  liver  is  enlarged,  the  fever 
is  remittent,  and  jaundice  is  seen  in  a  third  of  the  cases.  The  tongue 
is  dry,  and  the  patient  has  a  typhoid  look.  In  other  cases  the  hepatitis  is 
practically  latent  at  first.  The  local  symptoms  are  absent,  and  the  general 
symptoms  merely  comprise  malaise,  or  attacks  of  intermittent  or  remittent 
fever,  readily  taken  for  malaria.  The  pus  forms  from  the  eighth  to  the 
twelfth  day,  and  the  foregoing  modes  of  onset  indicate  that  tropical  abscess 
may  be  ushered  in  by  acute  symptoms  of  hepatitis  or  only  by  slight  gastro- 
intestinal troubles.  The  abscess  may  even  be  latent  without  fever  in  one 
case,  and  in  another  case  it  may  reveal  its  presence  by  most  grave  symp- 
toms. Locally  the  abscess  of  the  liver  cannot  be  recognized  unless  it  is 
of  fair  size.  The  extent  of  the  dullness,  the  deformity  of  the  Uver,  and  the 
projection  of  the  organ  towards  the  thoracic  or  iliac  region,  depend  on  the 
seat  of  the  abscess. 

The  abscess,  once  formed,  may  remain  stationary  for  weeks  and  months  ; 
but  most  commonly  in  about  three  weeks  it  tries  to  make  its  way  outwards. 
Rupture  of  the  abscess  into  the  peritoneum  is  not  always  followed,  as  might 
be  supposed,  by  rapid  and  fatal  peritonitis.  In  several  cases  surprising 
tolerance  of  the  peritoneum  has  been  noticed,  death  occurring  after  some 
days,  with  symptoms  of  prostration.  Rupture  of  the  abscess  into  the 
intestine  sometimes  leads  to  recovery,  which  may  also  follow  if  the  abscess 
opens  through  the  abdominal  wall  or  into  the  bronchi. 

I  may  mention,  as  exceptions,  rupture  of  the  abscess  into  the  stomach, 
pelvis,  kidney,  vena  cava,  or  pericardium.  It  appears  possible  that  the 
pus  may  be  absorbed,  the  abscess  being  replaced  by  a  cicatrix. 

The  foregoing  description  shows  that  the  diagnosis  is  often  difficult. 
The  prognosis  is  grave,  especially  because  endemic  hepatitis  is  subject  to 
recurrences,  and  sometimes  ends  in  a  chronic  form,  after  long  periods  of 
intermission.  An  opened  and  cured  abscess  does  not  protect  against  fresh 
abscesses.  No  limit  to  the  period  of  formation  of  abscesses  can  be  fixed, 
and  persons  may  leave  the  tropics  for  Europe,  but  yet  fresh  abscesses  may 
still  appear. 

Pathological  Anatomy. — The  liver  in  acute  hepatitis  is  large,  reddish, 
and  friable.  It  is  rare  for  several  abscesses  to  be  found,  and  suppurative 
hepatitis  in  three-quarters  of  the  cases  only  causes  one  abscess — a  marked 
difference  from  the  pj^semic  abscesses,  which  may  be  very  numerous. 

The  tropical  abscess  is  most  frequently  seated  in  the  right  lobe  of  the 


DISEASES  OF  THE  LIVER  955 

liver,  and  on  its  convex  surface  (Dutrouleau).  The  quantity  of  pus  may 
amount  to  2  or  3  pints.  It  is  yellowish  or  reddish,  thick,  creamy,  and 
sometimes  stained  with  bile.  It  may  become  foetid  from  the  close  connec- 
tion of  the  intestine,  or  in  consequence  of  communication  with  other  organs. 

The  walls  of  the  abscess  are  often  anfractuous,  formed  of  embryonic 
tissue.  Sloughs  often  detach  themselves  from  the  walls.  At  a  more 
advanced  period  the  pyogenic  membrane  becomes  surrounded  with  a  fibrous 
membrane.  The  abscess  commences  in  the  deep  parts  of  the  organ,  and 
gradually  reaches  the  surface.  When  it  comes  in  contact  with  Glisson's 
capsule,  it  behaves  differently,  according  to  circumstances.  Adhesions  are 
established  between  the  liver  and  the  neighbouring  organs.  Ulceration 
takes  place,  and  the  pus  makes  a  passage  for  itself  through  the  diaphragm 
and  into  the  bronchi  (vomica),  into  the  peritoneum,  the  pericardium,  the 
pleura,  or  the  intestine  ;  but  the  abscess  sometimes  opens  through  the 
abdominal  wall. 

Treatment. — Bleeding  has  been  recommended  (Dutrouleau),  and  ipe- 
cacuanha has  been  given  in  an  enema  (15  grains  of  ipecacuanha  in  twenty- 
four  hours)  (MacLean).  The  formation  of  the  abscess  must  be  watched 
in  order  to  open  it  without  delay. 

XIX.  APPENDICULAR  LIVER. 

I  have  given  the  name  of  appendicular  liver  to  the  toxi -infection  of  the  liver  con- 
Becutive  to  appendicitis.  From  its  situation  the  liver  receives  the  frontal  attack  of 
the  toxines  and  microbes,  whose  virulence  has  been  increased  in  the  closed  cavity.  The 
appendicular  veins  and  the  branches  of  the  portal  vein  carry  toxines  and  microbes  to 
the  liver.  It  is  nevertheless  important  to  distinguish  between  toxic  and  purulent 
hepatitis.  Soon  after  the  onset  of  appendicitis  the  liver  may  be  affected  by  the  toxines, 
which  are  carried  more  rapidly  than  the  microbes  ;  a  change  in  the  hepatic  cells, 
which  deserves  the  name  of  toxic  hepatitis,  is  the  result.  This  early  toxic  hepatitis  does 
not  suppurate.  Later,  during  the  second  or  third  week  of  appendicitis,  the  microbes 
are  carried  to  tlie  liver,  and  cause  purulent  hepatitis.  It  is,  therefore,  indispensable  to 
describe  separately  toxic  and  purulent  hepatitis. 

1.  Toxic  Hepatitis. 

I  have  already  described  toxic  appendicitis,  or  appendicsemia,  in  which  the  signs  may 
Ijo  jaundice,  choluria,  urobilinuria,  albuminuria,  hajmatomesis,  etc.  I  shall  hero  discuss 
one  of  these  signs,  jaundice,  with  the  concomitant  lesion  of  the  liver,  which  I  was  the 
first  to  point  out  in  my  conMnunication  to  the  Acadt'mie  in  1898. 

Clinical  Cases. — A  young  man  of  twenty  years  of  age  came  into  my  wards,  and  a 
student  remarked  :  "  There  is  a  man  with  jaundice."  The  man  had,  as  a  matter  of 
f  u't,  a  yellowish  tinge,  not  jironoimced  on  the  skin,  but  well  marked  on  the  conjunctiva*, 
lie  said  that  he  was  sufTtiring  from  his  stomach.  Abdominal  i)aiii  and  jaimdico 
naturally  aroused  at  first  the  idea  of  hepatic  colic.  The  jmin  in  tlie  belly  had  com- 
menced four  days  before,  on  Sunday  morning  ;  towards  evening  he  was  taken  ill  with 
fever  and  vomiting,  and  ih(-.  abdominal  pain  persisted  all  niglit.  On  Monday,  as  the 
situation  did  not  change  and    tlio    belly  remained  tender,  the  patient  came  to  the 


956  TEXT-BOOK  OF  MEDICINE 

hospital.  I  asked  him  to  indicate  the  exact  spot  where  the  pains  commenced,  and  also 
where  they  were  most  severe.  He  at  once  placed  his  finger  on  McBurney's  point. 
Palpation  revealed  tenderness  and  muscular  resistance  ;  the  hyperaesthesia  was  most 
marked  at  this  point.     The  diagnosis  was,  therefore,  appendicitis. 

An  explanation  had  still  to  be  found  for  the  jaundice  :  the  Uver  was  neither  enlarged 
nor  painful.  Was  the  jaundice  a  simple  coincidence,  or  was  there  some  relation  between 
it  and  the  appendicitis  ?  My  first  impression  was  that  it  was  not  a  case  of  true  jaundice. 
Examination  of  the  urine  with  nitric  acid  showed  no  ring  of  bihverdin  or  biUrubin, 
but  gave  a  brownish  disc.  Spectroscopic  examination  revealed  the  presence  of  urobihn 
and  of  brown  pigment.  The  yellow  tint  of  the  skin  and  of  the  conjunctivae  was,  then, 
not  the  result  of  true  jaimdice.  The  analysis  of  the  urine  hkewise  proved  the  presence 
of  albumin  in  fairly  considerable  quantity.  With  these  symptoms  I  expressed  the 
opinion  that  this  youth  was  suffering  from  toxic  appendicitis,  the  appendicular  toxine, 
elaborated  in  the  closed  cavity,  having  caused  changes  in  the  cells  of  the  Uver  and 
kidneys,  whence  the  urobiUnuria,  jaundice,  and  albuminuria. 

The  diagnosis  being  given,  treatment  had  to  be  decided.  After  having  obtained  the 
consent  of  the  patient,  and  in  spite  of  the  apparent  mildness  of  the  appendicitis,  I 
requested  Marion  to  operate.  He  found  a  collection  of  foul-smelling  pus  in  the  peri- 
toneum ;  the  appendix  was  gangrenous,  and  bathed  in  pus ;  a  large  calculus  was 
found  in  the  lower  portion  of  the  canal,  which  was  greatly  dilated,  and  converted  into 
a  closed  cavity.  It  is  easy  to  see  what  would  have  happened  had  the  appendicitis  in 
its  gangrenous  form  been  allowed  to  run  its  course. 

This  example  shows  once  more  that  the  gravity  of  the  appendical  lesions  is  not  always 
in  direct  relation  to  the  intensity  of  the  symptoms.  The  ablation  of  the  appendix 
removed  the  primary  focus,  but  the  Hver  and  the  kidneys  were  also  affected.  On  Wed- 
nesday the  situation  became  critical :  the  patient  was  prostrate ;  his  face  was  drawn 
and  yellowish  ;  hiccough  was  frequent ;  the  urine  was  scanty  and  albuminous  ;  the 
temperature  was  102°  F.,  and  the  pulse  106.  Two  injections  of  serum  (1  pint  in  each) 
were  administered.  He  passed  a  better  night.  Next  day,  Thursday,  the  hiccough  had 
almost  gone  ;  the  temperature  was  99°  F.  ;  but  sUght  jaundice  was  still  present. 
Urobilin  still  persisted  in  the  brownish  urine,  but,  an  important  point,  the  albumin 
had  disappeared.  Two  days  later  the  jaundice  disappeared  in  its  turn,  and  the 
urine  contained  no  more  urobihn  ;  a  few  days  later  the  patient  was  out  of  danger. 
This  case,  described  in  one  of  my  lectures  on  the  toxicity  of  appendicitis,  is  a  proof  of 
this  toxicity.  The  toxine  had  affected  the  hver  and  the  kidneys,  and  the  intoxication 
revealed  itself  by  urobihnuria,  jaundice,  and  albuminuria.  The  appendix  being 
removed,  the  albumin  disappeared  within  twenty-four  hours,  and  the  urobiUnuria 
ceased  three  days  later. 

Routier  has  mentioned  several  cases  to  me.  One  of  them  referred  to  a  young  girl 
who  was  operated  on  for  appendicitis,  and  cured.  From  the  commencement  of  the 
disease  she  had  jaundice,  which  became  more  pronounced  during  the  next  few  days. 
Another  case  referred  to  a  man  who  underwent  an  urgency  operation,  and  was  cured  of 
appendicitis.  The  jaundice,  which  was  present  on  the  day  of  the  operation,  persisted 
for  several  days. 

Valmont  saw  a  man  who  had  had  several  attacks  of  appendicitis.  He  was  taken 
ill  with  jaundice  during  the  last  attack,  and  died  in  three  days.  One  of  the  patients, 
whose  case  I  have  referred  to  under  Appendicular  Vomito  Negro,  was  taken  ill, 
at  the  commencement  of  appendicitis,  -with  jaundice,  which  became  general  over  the 
whole  body. 

In  some  cases  the  jaundice  is  obstinate,  and  may  last  for  weeks  and  months,  until 
the  appendix  is  removed.  Hartmarui  communicated  the  following  case  to  me  : 
In  September,  1897,  a  young  man  was  taken  ill  with  clearly-defined  pain  in  the  right 
iUac  fossa,     Dreyfus-Brissac  diagnosed  appendicitis.     The  acute  crisis  once  passed. 


DISEASES  OF  THE  LIVER  ,  957 

the  yoiing  man  still  had  a  somewhat  yellow  complexion,  and  the  liver  was  foimd  to  be 
enlarged.  Dreyfus-Brissac  sent  the  patient  to  Breda  for  a  cure.  On  October  2,  1898, 
a  fresh  attack  of  appendicitis  occurred.  This  time  there  was  also  jaundice,  and 
albumin  was  foimd  in  the  urine.  Hartmann  removed  the  appendix  on  October  14  ; 
on  October  25  the  jaundice  and  the  albumin  had  disappeared. 

In  August,  1903,  in  consultation  with  Segond,  I  saw  a  woman  who  had  had  jaundice 
since  February,  when  she  suffered  from  appendicitis.  The  pain  in  the  right  iliac  fossa 
had  never  completely  disappeared.  An  operation  was  performed,  and  ten  days  later 
the  jaundice  disappeared. 

A  woman  was  in  the  Salpetriere  for  appendicitis  in  February,  1903.  She  remained 
jaundiced  till  Segond  operated  for  appendicitis  three  months  later. 

Description. — This  toxic  jaurdice  may  appear  on  the  second  or  third 
day  of  an  attack  of  appendicitis,  but  we  must  not  expect  to  find  marked 
jaundice.  The  yellow  tint  is  often  slight.  It  is  most  pronounced  in  the 
conjunctivae  and  the  face,  and  it  is  only  in  exceptional  cases  that  it  becomes 
general,  hke  true  jaundice.  The  faeces  remain  coloured.  The  urine  is 
fairly  dark,  and  true  bile  pigments  may  be  found  in  it,  but  most  frequently 
it  contains  only  urobilin  or  brown  pigment.  In  some  cases  the  liver  is 
enlarged. 

The  jaundice  is  not  of  long  duration,  and  quickly  disappears  after 
appendectomy.  Patients  have  been  seen  who  with  each  attack  of  appendi- 
citis had  an  attack  of  jaundice.  Sometimes,  as  we  have  seen  in  the  cases 
quoted  above,  the  colour  remains  for  weeks  and  months,  and  only  disappears 
after  ablation  of  the  appendix.  In  view  of  these  facts,  I  think  that  the  in- 
toxication of  the  liver  consecutive  to  appendicitis  may  play  some  part  in 
the  causation  of  cirrhosis  of  the  liver. 

This  form  of  jaundice  is  sometimes  the  sole  evidence  of  the  appendicular 
toxicity,  but  most  frequently  it  is  associated  with  albuminuria  as  a  second 
sign.  In  patients  suffering  from  appendicitis  we  must  always  look  for 
jaundice  and  albuminuria,  and  the  urine  must  always  be  examined  for 
pigment,  albumin,  and  casts,  because  all  these  signs,  formerly,  and  even  now, 
too  much  neglected,  point  to  the  impregnation  of  the  system  by  the  appen- 
dicular toxines.  They  are  another  argument  in  favour  of  early  intervention, 
so  as  to  remove  the  focus  which  produces  the  poison. 

Jaundice  in  an  individual  with  appendicitis  does  not  simplify  the  diag- 
nosis. As  a  matter  of  fact,  there  are  cases  in  which  the  pain  of  appendicitis, 
though  present  at  McBurney's  point,  may  radiate  as  far  as  the  subhepatic 
region  (ascending  type  of  appendix).  Let  us  suppose  that  in  such  a  case 
the  patient  also  has  slight  jaundice.  The  idea  of  hepatic  colic  will  naturally 
present  itself.  How  are  we  to  make  a  diagnosis  ?  In  the  hepatic  colic  true 
bile  pigments  are  found  in  the  urine,  but  this  is  not  a  pathognomonic  sign, 
because  they  may  also  be  found  in  a|)pendicular  jaundice.  What  is  more  im- 
portant is  that  in  the  case  of  hepatic  colic  the  painful  focus  has  neither  its 
origin  not  its  maximum  intensity  at  McBurney's  point.     In  appendicitis, 


958  TEXT-BOOK  OF  MEDICINE 

even  when  the  pain  radiates  towards  the  hypochondrium,  the  maximum 
intensity  of  the  pain,  the  muscular  resistance,  and  the  h}^er8esthesia  are 
in  the  appendicular  region.  Hepatic  coHc  with  jaundice,  therefore,  will  not 
be  mistaken  for  the  icteric  tint  of  appendicitis. 

From  the  point  of  view  of  prognosis  we  must  always  mistrust  toxic 
jaundice  in  appendicitis,  for  it  is  sometimes  the  prelude  of  a  terrible  general 
mtoxication.  We  find  at  first  slight  jaundice  and  albuminuria,  and  later 
urinary  and  hepatic  insufiiciency,  haematemesis,  nervous  troubles,  and 
death. 

Pathological  Anatomy. — In  a  case  described  more  fully  under  Appen- 
dicular Kidney  I  was  able,  thanks  to  the  kindness  of  Letulle,  to  make  a  histo- 
logical examination.  Sections  of  the  fiver  treated  with  osmic  acid,  after 
fixation  in  10  per  cent,  formalin,  showed  an  accumulation  of  very  fine 
fatty  granules  in  the  interior  of  the  Liver  cells,  especially  near  the  centre  of 
the  lobule.  The  remainder  of  the  trabeculse,  however,  were  not  free  from 
fat.  One  detail  was  interesting  to  note  :  accumulation  of  fat  in  the  endo- 
thelial cells,  which  showed  a  fair  number  of  trabeculse,  and  in  the  interior 
of  the  capillary  vessels  a  large  number  of  leucocytes  charged  with  fatty 
granules.  In  sections  stained  with  haematoxyHn-eosin  the  lobulated  look 
of  the  liver  was  somewhat  remarkable.  This  disposition  was  partly  due 
to  condensation  of  the  periportal  connective  tissue  and  to  some  islets  of 
trabecular  atrophy,  with  pigmentation  of  the  cells,  grouped  around  the 
hepatic  veins  of  average  size.  There  was  no  necrobiosis  in  the  liver 
cells.  In  short,  I  found  in  the  fiver  lesions  of  granulo-fatty  degeneration 
of  the  centro-lobular  hepatic  cells  —  that  is,  lesions  due  to  superacute 
intoxication. 

In  another  case  of  toxic  appendicitis  published  by  Lorrain  the  histo- 
logical lesions  greatly  resembled  those  described  by  Letulle.  Certain  cells 
were  filled  with  very  fine  grains  of  the  colour  of  rust.  "  The  presence  of 
the  ochre  pigment  in  abundance  in  the  cells  of  the  liver  indicates  deep-seated 
trouble,  probably  resulting  from  acute  intoxication." 

In  another  case,  discussed  under  Appendicular  Kidney,  the  histological 
examination  made  by  Nattan-Larriei  proved  that  the  cells  of  the  organ 
were  undergoing  fatty  degeneration. 

2.  Infective  Purulent  Hepatitis. 

Toxic  hepatitis,  as  I  have  said,  occurs  early,  and  is  accompanied  by 
neither  hepatic  pain  nor  violent  symptoms.  Purulent  hepatitis,  due  to 
the  infection  by  the  appendicular  microbes,  is  quite  different.  It  appears 
during  the  decline  or  convalescence  of  appendicitis.  It  is  accompanied 
by  sharp  rigors,  severe  fever,  pains  in  the  hypochondrium,  rapid  increase 


DISEASES  OF  THE  LIVER  959 

in  tlie  size  of  the  liver,  jaundice,  etc.     The  reader  will  get  an  idea  of  it  from 
the  following  cases  taken  from  my  clinical  lectures  :* 

Clinical  Cases. — A  man  came  into  my  wards  on  March  12,  1898,  Tvith  febrile  icterus. 
The  temperature  was  102°  F.  on  admission,  and  reached  104°  F.  the  next  morning  ; 
the  pulse  was  rapid,  and  the  tongue  dry  and  parched  ;  the  yellow  colour  (though  not 
very  intense)  extended  over  the  whole  body  ;  the  urine  was  abundant,  of  a  mahogany 
colour,  fairly  rich  in  bile  pigment,  and  GmeUn's  reaction  gave  a  very  clear  ring  of 
bihrubin  ;  a  cloud  of  albumin  was  also  visible.  The  faeces  were  only  shghtly  coloured, 
but  still  they  had  not  the  whitish,  putty-Uke  appearance  seen  in  obstruction  of  the 
common  bile-duct,  when  the  bile  can  no  longer  reach  the  intestine.  The  case  was, 
therefore,  one  of  true  icterus,  with  high  fever,  and  as  the  patient  was  prostrate,  feverish, 
and  answered  questions  with  difficulty,  we  thought  at  first  of  icterus  gravis. 

Examination  of  the  hver  gave  valuable  information.  The  hepatic  region  formed  a 
bulging  which  extended  as  far  as  the  epigastrium  ;  this  bulging  was  so  marked  that  an 
exploratory  puncture  had  been  made,  without  any  result,  prior  to  the  admission  of  the 
patient,  on  the  hypothesis  that  it  might  be  a  fluid  tumour.  The  hver  was  enlarged, 
very  tender  on  pressure,  and  extended  below  the  false  ribs  by  the  wdth  of  two  fingers. 
The  other  abdominal  and  thoracic  organs  were  healthy,  and  the  entire  disease  seemed 
to  be  confined  to  the  hver.  The  man  told  us  that,  twelve  days  previously,  on 
February  27,  he  had  been  seized  %vith  a  violent  rigor  and  sharp  fever,  which  was  but  the 
prelude  of  many  similar  attacks.  Rigors  and  fever  had  since  recurred  almost  daily, 
without  any  periodicity. 

According  to  the  patient,  acute  hepatic  pain  appeared  with  the  fever ;  this  pain, 
though  less  severe,  was  still  present  ;  the  jaundice  had  come  on  some  days  after  the 
attack  of  fever. 

This  information  led  to  various  suppositions.  The  acute  attacks  of  fever,  the  hejiatic 
pain,  and  the  enlarged  liver  caused  us  to  think  of  suppuration  ;  but  what  could  be  the 
cause  ?  The  hypothesis  of  a  suppurating  hydatid  cyst  was  hardly  hkely,  and,  more- 
over, an  exploratory  puncture  had  been  without  result.  Had  we  to  deal  Avith  a  large 
abscess  of  the  hver,  analogous  to  the  so-called  tropical  "  abscess  "  which  generally 
follows  on  dysenteric  infection  ?  On  the  other  hand,  had  we  to  deal  with  small 
miliary  abscesses  associated  with  suppurative  angiochohtis  ?  The  former  hypothesis 
was  hardly  admissible  in  the  absence  of  any  cause  for  a  large  abscess  in  the  hver.  As 
for  a  large  abscess  from  dysentery  nostras,  its  symptomatology  is  so  masked  that  it 
often  passes  unnoticed.  The  second  hypothesis  was  debatable,  as  the  chnical  picture 
recalled  the  symptoms  of  infective  angiocholitis,  whether  due  to  gall-stones  or  not. 
Angiochohtis,  however,  does  not  cause  so  much  enlargement  of  the  hver  in  a  few  days. 

There  is  a  variety  of  suppurative  hepatitis  which  must  always  be  remembered  in 
these  cases.  I  refer  to  hepatic  abscesses  consecutive  to  appendicitis.  Sharp  attacks  of 
fever,  hepatic  pain,  rapid  increase  in  the  size  of  the  hver  and  icterus,  form  a  syndrome 
which  should  awaken  the  idea  of  hepatic  infection  consecutive  to  infection  of  the 
appendix.  It  became,  therefore,  necessary  to  know  whether  the  patient  had  recently 
had  an  attack  of  acute  appendicitis.  I  say  acute  appendicitis,  because  it  is  only  during 
the  active  pha.so  of  the  closed  cavity  that  such  complications  can  take  place.  On  this 
point  the  patient  rcphed  that  some  ten  days  prior  to  the  attacks  of  fever  he  had  felt  sharp 
abdominal  pain,  which  had  prevented  him  working.  Ho  indicated  the  region  which 
corre.spf)nds  exactly  with  McBurney'a  point.  The  appendicular  pain  had  lasted  only 
a  few  days,  but  it  was  undeniable,  and  had  been  accompanied  by  severe  constipation, 
as  is  customary. 

*  "  Lo  Foio  Appendiculaire,"  "  Abces  du  Foio  Consecutive  k  I'Appendicito " 
(Clinique  Medicate  de  VHotd-Dieu,  10m«  le9on). 


960  TEXT-BOOK  OF  MEDICINE 

We  were,  therefore,  able  to  state  that  the  man  had  at  this  time  an  apparently  benign 
attack  of  appendicitis.  Do  we  not,  however,  know  that  appendicitis  is  never  benign, 
in  the  true  sense  of  the  word  ?  Do  we  not  know  that  the  exaltation  of  virulence  in  the 
closed  cavity,  which  sums  up  the  entire  history  ol  appendicitis,  may  favour  the  emigra- 
tion of  the  pathogenic  microbes  in  all  directions,  and  thus,  by  means  of  the  lymphatics 
and  veins,  give  rise  to  remote  infections,  the  most  terrible  of  which  undoubtedly  is 
hepatic  infection  ?  In  consequence  I  diagnosed  purulent  infection  of  the  hver,  following 
appendicitis,  and  gave  a  fatal  prognosis. 

During  the  month  that  this  patient  was  in  my  ward  we  counted  fourteen  severe 
attacks  of  fever,  the  temperature  reaching  105°  F.,  and  the  attacks  being  preceded  by 
violent  rigors.  In  a  short  time  the  Uver  formed  an  enormous  abdominal  tumour, 
which  was  hard  and  smooth.  The  jaimdice  improved  at  times,  and  the  faeces  became 
more  or  less  coloured.  The  hepatic  region  was  painful,  the  pain  radiating  to  the 
abdomen  and  thorax.  Eespiration  became  difficult,  and  the  rales  due  to  pulmonary 
oedema  were  heard  at  the  base  of  the  chest,  especially  on  the  right  side. 

On  March  31  facial  erysipelas  broke  out,  and  disappeared  in  a  few  days.  During 
the  last  days  of  the  disease  the  hver  was  still  enlarged ;  the  jaundice  had,  so  to  say, 
disappeared ;  the  belly  was  much  distended ;  and  the  stools  were  loose,  foetid,  and 
almost  colourless.  The  patient  sank  into  a  typhoid  state.  He  died  with  a  temperature 
of  104°  F.  four  weeks  after  his  admission,  and  less  than  six  weeks  after  the  start  of  the 
hepatic  infection.  The  appendicitis,  which  was  the  cause  of  the  fatal  complications, 
was  two  months  old. 

As  far  as  the  treatment  was  concerned,  I  had  not  thought  of  surgical  intervention, 
because  surgery  is  practically  powerless  in  multiple  abscesses  due  to  appendicular 
infection  of  the  Uver.     A  single  abscess  is  absolutely  imique. 

The  post-mortem  examination  confirmed  the  diagnosis.  The  Uver  weighed 
100  ounces.  Its  surface  showed  at  various  points  yellowish  or  brownish  projections. 
At  first  sight  the  specimen  might  have  been  taken  for  secondary  cancer.  The  con- 
sistency of  the  organ  was  soft.  Sections  of  the  lobe  revealed  abscesses  everywhere, 
the  gland  being  riddled  with  them.  From  150  to  200  abscesses,  varying  in  size  from 
a  pin's  head  to  an  egg,  might  certainly  have  been  counted,  and  there  was  also  an  abscess 
of  the  size  of  an  orange  in  the  right  lobe.  Some  were  just  beneath  GUsson's  capsule, 
others  were  deeply  seated  in  the  parenchyma.  They  contained  fairly  thick  pus,  without 
foetid  odour,  the  colour  varying  from  yellow  to  green.  These  abscesses  were  mostly 
independent,  and  were  separated  by  septa  of  healthy  or  altered  hepatic  tissue,  but 
they  had  no  proper  walls.  Other  abscesses  communicated  with  one  another,  forming 
large  anfractuous  cavities.  On  section  a  fair  number  of  these  abscesses  had  a  spongy, 
areolar  aspect,  whence  the  name  areolar  abscesses  of  the  liver  (Chauffard). 

The  extrahepatic  bile-ducts  were  healthy  and  permeable,  and  such  was  also  the 
case  with  the  trimk  of  the  portal  vein.  The  organs  of  the  abdomen  were  absolutety 
normal,  and,  except  for  a  few  perihepatic  adlaesions,  we  found  no  peritoneal  lesion  and 
no  ascites  ;  nothing  in  the  spleen  ;  nothing  in  the  intestine. 

The  appendix  was  surrounded  by  false  membranes,  which  increased  its  size  threefold 
by  uniting  it  to  the  posterior  surface  of  the  caecum  and  to  the  front  of  the  psoas.  Dis- 
section of  the  adhesions,  so  as  to  isolate  the  appendix,  revealed  a  small  peri -appendicular 
abscess,  containing  about  a  teaspoonful  of  sUghtly  foetid  pus.  The  veins  at  the  base 
of  the  appendix  were  so  enlarged  as  to  form  a  prominent  varicose  network,  which,  after 
enveloping  the  appendix,  spread  over  the  caecum,  where  it  blended  with  the  mesenteric 
veins. 

I  have  never  seen  such  a  venous  network  in  a  case  of  appendicitis  ;  it  is  probable 
that  it  only  acquires  such  a  development  in  the  case  of  venous  infection.  The  appendix 
was  not  perforated,  but  the  mucosa  was  ulcerated  at  three  or  four  points,  and  towards  the 
tip  there  was  a  very  small  abscess.     Let  us  next  consider  the  histological  lesions  and 


DISEASES  OF  THE  LIVER 


961 


the  bacteriological  examination.  The  pus  from  the  small  peri-appendicular  abscess 
gave  a  pure  culture  of  coU  bacillus.  The  veins  of  the  cellular  coat  of  the  appendix  were, 
in  a  large  number  of  instances,  attacked  by  endophlebitis  and  periphlebitis. 

Several  of  these  veins  were  filled  -with  thrombi,  formed  in  j^art  by  endotheUal  cells 
and  fibrous  tissue.  By  the  side  of  these  thrombosed  veins,  especially  under  the  serous 
membrane,  very  dilated  veins,  which  contributed  to  form  the  appendicular  i)lexus,  were 
found.  Microbes  were  present  in  the  walls  of  the  thrombosed  veins,  and  in  the  inflamed 
tissue  roimd  them. 

The  microbes,  after  leaving  the  closed  cavity,  became  engaged  in  the  appendicular 
veins,  giving  rise  to  phlebitisand  thrombosis,  andreached  the  liver  through  the  portal  vein. 


Fig.  57. — Formation  of  Abscess  in  LivjiK,  .St*  undary  to  Appendicitis. 

After  reaching  the  hver,  they  followed>the  course  of  the  portal  veins — that  is  to  say, 
they  occupied  the  periphery  of  the  hepatic  lobules.  It  was,  therefore,  around  the  lobules 
that  the  infection  of  the  liver  had  commenced.  The  microbes  swarmed  there,  and 
embryonic  cells  sheathed  the  portal  vein  like  a  sleeve. 

The  process  gradually  extended,  and  in  the  end  the  liver  was  transformed  into  a 
sort  of  purulent  honeycomb. 

Summary.— In  this  case  it  was  possible  to  follow  the  organisms  in  their  migration 
from  the  a^ipendix  to  the  liver.     When  we  remember  that  hundreds  of  abscesses  were 


Fig.  58. 
L,  normal  lobule;  vp,  portal  vein  (normal) ;  a,  h,  c,  abscess  in  various  stages. 

formed  in  the  hv(!r  in  a  few  weeks,  the  virulence  of  the  microlies  will  be  understood. 
The  exaltation  of  the  virulence,  acquired  in  tlie  focus  of  the  appendix,  allowed  tho 
microbic  colonics  to  pass  througli  tlie  aj^pcndicular  veins,  to  follow  tho  Ijlood-stream 
as  far  as  the  portal  vein,  vena  porta  malorum,  and  rush  forward  in  infecting  columns  to 
the  conquest  of  tho  Hver. 

Such  is  the  hepatic  infection.  Tiiis  complication  of  appendicitis,  whicli  dilTcrs  from 
toxi(!  hepatitis,  is  far  from  being  rare.  Bcrtholin  has  collected  twenty-eight  cases  in  his 
thesia 

01 


962  TEXT-BOOK  OF  MEDICINE 

Description. — Events  usually  run  the  following  course  :  An  individual, 
either  a  child  or  an  adult,  is  attacked  with  severe  or  slight  appendicitis. 
The  physician  commences  to  investigate  carefully  the  area  in  which  the  pain 
has  first  shown  itself.  Palpation,  pressure,  muscular  resistance,  and  hyper- 
sesthesia  show  that  the  painful  spot  is  at  the  centre  of  a  line  drawn  from  the 
umbilicus  to  the  anterior  superior  iliac  spine.  Although  the  belly  may  be 
sensitive  in  other  regions,  it  is  here  that  the  pain  commences  and  reaches 
its  maximum.  He  inquires  as  to  the  onset  of  the  disease,  and  learns  that 
the  patient  was  in  a  state  of  perfect  health  when  he  experienced  the  first 
symptom.  At  that  time,  or  a  little  later,  attacks  of  nausea,  and  per- 
haps of  vomiting,  supervened.  The  diagnosis  of  appendicitis  is  clearly 
established,  and  the  doctor  explains  how  even  slight  appendicitis  exposes 
the  patient  to  the  greatest  dangers,  and  mentions  the  many  cases  where 


i  <m 


#   '■S^'t^ 


Fio.  59. — Invasion  of  Liver  by  the  Micro-orgaistisms  at  a. 

appendicitis,  looked  upon  as  almost  a  negligible  quantity,  has  been  followed 
later  by  peritonitis  or  suppurative  infection  of  the  liver  or  of  the  pleura,  etc., 
and  in  order  to  avoid  such  a  dire  result,  he  insists  on  an  operation. 

If  the  doctor  is  a  believer  in  the  erroneous  doctrine  "  that  there  is  time 
enough  to  see  how  things  will  develop,"  as  the  condition  of  the  patient 
appears  to  be  so  little  alarming,  the  fever  is  so  mild,  and  the  belly  is  so 
little  swollen  ;  if  he  remains  satisfied  with  an  approximate  diagnosis ;  or 
if  he  only  sees  in  the  case  typhlitis  or  typhlo-colitis,  which  in  a  few  days  will 
yield  to  purgatives,  appHcations  of  ice,  and  injections  of  morphia,  he  will 
consider  the  case  benign,  and  will  reject  surgical  intervention.  As  a  matter 
of  fact,  a  few  days  afterwards  convalescence  sets  in,  and  seems  to  justify 
the  treatment.  He  proclaims  aloud  that  it  is  wrong  to  hand  over  people 
to  the  surgeon  when  they  are  suffering  from  appendicitis  and  are  simply  in 
need  of  medical  treatment.  The  triumph  is,  however,  of  short  duration. 
During  the  few  days  when  the  patient  is  seemingly  recovering,  the  infec- 
tion is  silently  continuing  its  course,  and  the  pathogenic  microbes,  starting 
from  the  appendix,  and  armed  with  terrible  virulence,  have  already  reached 


DISEASES  OF  THE  LIVER  963 

the  liver.  After  a  silent  phase  of  incubation  the  severe  symptoms  of 
infection  of  the  liver — namely,  sharp  attacks  of  fever,  hepatic  pain,  rapid 
enlargement  of  the  organ,  and  jaundice — appear.  The  mischief  makes  speedy 
headway,  and  in  a  week  or  two  the  patient  succumbs.  Let  us  never  forget 
that  the  fatal  consequences  of  appendicitis  are  by  no  means  always  in  rela- 
tion to  the  intensity  of  the  symptoms.  I  have  discussed  this  question 
under  Appendicitis,  and  quoted  cases  of  patients  apparently  suffering  from 
slight  appendicitis,  and  yet  an  operation  performed  thirty  hours  after  the 
appearance  of  the  disease  revealed  gangrene  of  the  appendix  and  peritonitis, 
which  would  have  been  fatal  if  the  operation  had  been  postponed. 

Similar  considerations  are  applicable  to  hepatic  infection  following  on 
appendicitis.  The  appendicular  phase  is  sometimes  very  acute  and  painful, 
but  at  other  times  it  may  be  fairly  sHght,  and  so  escape  the  notice  of  an 
inexperienced  observer.  We  have  seen  the  small  space  occupied  by  this 
appendicular  phase  in  my  patient,  who  suffered  so  little  discomfort  that  he 
had  only  stopped  work  for  a  few  days,  and  yet  the  consequences  were  to 
be  fatal.  Hepatic  infection  may  supervene  in  any  case  of  appendicitis, 
whether  the  appendix  is  or  is  not  perforated  and  whether  peritoneal  or 
peri-appendicular  lesions  are  present  or  absent.  It  is  not  the  extra-appen- 
dicular  lesions  which  constitute  the  danger.  The  whole  danger  comes  from 
the  closed  cavity  where  the  toxi-infection  gathers  strength. 

We  find  here  a  new  application  of  this  exaltation  of  virulence  in  the 
closed  cavity,  which  has  been  so  clearly  proved  by  experiment,  and  which 
has  enabled  me  to  explain  the  whole  history  of  appendicitis.     It  is  in  the 
closed  cavity  that  the  microbes  acquire  the  increase  of  virulence  and  the 
power  of  expansion,  enabling  them  to  traverse  the  walls  of  the  appendix 
and  establish  themselves  in  the  peritoneum,  even  though  the  walls  are  not 
perforated.     It  is  likewise  the  increase  of  virulence  and  the  power  of  expan- 
sion acquired  in  the  closed  cavity  which  facilitate  the  migration  of  the 
microbes  through  the  bloodvessels,  and  enable  them  to  cause  fatal  remote 
infection.    Hepatic  infection  is  one  of  these  remote  infections  peculiar  to 
appendicitis.     The  microbes — coli  bacilli  and  others — by  virtue  of  their 
increased  virulence,  enter  the  appendicular  veins,  and  reach  the  great  mesen 
teric  vein,  the  portal  vein,  and  the  liver.     In  some  cases,  as  in  my  patient 
the  infected  veins  form  a  varicose  network.     Some  small  veins  are  throm 
bosed  ;  others  are  not.     Phlebitis  sometimes  affects  the  larger  venous  trunks 
such  as  the  great  mesenteric  vein,  which  receives  the  appendicular  veins 
and  even  the  trunk  of  the  portal  vein,  which  starts  from  the  mesenteric 
vein. 

I  would  remind  the  reader  how  this  hepatic  infection  announces  itself. 
The  patient  has  been  suffering  from  appendicitis,  and  it  matters  little  whether 
the   attack   has   been   severe  or  mild.      Sometimes,   indeed,   an  operation 

Gl— 2 


964  ■         TEXT-BOOK  OF  MEDICINE 

has  been  performed  (too  late),  and  the  patient  is  on  the  highroad  to  con- 
valescence. And  yet  rigors,  temperature  rising  to  104°  F.,  and  profuse 
sweats  open  the  scene.  The  attacks  return  daily,  and  the  fever  is  con- 
tinuous. The  attacks  of  fever  are  accompanied  by  hepatic  or  epigastric  pain, 
jaundice,  gastric  intolerance,  and  vomiting.  These  symptoms  are  accom- 
panied by  rapid  swelling  of  the  liver,  which  may  become  enormous.  The 
spleen  remains  normal.  Diarrhoea  is  as  frequent  as  constipation.  In  one  of 
my  cases  it  was  exceedingly  profuse.  Jaundice  may  be  early  or  late,  slight 
or  intense.  The  general  symptoms  are  those  of  the  typhoid  state.  The 
pulse  is  quick,  the  tongue  is  dry  and  red,  and  the  attacks  of  fever  persist 
for  one  or  two  weeks.  Sometimes  the  fever  improves,  and  there  is  a  tem- 
porary remission,  but  in  the  end  the  patient  succumbs  in  a  state  of  adynamia, 
collapse,  or  syncope,  or  with  symptoms  of  icterus  gravis,  multiple  haemor- 
rhages, albuminuria,  and  anuria. 

The  hepatic  infection  is  always  consecutive  to  the  acute  phase  of  appen- 
dicitis. It  is  not  to  be  feared  when  the  active  process  of  appendicitis  has 
been  extinct  for  some  time.  On  the  other  hand,  I  do  not  know  of  a  single 
example  where  hepatic  infection  supervened  quickly  during  the  early  stage 
of  appendicitis.  The  migration  of  the  microbes  into  the  veins  of  the 
appendix  never  commences — at  least,  so  I  believe — before  the  fifth  or  sixth 
day.  Surgery  has,  therefore,  ample  time  to  intervene  before  the  commence- 
ment of  the  appendiculo-portal  migration. 

This  hepatic  infection  is  one  of  the  most  terrible  complications  of  appen- 
dicitis, because  I  am  only  acquainted  with  two  cases  of  recovery  (Kcerte, 
Loison).  The  operation  was  successful  because,  extraordinary  to  relate, 
there  was  a  solitary  hepatic  abscess.  In  Loison's  case  radioscopy  gave 
considerable  support  to  the  diagnosis.  Summary :  Except  in  very  rare 
cases,  medicine  and  surgery  are  powerless  to  avert  the  evil  once  it  has 
declared  itself.  As  a  matter  of  fact,  however  successful  the  surgeon  may 
be  in  solitary  abscess  of  the  liver,  intervention  is  hopeless  in  appendicular 
infection,  where  abscesses  of  the  liver  are  almost  always  counted  by  dozens. 
What  a  lesson,  however,  for  those  who  say  that  we  must  only  perform 
interval  operations  !  Once  again  I  protest  against  such  an  assertion.  In 
appendicitis  we  must  never  wait,  for  we  can  never  know  what  the  future 
has  in  store  for  us. 


XX.  GALL-STONES. 

Structure  and  Formation  of  Gall-Stones. — The  production  of  gall- 
stones is  one  of  the  most  common  troubles  in  the  human  race  (Cruveilhier). 
They  may  be  formed  in  the  intra-  or  extrahepatic  ducts,  or  in  the  liver, 
but  the  gall-bladder  is  the  most  common  situation. 


DISEASES  OF  THE  LIVER  965 

Biliary  concretions  of  all  sizes  are  found  in  the  gall-bladder,  from  gravel 
to  calculi  larger  than  an  egg.  They  may  be  solitary,  multiple,  or  indefinite 
in  number.  The  solitary  calculus  has  no  facets,  and  may  be  oval  or  pear- 
shaped.  Multiple  calculi  are  rounded  or  pyramidal  and  faceted  from  the 
rubbing  and  pressure  of  neighbouring  calculi.  They  are  elongated  when 
they  have  been  long  in  the  common  duct.  Their  colour  is  brown,  greenish- 
yellow,  or  blackish.  It  is  whitish  in  the  case  of  calculi  of  cholesterin. 
Their  density,  though  low,  is  greater  than  that  of  water.  Wlien  they  have 
not  been  dried,  their  structure  varies,  according  as  they  are  simple  or  com- 
pound. The  compound  calcali  have  a  nucleus  and  a  crust.  The  nucleus 
is  formed  of  bile  pigment,  chalk,  epithelial  cells,  and  rarely  foreign  bodies.  It 
is  surrounded  by  a  middle  radiating  layer,  in  which  crystals  of  cholesterin 
predominate.  The  crust  is  stratified  and  composed  of  cholesterin,  bile 
pigment,  or  chalk.  Calculi  without  a  crust  may  be  met  with.  Others, 
again,  called  simple  calculi,  are  homogeneous  throughout  their  whole  thick- 
ness. The  calculi  contained  in  the  same  gall-bladder  are  identical  as  regards 
structure,  colour,  and  chemical  composition.  Agglomerated  and  frag- 
mented calculi  are  found.  The  consistency  of  the  biliary  concretions  is 
moderate,  and  the  most  resistant  ones  are  fonned  of  pure  cholesterin.  The 
calculi  are  free  in  the  bladder.  They  may  sometimes  be  adherent  to  the 
wall.  They  are  then  let  into  the  walls  of  the  gall-bladder  which  have 
become  alveolar,  as  Terrier  observed  when  performing  cholecystotomy. 
The  chief  components  of  gall-stones  are  crystalline  or  amorphous  chole- 
sterin, and  next  the  colouring  matters  of  the  bile  and  the  calcareous  salts. 
It  is  curious  to  note  that  cholesterin  and  chalk,  which  are  found  in  very 
small  quantities  in  the  bile  as  compared  with  the  other  elements,  form  the 
chief  constituent  parts  of  the  calculus.  Thus,  cholesterin,  on  an  average, 
forms  70  per  cent,  of  the  constituent  parts  of  the  calculus,  whilst  the  bile 
barely  contains  2  per  cent.  The  salts  of  potassium  and  of  sodium,  which 
alone  form  some  calculi,  are  found  in  very  small  quantities  in  the  bile. 
Throughout  the  whole  thickness  of  the  calculi  there  is  a  kind  of  organic 
albuminoid  web,  which  indicates  the  participation  of  the  mucosa  in  the 
formation  of  calculi. 

The  exact  manner  in  which  the  stones  are  formed  is  still  imperfectly 
known.  The  substances  contained  in  the  bile  must  be  precipitated  and 
agglomerated,  and  nmst  be  ke])t  agglomerated.  It  is  supjwsed  that  chalk  is  a 
product  of  the  secretion  of  the  gall-hladder  (see  Catarrh  of  the  Gail-Bladder). 
Catarrh  of  the  gall-bladder  is  said  to  have  the  power  of  acidifying  the  bile, 
and  the  acidity  of  the  bile  is  said  to  split  up  the  bile  salts ;  by  the  dissolution 
of  the  salts,  cholesterin  and  bilirubin  are  set  free  and  precipitated— the 
former  in  a  crystalline  form  ;  the  latter  either  in  a  crystalline  form  or  mixed 
with  the  chalk. 


966  TEXT-BOOK  OF  MEDICINE 

It  is  admitted  tliat  microbic  infection  plays  an  important  part  in  the  pro- 
cess, by  favouring  cholecystitis,  altering  the  composition  of  the  bile,  and 
contributing  to  the  formation  of  the  nuclei.  It  may,  perhaps,  be  that 
typhoid  fever  and  other  infectious  diseases  which  affect  the  gall-bladder 
are,  by  reason  of  the  microbes,  the  remote  origin  of  biliary  calculi  (Dupre). 
Dufour  was  able  to  collect  fourteen  cases  of  patients  of  various  ages  who 
had  hepatic  colic  some  months  after  an  attack  of  typhoid  fever,  while  they 
had  had  no  symptoms  of  gall-stones  prior  to  the  fever.  Several  writers  accept 
this  pathogenesis  of  biliary  lithiasis  (Chiari,  Gilbert),  and  Hanot  thus  sums 
up  the  question  :  "  If  the  intestinal  catarrh  spreads  to  the  biliary  passages 
and  becomes  lithogenous  catarrh — that  is,  if  the  micro-organism  of  typhoid 
fever  is,  after  all,  capable  of  causing  biliary  lithiasis — the  question  of  a 
microbic  origin  is  settled.  It  would,  then,  remain  to  be  decided  which 
microbes,  other  than  those  of  typhoid  fever,  intervene.  It  may  be  possible 
that  every  microbe,  from  the  very  fact  that  it  swarms  in  the  bile-ducts, 
causes  chemical  changes  leading  to  the  deposit  of  the  mineral  principles. 
Thus,  Galippe  actually  saw  the  formation  of  crystals  of  carbonate  of  lime 
in  saliva  placed  in  a  flask,  around  masses  of  micro-organisms  which  were 
growing  therein." 

"  Biliary  lithiasis  would,  then,  result  from  the  mode  of  penetration  of  the 
micro-organisms  into  the  bile-ducts,  from  their  greater  or  smaller  number, 
and  particularly  from  the  constitution  of  the  mucus,  which  is  more  or  less 
readily  deposited.  If  this  last  theory  is  true,  the  soil  is  more  important 
than  the  seed,  and  biliary  lithiasis  would  no  longer  be  an  accidental 
phenomenon,  but  would  remain  the  expression  of  a  previous  state  of 
the  organism,  of  a  hereditary  or  congenital  modification,  totius  suhstantice 
— that  is,  of  a  diathesis."  My  ideas  agree  absolutely  with  those  ex- 
pressed by  Hanot — that  the  diathesis  is  the  factor  in  the  pathogenesis  of 
lithiasis. 

i^tiology. — Biliary  lithiasis  is  more  frequent  in  women  ;  it  is  most  prone 
to  occur  in  heavy  eaters,  in  fat  people  who  take  Httle  exercise,  and  in  indi- 
viduals past  middle  life.  Often,  says  Trousseau,  the  real  causes  of  the 
disease  escape  us,  and  a  clear  point  is  that  these  causes,  no  matter  what 
they  be,  are  dominated  by  a  predisposition  special  to  the  individual.  As  a 
matter  of  fact,  biliary  lithiasis  is  often  associated  with  the  diathetic  condi- 
tions that  form  a  part  of  the  group  of  arthritic  diseases — migraine,  gout, 
or  rheumatism,  urinary  lithiasis,  obesity,  asthma,  diabetes,  and  eczema — 
which  have  been  described  by  Bouchard  in  his  work  on  "  Les  Maladies  par 
Kalentissement  de  la  Nutrition."  Urinary  lithiasis  is  closely  related  to 
hepatic  lithiasis,  and  these  two  manifestations  may  occur  successively  in 
the  same  individual,  or  exist  simultaneously  in  one  family,  where  they  are 
hereditary.     The  same  remark  applies  to   appendicular  lithiasis,  and  the 


DISEASES  OF  THE  LIVER  967 

numerous  cases  quoted  under  Appendicitis  show  that  hepatic,  intestinal, 
renal,  and  appendicular  Hthiasis  belong  to  the  same  pathological  family. 
After  the  diathetic  causes,  or  side  by  side  with  them,  come  infections  of 
microbic  origin,  as  I  have  mentioned  above. 

Pregnancy— Puerperal  Condition.— Pregnancy  plays  a  large  part  in 
biliary  hthiasis.  I  have  devoted  a  chnical  lecture  to  this  question.*  Hepatic 
coUc  is  frequent  in  pregnant  women.  In  a  comprehensive  work,  the  first 
which  has  appeared  on  the  subject,  Huchard  has  pubhshed  several  cases. 
The  cases  of  Depaul,  Tarnier,  and  Pinard  are  positive  evidence.  I  have 
reported  several  cases.  According  to  Leyden's  statistics,  in  one  hundred 
cases  of  women  suffering  from  hepatic  colic,  concomitant  or  anterior  preg- 
nancy has  been  noticed  in  ninety  of  them.  Authorities  are  not  absolutely 
agreed  as  to  what  period  of  the  puerperal  state  is  most  favourable  to  the 
appearance  of  hepatic  cohc.  Some  maintain  that  it  is  during  pregnancy ; 
others  that  it  is  during  accouchement.  Cyr  has  published  the  following 
statistics  :  In  fifty-one  women  with  gall-stones,  hepatic  cohc  has  been  noticed 
eleven  times  during  pregnancy,  four  times  after  miscarriage,  and  thirty-six 
times  after  accouchement.  The  period  between  the  accouchement  and  the 
attack  of  cohc  varied  from  one  day  to  a  month  in  twenty-two  cases,  and  from 
one  to  twelve  months  in  fourteen  cases.  In  the  statistics  sent  me  by  Bou- 
loumie,  of  Vittel,  hepatic  cohc  figures  as  follows  :  twenty-two  times  during 
pregnancy,  and  fifty-five  times  from  a  day  to  a  year  after  accouchement. 
In  the  statistics  forwarded  to  me  by  Deleage,  of  Vichy,  hepatic  colic  figures 
as  follows  :  fifty-nine  times  during  pregnancy,  and  forty-five  times  after 
accouchement. 

Whether  hepatic  colic  appears  during  pregnancy  or  after  delivery,  it  is 
none  the  less  true  that  the  puerperal  condition  has  a  great  influence  in  the 
pathogenesis  of  biliary  Hthiasis.  Hepatic  colic  appears  in  various  ways. 
First  variety  :  A  young  girl  who  has  never  had  hepatic  colic  marries  ;  during 
her  first  pregnancy  hepatic  colic  appears,  and  reappears  during  subsequent 
pregnancies ;  but  never  apart  from  the  puerperal  condition.  Second  variety  : 
A  woman  who  has  never  had  hepatic  colic,  either  as  a  girl  or  later  during 
pregnancy,  is  seized  with  hepatic  colic  some  days  or  weeks  after  delivery. 
The  colic  recurs  after  subsequent  deliveries,  and  is  never  present  except  at 
this  time.  Third  variety  :  Hepatic  colic  appears,  either  during  pregnancy 
or  after  labour,  and  again  later,  at  indeterminate  periods,  when  the  woman 
is  not  pregnant. 

Hepatic  colic  during  pregnancy  or  after  delivery  does  not  differ  from 

the  ordinary  form.     The  diagnosis  is  generally  easy  ;  nevertheless,  when  it 

a))pears  during  pregnancy,  it  may,  for  want  of  clear  symptoms,  be  mistaken 

*  "  La  Grossesse  et  les  Lithiasea "  {Clinique  Mediccde  de  VHUel-Dieu,  1898, 
If)""-  10900). 


9G8  TEXT-BOOK  OF  MEDICINE 

for  a  miscarriage.     When  it  appears  after  delivery,  it  may,  for  want  of  atten- 
tion, be  loolced  upon  as  commencing  peritonitis. 

Many  theories  exist  regarding  the  occurrence  of  biUary  lithiasis  during 
pregnancy.  Pregnancy  is  said  to  favour  stagnation  of  bile  in  the  bile-ducts, 
and,  as  a  consequence,  the  formation  of  calculi.  It  has  been  said  that  preg- 
nancy favours  mobility  of  the  kidneys  and  liver.  On  account  of  the  flaccidity 
of  the  abdominal  walls,  the  gall-bladder,  since  its  means  of  fixation  have 
been  relaxed,  tends  to  swing  backwards,  and  the  common  bile-duct  being 
dragged  on  by  this  swinging  movement,  becomes  narrowed ;  this  narrowing 
favours  stagnation  of  the  bile  in  the  gall-bladder.  Pregnancy,  according  to 
Heidenhain,  is  also  said  to  provoke  stagnation  of  the  bile,  by  hindering  the 
play  of  the  diaphragm,  especially  as  the  corset  fixes  the  costal  insertions  of 
the  muscle.  This  pathogenesis  might  be  classified  under  the  mechanical 
causes,  but  the  chemical  causes  (malnutrition),  the  bacteriological  causes 
(action  of  the  microbes  in  forming  calculi),  and  the  constitution  of  the 
patient  (arthritism,  heredity),  have  also  to  be  considered.  All  these  theories 
are  possible,  but  not  one  seems  to  me  to  be  sufficient.  The  undeniable 
clinical  fact  is  that  the  puerperal  condition  exercises  a  considerable  influence 
on  the  pathogenesis  of  gall-stones. 

After  having  shown  the  influence  of  pregnancy  on  the  pathogenesis  of 
hepatic  colic,  let  us  invert  the  question  and  inquire  what  influence  hepatic 
colic  may  have  on  pregnancy  and  the  sequelae  of  labour.  The  prognosis  in  preg- 
nancy is  scarcely  affected  by  hepatic  colic ;  severe  and  repeated  attacks  of  colic 
do  not  interrupt  it.  The  jaundice  which  in  many  cases  follows  hepatic  coUc 
is  not  dangerous  to  the  pregnant  woman  ;  it  is  merely  jaundice  by  retention, 
which  habitually  ceases  a  few  days  after  the  colic,  and  does  not  injure  the 
cells  of  the  liver.  If,  however,  it  lasts  too  long,  as  in  permanent  obliteration 
of  the  common  duct,  the  normal  activity  of  the  cell  may  suffer,  and  for- 
midable mischief  may  ensue.  Hepatic  colic  and  jaundice  do  not,  as  a  rule, 
render  the  prognosis  serious,  either  in  the  pregnant  woman  or  the  recently 
delivered  woman.  And  though  jaundice  due  to  a  stone  is  not,  as  a  rule, 
dangerous  in  the  pregnant  woman,  this  is  not  the  case  in  the  other 
varieties  included  under  infective  jaundice.  It  matters  little  what  theory 
is  formulated  to  explain  the  affection  of  the  hepatic  cell.  As  soon  as  the 
cell  participates  in  the  toxic  process,  it  undergoes  a  change  which  under 
other  circumstances  might  not  have  serious  consequences,  but  which  in 
the  gravid  condition  is  always  to  be  feared.  Jaundice  supervening  in  a 
pregnant  woman,  therefore  (I  speak  of  jaundice  apart  from  hepatic  colic), 
is  always  a  suspicious  symptom,  because  it  points  to  possible  hepatic 
insufficiency,  with  all  its  consequences.  This  question  will  again  be  re- 
ferred to  under  Jaundice,  when  we  shall  consider  the  relations  betw^een 
pregnancy  and  infective  jaundice. 


DISEASES  OF  THE  LIVER  969 

Symptoms  and  Complications  of  Gail-Stones. — In  some  cases  (in  old 
people  particularly)  gall-stones  cause  no  symptoms.  At  a  post-mortem 
examination  it  is  by  no  means  rare  to  l&nd  a  calcified  and  enlarged  gall- 
bladder, containing  numerous  calculi,  in  people  who  have  shown  none  of 
the  symptoms  of  gall-stones.  More  frequently,  however,  the  stones  cause 
various  troubles  and  more  or  less  grave  complications,  divisible  into  several 
groups  : 

1.  Migration  of  the  calculi  into  the  large  bile-ducts — hepatic  colic. 

2.  Migration  and  arrest  of  the  calculi  in  the  intestine — obstruction  of 
the  pyloric  orifice. 

3.  Persistent  obHteration  of  the  large  ducts.— biliary  cirrhosis. 

4.  Infection  of  the  ducts — angiocholitis,  cholecystitis,  hepatitis,  endo- 
carditis. 

5.  Passage  of  the  calculi  outside  the  natural  passages — perforation  of 
the  gall-bladder  and  bile-ducts,  peritonitis,  biliary  fistulse. 

1.  Hepatic  Colic. 

Anatomy. — Hepatic  colic  is  the  most  common  complication  of  gall-stones.  In  order 
ta  understand  the  mechanism,  it  will  be  well  to  mention  certain  anatomical  facts  con- 
cerning the  ducts  through  which  the  calculus  has  to  pass. 

In  the  normal  condition  the  gall-bladder  contains  about  2  ounces  of  bile,  but  its 
walls  are  capable  of  such  distension  that  it  may  contain  more  than  2  pints  without 
rupture.  The  gall-bladder  ends  in  a  neck,  which  is  very  flexible,  and  is  continuous 
with  the  cystic  duct.  The  neck  of  the  bladder  presents  a  swelling,  or  pelvis.  In  an 
opened  bladder  we  see  that  this  swelling  is  limited  above  by  a  valve,  which  considerably 
narrows  the  orifice,  and  below  by  a  second  and  less  important  valve.  The  gall-bladder 
is  contractile,  and  possesses  muscular  fibres,  forming  a  muscularis  mucos;e,  which 
becomes  hypertrophied  in  biliary  lithiasis.  The  mucosa  shows  both  temporary  and 
permanent  folds.  The  former  disappear  as  soon  as  the  bladder  is  sufficiently  distended  ; 
the  latter  anastomose,  and  circumsci'ibe  areola?  of  various  forms. 

The  cystic  duct  is  the  continuation  of  the  neck  of  the  gall-bladder.  It  is  nearly 
2  inches  long  and  ^  inch  in  diameter  ;  it  opens  into  the  common  duct.  On  opening  the 
cystic  duct  we  .see  that  its  internal  walls  show  projections  (the  semilimar  valves  of 
Heister),  which  prevent  the  migration  of  calculi.  The  common  duct  is  formed  by  the 
fusion  of  the  cystic  and  hepatic  ducts.  It  is  .3  inches  long  and  about  ^  inch  in 
diameter  ;  it  opens  into  the  duodenum  at  Vater's  ampulla,  in  common  -WTth  the  pancreatic 
duct.  The  common  duct  is  not  provided  with  valves,  but  at  its  entrance  inl^  Vater's 
ampulla  it  possesses  a  sphincter,  composed  of  muscle  fibres.  As  a  matter  of  fact,  tlio 
real  opening  is  situated  at  the  duodennl  opening  of  Vater's  ampulla,  and  at  (his  point 
there  is  a  very  marked  constriction,  which  is  a  final  obslaolo  to  the  calculi  coming  from 
the  bladder.  The  cystic  and  common  ducts  possess  longitudinal  muscle  fibres,  which 
disappear  late  in  life.  Thoy  are  capable  of  such  distension  that  they  may  allow  the 
passage  of  calculi  as  big  as  a  hazel-nut.  The  common  duct  when  distended  mr\y  bo  as 
large  as  a  coil  of  bowel. 

Hepatic  Colic. — The  contraction  of  the  gall-bladder,  bile-duct,  and  abdo- 
minal musck's  causes  a  calculus  to  (Migage  in  the  cystic  duct.  If  the  stone 
is  neither  large  nor  angular,  it  will  pass  through  the  cystic  and  conimoi^  ducts 


970  TEXT-BOOK  OF  MEDICINE 

into  the  intestine  without  causing  colic  ;  if  the  stone  is  larger  than  the 
lumen  of  the  bOe-ducts,  it  produces  in  its  migration  the  symptom- complex 
of  hepatic  cohc. 

In  the  struggle  between  the  calculus  and  the  ducts,  the  former  is  pushed 
onwards,  but  causes,  in  its  migration,  spasm  and  contraction  of  the  latter. 
It  meets  with  numerous  obstacles  to  its  passage  :  in  the  cystic  duct,  which 
is  of  small  calibre,  it  must  pass  a  series  of  valves  ;  and  in  the  common  duct, 
which  is  larger,  it  meets,  at  the  last  moment,  with  the  narrow  orifice  of 
Vater's  ampulla.  Hepatic  colic  appears  most  frequently  a  few  hours  after 
a  meal,  "post  frandium,  probably  because  at  this  moment  the  gaU-bladder 
contracts,  in  order  to  empty  the  bile  into  the  intestine.  The  onset  is  sudden, 
and  the  subject  complains  of  sharp  pain,  radiating  in  several  directions  :  to 
the  pit  of  the  stomach  (epigastric  point),  around  the  umbilicus,  to  the  right 
hypochondrium,  the  right  shoulder,  and  the  lower  extremity  of  the  scapula 
on  the  same  side  (scapular  point).  The  pains  rapidly  become  very  severe, 
and  cause  the  patient  intense  agony.  They  may  be  continuous  or  inter- 
mittent, following  one  another  at  more  or  less  close  intervals,  and  consti- 
tuting an  attack  of  hepatic  colic.  The  attack  lasts,  on  an  average,  from  six 
to  twelve  hours,  though  it  may  persist  for  several  days.  It  is  most  fre- 
quently apyretic,  but  in  some  cases  fever  is  also  present. 

Hepatic  colic  is,  as  a  rule,  accompanied  by  vomiting,  which  is  at  first 
alimentar}%  if  the  colic  appears  soon  after  a  meal,  and  subsequently  becomes 
glairy  and  bilious.  As  long  as  the  calculus  remains  in  the  cystic  duct,  the 
vomit  may  be  bilious,  because  the  bile  continues  to  pass  into  the  intestine, 
whence  it  regurgitates  into  the  stomach  ;  if,  however,  the  calculus  is  arrested 
in  the  common  duct,  the  passage  of  the  bile  into  the  intestine  is  interrupted, 
and  bilious  vomiting  cannot  occur.  The  same  remark  applies  to  the  de- 
ooloration  of  the  faeces.  As  long  as  the  calculus  remains  in  the  cystic  duct, 
the  bile  flows  freely  into  the  intestine,  and  the  faeces  are  coloured;  but  if 
the  calculus  is  impacted  in  the  common  duct  for  some  time,  the  faeces  become 
colourless,  and  the  yellow  colour  of  the  skin  and  of  the  urine  reaches  its 
maximum.  Generally  speaking,  the  attack  of  hepatic  colic  ceases  suddenly, 
and  the  patient  at  once  feels  a  delightful  sensation  of  relief.  The  calculus 
has,  then,  gone  back  into  the  gall-bladder,  after  a  vain  attempt  to  pass  through 
the  cystic  duct,  or  has  reached  the  duodenum,  after  a  painful  migration 
through  the  ducts.  The  end  of  the  attack  is  often  accompanied  by  the 
passage  of  much  watery  urine  (nervous  urine).  During  the  attack  the  fiver 
is  often  enlarged,  and  the  region  of  the  gall-bladder  is  extremely  tender  on 
pressure. 

^Vhen  the  colic  has  been  long  and  severe,  the  liver  remains  enlarged  and 
painful  for  several  days ;  it  reaches  below  the  false  ribs,  and  is  so  tender  on 
pressure  that  women  cannot  wear  their  corsets. 


DISEASES  OF  THE  LIVER  971 

I  have  just  described  a  severe  attack,  but  hepatic  colic  is  often  much  less 
acute.  Many  people  with  gall-stones  merely  complain  of  cramp  in  the 
stomach,  which  may  be  looked  on  as  gastralgia,  but  is,  in  reality,  rudimentary 
hepatic  colic.  The  yellowish  tint  which  often  follows  this  so-called  cramp  in 
the  stomach  explains  the  nature  and  the  origin  of  the  mischief. 

Jaundice  is  a  frequent  symptom  of  hepatic  colic,  provided  the  calculus 
blocks  the  common  duct  completely  and  for  a  sufficient  time.  The  result  is 
jaundice  by  retention  some  hours  after  the  colic.  If  the  obUteration  of  the 
common  duct  lasts  long  enough,  the  faeces  have  a  whitish  look,  due  partly 
to  the  absence  of  bile  and  to  the  presence  of  non-emulsified  fats.  The  urine 
is  loaded  with  bile  pigment,  and  has  a  characteristic  mahogany  colour. 
Jaundice  is,  however,  not  constant  :  in  forty-five  cases  of  hepatic  colic 
analyzed  by,  Wolff  where  gall-stones  had  been  found  in  the  stools,  jaundice 
was  absent  in  twenty-five,  proving  that  the  stone  may  traverse  the  common 
duct  without,  however,  completely  obliterating  it.  The  icteric  tint  may 
be  very  slight,  and  must  be  looked  for  carefully.  We  must  not  forget,  too, 
that  the  seat  of  the  trouble  may  be  the  cystic  duct,  in  which  case  there  will 
be  no  jaundice.  Finally,  we  must  remember  that  attacks  of  pain,  mistaken 
for  hepatic  colic  without  icterus,  may  in  reality  be  due  to  cholecystitis. 

If  the  stools  are  examined  by  sifting  them,  the  calculus  or  the  calculi 
which  have  caused  the  complications,  will  be  found,  unless  the  calculus  in  the 
cystic  duct  has  passed  back  into  the  gall-bladder,  or  has  been  pushed  back 
from  the  duodenum  into  the  stomach  and  rejected  by  vomiting.  The 
calculi  may  not  appear  in  the  stools  till  three  or  four  days  after  the  attack. 
To  find  them,  the  stools  nmst  be  carefully  sifted  ;  otherwise  the  calculi  may 
pass  unnoticed.  The  syndrome  of  hepatic  colic  may  likewise  be  caused  by 
worms  or  by  hydatids  impacted  in  the  excretory  canals,  but  these  cases  are 
very  exceptional. 

Accompanying  Symptoms. — I  have  given  the  name  of  "  satellite  symp- 
toms "  to  certain  pheuomena  which  sometimes  accompany  hepatic  colic,  or 
which  may,  indeed,  exist  without  typical  colic  ;  in  the  latter  event  we  have  to 
deal  with  defaced  hepatic  colic. 

Vertigo  is  one  of  these  symptoms,  and  I  may  say  that  it  is  frequent, 
if  trouble  is  taken  to  seek  it.  1  do  not  know  the  exact  pathogenesis,  but  it 
is  certain  that  a  fair  number  of  persons  with  gall-stones  suffer  from  vertigo, 
whereas  I  have  not  noticed  this  symptom  in  renal  calculi.  A  few  years  ago  I 
saw  a  lady  in  whom  the  attacks  of  hepatic  colic  were  ushered  in,  accompanied, 
and  even  replaced,  by  attacks  of  vertigo,  lasting  for  several  days.  The 
vertigo  may  be  sliglit  or  intense,  transitory  or  lasting  ;  it  must  have  fre- 
quently been  confounded  with  gastric  vertigo,  the  so-called  cramps  in  the 
stomach  often  lieing  abnormal  hepatic  colic.  Vertigo  due  to  calculus  (as, 
by  the  way,  all  forms  of  vertigo)  distresses  patients,  who  believe  that  they  are 


972  TEXT-BOOK  OF  MEDICINE 

threatened  with  "  a  stroke."  Such  was  the  case  in  a  lady  whom  I  saw  some 
years  ago  with  Jacquet.  The  patient,  who  suffered  from  gall-stones,  dared 
not  move  from  the  bed  to  the  sofa,  because  the  feeling  of  vertigo  and  faint- 
ness  was  so  strong  ;  she  fancied  that  she  was  threatened  with  "  a  fit  of  apo- 
plexy." In  the  hospital,  when  questioning  patients  with  hepatic  colic,  we 
find  that  vertigo  is  a  marked  symptom. 

A  tendency  to  syncope  is  met  with  in  many  cases  of  gall-stones.  And  I  am 
not  alluding  to  syncope  caused  by  the  excessive  pain,  but  the  prostration  and 
distress,  satellite  symptoms  of  the  passage  of  a  stone,  and  of  hepatic  cohc, 
which  cause  the  victims  to  say  that  "  they  are  going  to  faint."  A  satellite 
symptom  of  real  importance  is  rigors  and  severe  attacks  of  fever.  The 
fever  is  not  due  to  angiocholitis,  cholecystitis,  or  abscess  of  the  liver ;  in 
these  cases  the  fever,  which  is  the  result  and  the  index  of  biliary  infections 
to  be  discussed  later,  has  generally  a  grave  prognostic  signification,  and 
furnishes  valuable  indications  as  to  surgical  intervention.  The  febrile 
complications  that  I  am  about  to  describe  have  another  signification,  as 
the  following  examples  will  show  : 

Some  years  ago  I  was  called  in  consultation  to  a  lady  who  was  subject  to  hepatic 
colic.  She  had  been  ill  for  some  days  with  pain,  jaundice,  decoloration  of  the  faeces,  and 
vomiting.  The  attack  had  so  far  been  normal,  but  suddenly  severe  rigors  appeared, 
with  a  rise  of  temperature  to  104°  F.  and  profuse  sweats.  The  attacks  returned  every 
day,  but  not  at  a  fixed  hour.  Quinine  had  no  effect,  and  infection  of  the  bile-ducts 
or  abscess  of  the  liver  was  feared.  I  felt  justified  in  giving  a  favourable  prognosis,  and 
made  a  diagnosis  of  satellite  attacks  of  fever  due  to  the  passage  of  gall-stones.  As  a 
matter  of  fact,  a  few  days  later  the  patient  recovered  from  the  coUc  and  the  fever,  after 
having  passed  about  a  dozen  large  stones. 

Another  example  :  I  had  in  my  ward  at  the  Necker  Hospital  a  patient  in  whom  the 
diagnosis  was  not  obvious.  The  liver  was  somewhat  enlarged  and  painful,  and  the 
conjunctivae  were  yellowish.  The  patient  was  seized  with  a  violent  and  prolonged 
rigor,  such  as  occurs  in  malaria  or  lobar  pneumonia,  the  attack  lasting  for  fifteen 
minutes.  The  slight  jaimdice  attracted  my  attention,  and  I  questioned  him  regarding 
gall-stones.  I  learnt  that  he  had  had  hepatic  cohc,  and  though  the  pains  were  only 
very  slight,  I  diagnosed  satelhte  fever  due  to  the  passage  of  stones.  At  the  end  of  a 
quarter  of  an  hour  the  temperature  rose  to  104°  F.,  and  the  hot  stage  was  followed  by 
profuse  sweating,  which  ended  the  attack.  Two  days  later  two  gall-stones  were  found 
in  the  faeces,  showing  the  nature  of  the  case. 

I  have  noticed  these  attacks  frequently,  and  in  hospital,  on  questioning 
my  patients  with  hepatic  colic,  I  have  obtained  a  history  of  severe  attacks 
of  fever.  I  have  dwelt  on  this  variety  of  fever  because  it  is  not  yet  recog- 
nized, in  spite  of  the  labours  of  Charcot  and  Magnin.  It  is  very  important 
to  distinguish  it  from  other  attacks  of  fever  due  to  acute  infection  of  the 
biliary  passages. 

The  distinction  between  satellite  fever  and  infectious  fever  has  long  been 
known.  Pentray,  Magnin,  Charcot,  and  Besnier  have  stated  "  that  the  inter- 
mittent fever  which  supervenes  in  biliary  Uthiasis  appears  in  two  different 


DISEASES  OF  THE  LIVER  973 

conditions,  and  may  indicate  two  different  morbid  states."  In  order  to  dis- 
tinguish these  two  varieties  of  intermittent  fever,  Charcot  called  the  former 
heptalgic  fever,  or  the  satellite  fever  of  hepatic  colic  ;  and  the  latter  hepatic 
or  biliary  fever  (of  toxic  origin).  Even  acute  attacks  of  satellite  fever  may 
exist  with  slight  forms  of  hepatic  colic  ;  they  are  at  times  so  severe  that  the 
colic  is  defaced  and  of  minor  importance.  Magnin  quoted  a  case  in  which 
the  satellite  fever,  due  to  the  passage  of  gall-stones,  preceded  the  colic  by 
several  months.  One  attack  of  satellite  fever  is  rare  ;  as  a  rule,  we  see 
a  series  of  attacks,  which  return  several  days  following,  without  well-marked 
periodicity.  I  am  not  certain  of  the  cause  of  these  satellite  attacks.  Charcot 
thought  they  weie  the  result  of  slight  infection,  in  which  case  they  might  be 
considered  as  a  kind  of  bilio-septic  fever.  It  is  possible,  but  I  am  not  con- 
vinced, because  we  see  many  people  who  are  suffering  from  gall-stones,  but 
in  whom  the  attacks  of  satellite  fever  never  end  in  bilio-septic  fever  and  are 
never  followed  by  infective  lesions  of  the  gall-bladder  or  of  the  liver. 

The  prognosis  of  the  attacks  is  generally  good  ;  although  they  cause  great 
alarm,  they  generally  end  in  recovery.  We  must  not,  however,  be  too 
optimistic,  for  attacks  which  have  at  first  presented  the  characteristics  of 
heptalgic  fever  may  have  a  fatal  ending,  as  in  the  case  reported  by  Besnier — 
an  exceptional  case,  however,  the-  patient  having,  in  a  few  days,  passed  148 
stones.  On  the  other  hand,  I  saw  a  patient  who  had  fifty-five  satellite 
attacks,  in  series  of  six  to  eight  intermittent  attacks,  with  hepatic  colic 
and  jaundice,  and  yet  recovered,  without  other  complications  occurring. 

The  diagnosis  between  satellite  fever  and  bilio-septic  fever  is  often  diffi- 
cult, but  it  may  nevertheless  be  said  that  satellite  attacks  are  generally  asso- 
ciated with  hepatic  colic,  pain  and  vomiting,  while  in  bilio-septic  fever 
these  troubles  are  often  absent.  The  satelUte  attacks  are  almost  always 
followed  by  the  passage  of  calculi,  which  is  not  the  case  in  bilio-septic  fever 
due  to  cholecystitis  and  angiocholitis.  Finally,  satellite  attacks  are  often 
coexistent  with  other  satellite  symptoms  due  to  passage  of  stones — vertigo, 
fainting-fits,  and  syncope — which  is  not  the  case  in  bilio-septic  fever. 
Summary  :  It  cannot  be  said  of  hepatic  colic  that  it  is  always  apyretic, 
whilst  I  have  never  noticed  satellite  attacks  in  renal  colic. 

In  addition  to  the  attacks  of  fever  just  described,  we  also  find  fever,  due 
to  biliary  stagnation,  in  persistent  obliteration  of  the  common  duct.  This 
question  will  1k>  discussed  under  Persistent  Obliteration  of  the  Common  Duct. 
Complications. — Hepatic  colic  is  sometimes  accompanied  by  complications. 
Even  at  the  commencement  of  the  attack  rupture  of  the  cystic  and  of  the 
common  ducts,  followed  by  peritonitis,  may  occur.  Sudden  death  in  an  attack 
is  not  quite  unknown.  It  is  probably  due  to  reflex  action,  and  at  the 
post-mortem  examination  a  large  calculus  is  found  impacted  in  the  cystic 
or  the  common  duct.     Hepatic  colic  may  be  accompanied  by  vascular 


974  TEXT-BOOK  OF  MEDICINE 

troubles,  whicli  show  themselves  by  pulmonary  congestion  on  the  right 
side,  cEdema  of  the  lower  limbs,  and  dilatation  of  the  right  side  of  the  heart, 
with  tricuspid  insufficiency.  The  reaction  of  the  biliary  lesions  on  the  right 
side  of  the  heart  has  been  pointed  out  by  Potain.  Gangolphe  has  indicated 
the  existence  of  a  murmur  in  jaundice,  and  placed  it  at  the  mitral  opening ; 
but  it  seems  that  this  murmur  should  be  located  in  the  tricuspid  opening. 
Potain  has  shown  that  acute  affections  of  the  biliary  passages  and  calculous 
jaundice  in  particular  may  cause  transitory  dilatation  of  the  right  heart, 
with  tricuspid  insufficiency  and  hypertrophy  of  the  ventricle.  The  dilata- 
tion is  probably  due  to  excess  of  pressure  in  the  pulmonary  artery,  and 
depends  upon  diminution  in  the  calibre  of  the  arterioles  of  the  lungs,  the 
diminution  being  doubtless  the  result  of  reflex  action  transmitted  to  the  bulb, 
and  reflected  to  the  lungs  by  the  branches  of  the  great  sympathetic. 

We  shaU  see  later  that  biliary  hthiasis  may  cause  infective  endocarditis, 
through  organisms  present  in  the  bile  ducts  and  derived  from  the  intestine. 

Diagnosis. — The  diagnosis  of  hepatic  cohc  is  generally  easy.  It  is  dis- 
tinguished from  renal  colic  in  that  the  liver  is  not  painful ;  the  pain  starts 
from  the  kidneys,  follows  the  course  of  the  ureters,  and  spreads  to  the  tes- 
ticles, the  neck  of  the  bladder,  and  the  extremity- of  the  penis,  and  jaundice 
is  absent.  Idiopathic  heptalgia,  or  simple  hepatic  neuralgia  (which  Beau 
thought  so  frequent),  is  very  rare,  since  gall-stones  have,  after  careful  search, 
been  almost  always  found  in  the  stools  shortly  after-  the  attack  of  colic. 
The  diagnosis  from  gastralgia  is  sometimes  difficult ;  some  patients  merely 
complain  of  cramp  in  the  stomach,  but  closer  examination  shows  that  the 
so-called  cramp  means  hepatic  colic.  The  urine  contains  bile  pigment,  the 
conjunctivae  become  yellow,  the  hver  is  enlarged  and  painful,  and  the  pain 
reaches  the  right  shoulder.  When  the  diagnosis  of  biliary  lithiasis  is  difficult, 
urobilinuria  and  peptonuria  (Bouchard)  are  in  favour  of  it. 

I  may  mention  the  diagnosis  of  renal  from  lead  colic,  and  I  would  insist 
on  the  diagnosis  of  defaced  hepatic  colic,  which  may  be  painless,  the  presence 
and  the  migration  of  the  calculus  being  shown  by  rigors,  fever,  vertigo  and 
syncope.  The  diagnosis  from  the  pain  of  intestinal  hthiasis  may  present 
some  difficulties.  In  order  to  avoid  repetition,  I  refer  the  reader  to  the 
section  on  Entero-typhlo-colitis. 

The  diagnosis  of  hepatic  colic  from  appendicitis  has  been  already  dis- 
cussed. Hepatic  colic  must  not  be  confounded  with  hepatic  pseudo-colic, 
which  is  due  to  adhesive  pericholecystitis. 

The  prognosis  of  hepatic  colic  must  always  be  reserved — first,  because 
the  gravest  complications,  such  as  perforation  of  the  bile-ducts,  syncope, 
and  sudden  death,  are  possible  during  the  attack ;  and,  secondly,  because 
the  calculi  may  give  rise  to  a  series  of  complications,  described  in  the  following 
sections. 


DISEASES  OF  THE  LIVER  975 

Treatment. — The  objects  in  view  are — (1)  to  relieve  the  pain ;  (2)  to  facili- 
tate the  expulsion  of  the  calculus  ;  and  (3)  to  prevent  the  formation  of  new 
calculi.  In  order  to  ease  the  pain,  aspirin  may  be  given  in  doses  of  30  to 
60  grains  daily.  Subcutaneous  injections  of  morphia  are  of  much  service. 
To  these  means  may  be  added  enemata  of  chloral  and  the  appUcation  of  ice- 
bags  to  the  hypochondrium.  Prolonged  baths  also  give  good  results.  In 
order  to  facHitate  the  expulsion  of  the  calculus,  large  quantities  of  oil  and 
massage  of  the  hepatic  region  have  been  recommended  (Pujol).  AlkaUs 
have  a  twofold  action  :  they  facQitate  the  expulsion  of  the  calculi  and  prevent 
the  formation  of  new  ones.  With  this  object  in  view,  cures  at  Vichy,  Carls- 
bad, Contrexeville,  and  Vittel  may  be  described.  Durande's  remedy, 
given  in  perles  containing  3  parts  of  ether  to  2  parts  of  essence  of  turpen- 
tine, was  frequently  used  by  Trousseau.  The  patient  must  be  careful  to 
avoid  fat,  acid  foods,  and  drinks. 

2.  Migration  and  Arrest  of  the  Biliary  Calculi  in  the  Intestine — 
Stenosis  and  Obliteration  of  the  Pylorus. 

Intestinal  Obstruction. — Obstruction  of  the  intestine  by  gall-stones  is 
not  extremely  rare,  because  Dragon  has  collected  1-iO  cases.  In  order  to 
cause  obstruction,  the  calculus  must  be  as  large  as  a  walnut  or  an  egg.  The 
passage  of  these  large  calculi  remains  to  be  explained.  While  large  stones 
can  pass  through  the  bile-ducts,  when  much  dilated,  the  majority  of  these 
stones  pass  into  the  intestine  through  a  fistula  between  the  gall-bladder  and 
the  duodenum. 

The  reason  for  the  behef  that  these  large  calculi  have  not  passed  through 
the  bile-ducts  is  that  patients  may  have  previously  experienced  neither 
hepatic  colic  nor  jaundice.  Some  of  them,  however,  have  had  symptoms 
of  calculous  cholecystitis.  The  gall-bladder  forms  adhesions  with  the  in- 
testinal coil  (pericholecystitis)  ;  a  large  fistula  is  established,  and  the  calculus 
then  passes  from  the  gall-bladder  into  the  intestine.  Sometimes  the  calculus 
passes  into  the  intestine  without  encumbrance  ;  at  other  times  it  causes 
grave  mischief.  In  the  latter  event  the  symptoms  of  intestinal  occlusion 
are  sudden,  but  in  a  third  of  the  cases  recovery  supervenes  spontaneously, 
and  the  calculus  or  calculi  are  passed  per  anum.  When  intestinal  occlusion 
persists,  symptoms  of  peiitonitis  are  often  present.  The  calcuh  are  generally 
arrested  in  the  jejunum,  the  ileum,  or  the  lower  portion  of  the  rectum.  In 
some  cases  it  has  been  found  that  the  large  size  of  the  calculi  was  due  to  the 
addition  of  calcareous  deposits  of  fsecal  matter.  Intestinal  spasm  is  also 
an  important  factor  in  the  pathogenesis  of  obstruction  by  gall-stones.  The 
following  cases  will  give  an  idea  of  these  complications  : 

Merklen  :  A  woman  with  no  previous  history  of  gall-stones  was  suddonly  taken  ill 
with  colic,  vomiting,  arrest  of  faecofc,  and  liatus,  followed  by  faecal  vomiting,  a  cholera- 


976  TEXT-BOOK  OF  MEDICINE 

like  condition,  and  lowering  of  the  temperature.  After  a  short  respite  the  symptoms 
again  became  acute  ;  hiccough,  tympanites,  and  chilliness  were  present,  and  the  patient 
succumbed.  The  occlusion  was  seated  in  the  small  intestine,  and  was  due  to  an 
enormous  calculus,  measuring  more  than  3  inches  in  circumference.  It  had  passed 
into  the  intestine  through  a  cystico-duodenal  fistula.  The  gall-bladder  contained 
another  large  calculus. 

Audry :  A  patient  was  taken  suddenly  ill  with  symptoms  of  intestinal  occlusion : 
sharp  abdominal  pain,  vomiting,  absolute  constijDation,  and  meteorism.  A  respite  then 
supervened,  but  was  soon  followed  by  rapid  aggravation  of  the  symptoms,  and  the 
patient  succumbed  in  an  algid  condition.  At  the  post-mortem  examination  recent 
peritonitis  and  obstiniction  of  the  small  intestine,  due  to  an  enormous  calculus,  weighing 
IJ  oimces,  and  measuring  4^  inches  in  circumference,  were  fovmd.  The  calculus  had 
entered  into  the  intestine  through  a  cystico-duodenal  fistula. 

English  Cases. — Maclagan  reported  to  the  Chnical  Society  of  London  the  case  of  a 
patient  who  was  seized  on  four  occasions  ^^ith  sharp  abdominal  pain  and  constipation. 
The  attacks  lasted  from  three  to  six  daj's,  and  after  each  attack  the  patient  passed  gall- 
stones of  the  size  of  a  walnut.  The  patient  died,  and  at  the  post-mortem  examination 
a  cystico-duodenal  fistula  was  fomid.  The  gall-bladder  contained  another  large  calculus. 
Broadbent  had  a  case  of  intestinal  occlusion  in  an  old  man  who  succumbed  in  four  days. 
At  the  post-mortem  examination  an  enormous  gall-stone  was  found  in  the  small 
intestine.  Ord  saw  three  analogous  cases.  Enormous  gall-stones  were  arrested  at  the 
end  of  the  ileum  in  the  first  case,  in  the  small  intestine  in  the  second  case,  and  at  the 
anal  sphincter  in  the  third  case.  Harrington  pubhshed  a  case  of  an  aged  woman  -svith 
symptoms  of  intestinal  occlusion.  She  was  operated  on,  and  a  gall-stone  was  foimd  in 
the  ileum. 

We  see  that  intestinal  occlusion,  caused  by  gall-stones,  supervenes  in  old 
people  who  have  not  suffered  from  hepatic  colic  or 'from  any  sjnnptoms 
indicative  of  the  passage  or  the  arrest  of  the  calculi  in  the  bile-ducts.  These 
large  calculi  are  slowly  formed  in  the  gall-bladder,  which  becomes 
infected,  and  enter  the  intestine  generally  through  a  cystico-duodenal 
fistula.  In  ninety-two  cases  collected  by  Lobstein,  the  symptoms  of 
intestinal  occlusion  were  preceded  in  seventeen  cases  only  by  symptoms  of 
cholelithiasis. 

The  treatment  is  surgical.  According  to  Lobstein's  statistics,  out  of 
sixty-one  cases  which  were  operated  on,  twenty-nine  ended  fatally  ;  and  out 
of  thirty-one  cases,  nineteen  succumbed.  It  must  be  added  that  most  of  the 
operations  in  which  death  supervened  were  performed  on  exhausted  patients 
with  peritonitis.  In  order  to  have  the  best  chances  of  success,  the  operation 
should  be  performed  as  early  as  po.ssible. 

Stenosis  and  Obstruction  of  the  Pylorus.— The  close  relation  between 
the  gall-bladder  and  the  pylorus  explains  the  pathological  connections 
of  these  two  organs  in  calculous  cholecystitis,  which  may  react  in 
different  ways  on  the  pylorus  and  its  orifice.  Sometimes  a  large  calculus 
from  the  perforated  gall-bladder  becomes  embedded  in  the  wall  of  the 
pylorus,  forming  a, pouch  for  itself,  and  obliterating  the  orifice.  In  other 
cases  the  calculus  is  juxta-pyloric,  and  causes  fibrous  changes  in  the 
pylorus,  with  stenosis.     Marchant  quotes  three  such  cases  in  his  work. 


DISEASES  OF  THE  LIVER  977 

The  contraction  of  the  pylorus  may  not  be  due  directly  to  the  gall-stone  ; 
it  may  be  due  to  adhesions  and  to  perigastritis,  which  is  secondary  to  cal- 
culous pericholecystitis. 

Summary  :  Calculous  cholecystitis  may  cause  stenosis  and  obstruction 
of  the  pyloric  orifice,  either  directly  by  the  presence  of  large  calcuh,  or  in- 
directly by  adhesions,  by  retraction  of  fibrous  tissue,  or  by  perigastritis, 
consequent  on  pericholecystitis.  The  more  or  less  marked  contraction  of 
the  pyloric  orifice  shows  itself  by  the  following  sjonptoms  :  epigastric  pains  ; 
vomiting  several  hours  after  the  ingestion  of  food  ;  considerable  dilata- 
tion of  the  stomach,  with  tympanites  and  "  clapotement "  ;  constipation ; 
loss  of  flesh  due  to  insufficient  nourishment ;  cachexia  ;  induration  or  tumour 
of  the  epigastric  region. 

A  patient  vomits,  loses  flesh,  and  becomes  cachectic.  He  complains  of 
sharp  pains  in  the  epigastric  region.  On  examination,  we  find  dilatation  of 
the  stomach  and  pyloric  tumour,  and  we  cannot  eliminate  at  first  the  idea  of 
cancer ;  the  induration,  and  particularly  the  tumour,  obscure  the  diagnosis. 
After  all,  vomiting,  progressive  loss  of  flesh,  cachexia,  pain,  induration, 
tumour,  and  dilatation  of  the  stomach  may  all  be  present  in  pyloric  stenosis, 
whether  it  is  due  to  ulcer,  cancer,  perigastritis,  adhesions,  biliary  calculi, 
etc. ;  and  if  the  patient  has  a  history  of  hepatic  colic,  jaundice,  or  signs  of 
cholecystitis,  we  must  think  of  pyloric  stenosis,  consequent  on  calculous 
cholecystitis,  and  have  recourse  to  prompt  surgical  intervention. 

3.  Persistent  Obliteration  of  the  Bile-Ducts — Biliary  Cirrhosis. 

Hepatic  colic  is  only  accompanied  by  a  temporary  and  sometimes  in- 
complete obhteration  of  the  cystic  and  common  ducts.  I  shall  now  deal 
with  the  persistent  obliteration  of  these  canals,  and  with  the  many  com- 
plications resulting  therefrom. 

When  the  cystic  duct  is  permanently  obstructed  by  a  calculus,  the  bile 
no  longer  reaches  the  gall-])ladder ;  the  bile  already  present  is  absorbed ; 
the  walls  of  the  gall-bladder,  as  the  result  of  chronic  inflammation,  become 
thickened  and  converted  into  fibrous  tissue  ;  and  the  gall-bladder  atrophies. 
In  some  cases  the  walls  of  the  gall-bladder  become  infiltrated  with  lime-salts. 
In  other  cases  the  bile  gives  place  to  a  sero-mucous  secretion,  and  the  gall- 
bladder (hydroj)s)  may  be  much  enlarged.  The  fluid  in  hydrocholecystitis 
is  mucous,  .shreddy,  whitish,  and  sometimes  rich  iu  muco-pus.  As  the 
obstruction  of  the  cystic  ducts  allows  the  free  passage  of  the  Inle  into  the 
intestine,  this  complication  is  by  no  means  as  serious  as  obstruction  of  the 
common  duct. 

When  the  common  duct  is  permaiiently  oblitciated  by  one  or  more 
calculi,  it  matters  httle  whether  the  obliteration  occurs  at  some  point  of  its 
course  or  at  Vater's  ampulla  ;  the  bile  no  longer  passes  into  the  intestine, 

02 


1)78  TEXT-BOOK  OF  MEDICINE 

and  clironic  jaundice  appears.  There  are,  nevertheless,  examples  where, 
in  spite  of  the  presence  of  several  calculi  (Cruveilhier),  the  common  duct 
has  remained  sufficiently  patent  to  allow  the  bile  to  pass  into  the  duodenum. 

.Obliteration  of  the  common  duct,  as  also  of  the  cystic  duct,  is  not  always 
preceded  by  colic  ;  the  obHteration  may  come  on  silently,  without  pain.  Per- 
sistent obliteration  may  last  for  weeks  and  months,  without  other  symptoms 
than  chronic  jaundice,  with  clay-coloured  stools,  distension  of  the  gall- 
bladder, and  enlargement  of  the  hver.  Sometimes,  also,  persistent  obHtera- 
tion of  the  common  duct  may  at  length  cause  lesions  in  the  Hver,  gall-bladder, 
and  ducts ;  dilatation  and  suppuration  in  the  bile-ducts  and  gall-bladder ; 
fibrosis  of  the  liver  (biliary  cirrhosis) ;  suppurative  angiocholitis  and  abscess 
of  the  liver  ;  and  changes  in  the  hepatic  cells  (parenchymatous  hepatitis  and 
pancreatitis). 

Dilatation  of  the  Ducts  and  Gall-Bladder. — In  consequence  of  complete 
and  permanent  obstruction  of  the  common  duct,  the  cystic  and  hepatic 
ducts  may  undergo  enormous  dilatation,  while  the  common  duct  may  be  as 
large  as  an  intestinal  coil ;  the  bile  accumulates  in  the  gall-bladder,  which 
may,  then,  descend  as  far  as  the  umbilicus,  and  even  into  the  right  ihac  fossa. 
The  distended  gall-bladder  may  contain  several  pints  of  fluid.  Cruveilhier 
in  his  atlas  has  figured  a  gall-bladder  descending  into  the  right  ihac  fossa  ; 
and  in  Benson's  case  the  gaU-bladder  was  punctured,  under  the  impression 
that  the  case  was  one  of  ascites,  4  pints  of  bile  being  withdrawn.  The  fluid 
in  obHteration  of  the  common  duct  does  not  resemble  the  thready  mucous 
liquid  of  hydrocholecystitis  due  to  obHteration  of  the  cystic  duct. 

The  obstruction  of  the  common  duct  also  determines  enlargement  of 
the  superficial  and  deep  intrahepatic  ducts,  and  the  latter  assume  a  cylindrical 
or  ampuUa-Hke  form,  analogous,  says  Monneret,  to  bronchial  dilatations. 
The  dilatation  is  sometimes  so  general  that  the  parenchyma  of  the  liver 
resembles  cavernous  tissue.  The  retention  of  the  bile  causes  great  enlarge- 
ment of  the  Hver  ;  the  surface  is  smooth  and  of  an  olive  colour.  On  section, 
the  bile-ducts  are  seen  to  be  dilated  and  to  exude  bile,  which  is  often  mixed 
with  muco-pus,  sand,  and  biliary  concretions,  which  have  formed  owing  to 
the  stagnation  of  the  bile.  The  biliary  canals  are  attacked  with  chronic 
inflammation  (angiochoHtis),  which  commences  in  the  mucosa,  and  later 
involves  the  entire  wall  of  the  duct. 

Chronic  jaundice,  clay-coloured  faeces,  swelHng  of  the  Hver  which  may 
descend  as  far  as  the  umbilicus,  and  distension  of  the  gaU-bladder,  are  the 
first  results  of  the  permanent  obstruction  of  the  common  duct.  The  faeces 
may,  however,  from  time  to  time  regain  their  colour,  if  the  calculus 
or  the  calcuH  engaged  in  the  common  duct  do  not  completely  obstruct  the 
lumen,  and  allow  an  intermittent  flow  of  bile  into  the  intestine.  When  these 
compHcations  supervene  in  an  indixddual  who  has  had  hepatic  coHc,  it  is 


DISEASES  OF  THE  LIVER  979 

easy  to  trace  the  cause  of  the  lesion ;  but  when  the  symptoms  of  Hthiasis 
are  not  clearly  defined,  it  is  necessary  to  eliminate  prolonged  catarrhal 
jaundice,  ijrimary  cancer  of  the  bile-ducts,  and  cancer  of  the  head  of  the 
pancreas  and  of  Vater's  ampulla.  The  clinical  side  of  the  question  will  be 
discussed  in  Section  XXI. 

Biliary  Cirrhosis. — Obstruction  of  the  common  duct  produces  enlarge- 
ment of  the  hver,  but  this  hypertrophy  is  often  replaced  by  atrophic  cirrhosis. 
In  no  case  does  this  cirrhosis  resemble  Laennec's  atrophic  cirrhosis ;  the 
surface  of  the  liver  is  smooth,  and  the  parenchyma  is  but  moderately  in- 
durated ;  it  is  therefore  a  special  cirrhotic  process.  Experimental  oblitera- 
tion of  the  common  duct  in  animals  by  a  ligature,  and  the  pathological 
obstruction  of  this  canal  in  man  by  primary  cancer  of  the  biliary  passages, 
or  by  cancer  of  the  head  of  the  pancreas,  cause  similar  cirrhotic  changes. 
The  retention  of  the  bile  produces  angiochohtis  and  peri-angiocholitis,  the 
process  ending  in  diffuse  interstitial  hepatitis.  This  connective  hyperplasia 
affects  at  first  the  large  ducts,  and  then  the  smaller  canaliculi.  It  shows 
itself  first  in  the  spaces,  next  in  the  fissures,  and  circumscribes  the  hepatic 
lobule,  without  ever  ending,  like  Laennec's  atrophic  cirrhosis,  in  the  forma- 
tion of  nodules.  Formation  of  bjliary  canalicuU,  which  invade  the  lobule, 
pigmentation  of  the  cells,  and  invasion  of  the  lobule  by  connective  hyper- 
plasia, are  also  found. 

The  differences  are  great  between  hypertrophic  biliary  cirrhosis  (Hanot's 
disease)  and  the  biliary  liver.  The  latter  is  not  hypertrophied,  but  is 
rather  small  and  contracted ;  dilatations  of  the  biliary  canals  are  often 
found,  with  or  without  abscesses,  and  the  angiocholitis  commences  in  the 
large  bile-ducts,  which  are  healthy  in  hypertrophic  biliary  cirrhosis. 

These  lesions  may,  like  the  various  diseases  of  the  liver,  become  com- 
plicated at  any  moment  by  symptoms  of  icterus  gravis,  which  causes 
death  in  a  more  or  less  rapid  manner.  Moreover,  no  matter  what  arc  the 
lesions  of  the  liver,  no  matter  what  are  the  causes  of  its  anatomical  and 
physiological  decay,  as  soon  as  it  is  unable  to  fight,  it  is  invaded  by  secondary 
infections  (microbes  and  toxines),  and  the  complex  symptoms  of  hepatic 
insufficiency  appear. 

Pancreatitis. — This  question  is  discussed  later,  in  Section  VII.  of  Diseases 
of  the  Tancreas. 

4.  Infection  of  the  Biliary  Passages:  Angiocholitis,  Cholecystitis, 

Hepatitis,  Endocarditis. 
In  the  normal  state,  the  bile-ducts,  the  gall-bladder,  and  the  bile  are 
aseptic.     Gilbert,  Girode,  and  Thircloix  have  found  that  bile  from  the  gall- 
bladders of  ])erson8  who  had  not  succumbed  to  an  infectious  or  biliary  disease 
was  always  sterile.     In  animals  the  bile  in  the  gall- bladder  is  aseptic.     The 

62—2 


980  TEXT-BOOK  OF  MEDICINE 

effusion  of  pure  bile  into  the  peritoneum  does  not  cause  peritonitis.  Normal 
bile  is,  therefore,  aseptic  and  sterile.  The  bile  is  not  antiseptic,  and  does  not 
destroy  germs,  as  has  been  supposed.  As  far  as  the  microbes  are  concerned, 
it  is  as  favourable  a  culture  medium  as  ordinary  broth,  and  does  not  lessen 
their  virulence  in  any  way.  The  coli  bacillus,  streptococcus,  staphylococcus, 
etc.,  grow  readily  in  the  bile  (Gilbert  and  Dominici). 

How,  then,  does  infection  of  the  biliary  passages  take  place  ?  I  said 
that  the  canals  were  aseptic,  but  the  last  portion  of  the  common  duct  forms 
an  exception.  Numerous  microbes  have  been  found  there,  especially  the 
coli  bacillus  ;  they  come  from  the  duodenum,  which  is  very  rich  in  germs 
(Gessner).  The  common  duct  is,  therefore,  in  danger  of  being  infected,  and 
the  duodenum  is  a  constant  menace  to  the  bile-ducts.  In  the  normal  con- 
dition, the  flow  of  the  bile  mechanically  maintains  the  asepsis  of  the  ducts, 
but  any  obstacle  to  the  flow  favours  invasion  of  the  biliary  canals  by  the 
microbes  normally  present  in  the  duodenum,  and  the  terminal  portion  of  the 
common  duct.  The  infection  ascends  from  the  ducts  to  the  gall-bladder 
and  to  the  liver.  (The  infection  of  the  liver  through  the  bloodvessels  is  quite 
different,  and  was  described  in  Section  XIX.) 

By  ligaturing  the  common  duct,  biliary  infection  has  been  reproduced 
experimentally  (Gilbert,  Netter,  Girode).  The  ligature  produces  at  the 
same  time  arrest  of  the  flow  of  bile  and  trauma  of  the  walls,  two  con- 
ditions favourable  to  the  entrance  of  microbes.  Thesis  experimental  con- 
ditions are  fulfilled  pathologically  by  the  obstruction  of  the  common  duct ; 
calculi,  by  obliterating  the  canal,  prevent  the  exit  of  the  bile,  and  cause 
traumatic  erosion  of  the  mucosa  ;  the  door  is,  then,  open  to  infection,  and  the 
soil  is  prepared.  In  this  way  angiocholitis,  cholecystitis,  and  abscesses 
arise. 

Calculous  infection  of  the  biliary  passages  (angiocholitis,  cholecystitis, 
and  abscess  of  the  liver)  generally  occurs  in  people  who  have  had  colic, 
jaundice,  swelling  of  the  liver,  pains  in  the  hypochondrium,  etc.  These 
symptoms  may,  however,  be  absent,  or  may  have  disappeared  a  long  time 
before  the  symptoms  of  infection  appear.  Fever  is  sometimes  the  prominent 
feature,  and  is  bilio-septic  (Chauffard).  There  is  no  question  here  of  the 
satellite  fever  due  to  the  passage  of  a  stone,  and  we  have  to  deal  with  true 
infective  fever,  which  is  also  intermittent,  characterized,  like  satellite  fever, 
by  more  or  less  violent  rigors,  with  a  rise  of  temperature  to  103°  or 
104°  F.,  and  followed  by  profuse  sweating  after  the  attack.  These  attacks 
recur  every  night,  or  every  other  night,  almost  with  the  periodicity  of  swamp 
fever.  The  apyrexia  between  the  attacks  may  be  complete  (intermittent 
form)  or  incomplete  (remittent  form)  ;  or,  again,  the  fever  may  show 
but  slight  remissions  (contiimous  form),  and  is,  then,  more  serious.  Inter- 
mittent bilio-septic  fever  may  accompany  all  the  localizations  of  biliary 


DISEASES  OF  THE  LIVER  981 

infection,  but  it  is  in  hepatic  infection  that  it  attains  its  greatest  intensity, 
and  it  is  much  less  marked  or  fairly  often  absent  in  the  case  of  cholecystitis. 

Angiocholitis — Hepatitis. — Angiocholitis  may  attack  the  extra-  and 
intrahepatic  bile-ducts.  In  the  latter  case  lesions  of  the  liver  are  the  most 
important.  In  patients  who  have  died  of  these  complications  we  find  post 
mortem  that  the  liver  is  soft,  enlarged,  and  surrounded  by  adhesions,  due 
to  simple  or  to  suppurative  perihepatitis.  On  section  it  seems  to  be 
converted  into  a  spongy,  bilious,  and  purulent  tissue  ;  the  bile  flows  in 
abundance  through  the  dilated  ducts,  and  the  hepatic  parenchpna  is  riddled 
with  abscesses  of  various  forms  and  sizes.  Some  are  miliary ;  others  are 
larger  than  an  orange.  Some  of  them  have  been  well  described  by  Chauf- 
fard  under  the  name  of  areolar  abscesses.  These  biliary  abscesses  have- 
several  origins  :  some  are  due  to  the  cyhndrical,  moniliform,  or  ampullar y 
dilatations  of  the  bihary  canaHcuH,  and  are  not  true  abscesses  ;  while  others, 
true  abscesses,  are  much  more  common,  and  arise  in  the  connective  tissue 
around  the  ducts  (suppurative  peri-angiocholitis),  whether  the  walls  of  the 
duct  have  been  destroyed  by  the  suppurative  inflammation,  or  whether 
the  abscess  has  ulcerated  into  the  bile-duct.  The  rupture  of  a  dilated  bile- 
duct  in  the  parenchyma  of  the  liver  may  also  become  the  origin  of  a  large 
abscess.  The  pus  is  whitish,  yellowish-green,  or  brownish,  and  contains 
biliary  sand  and  debris  of  the  hepatic  tissue  ;  the  purulent  collection  has  no 
limiting  membrane,  or,  if  the  membrane  is  found,  it  is  never  lined  with 
cylindrical  epithelium.  If  cylindrical  epithelium  is  found  in  the  pus,  it 
indicates  communication  between  the  abscess  and  a  biliary  canaliculus. 
Micro-organisms,  especially  the  Bacillus  coli,  abound  in  the  pus  from  these 
biliary  abscesses. 

Calculous  Cholecystitis. — In  exceptional  cases  the  calculi  may  be  formed 
in  the  Uver,  but  they  are  almost  always  formed  in  the  gall-bladder.  The 
number  may  be  considerable  ;  sometimes  there  is  only  one,  which  may 
be  larger  than  an  egg.  The  calculi  may  remain  for  a  long  time  in  the  gall- 
bladder without  causing  cholecystitis  in  the  true  sense  of  the  word.  This 
calculosis  of  the  gall-bladder  becomes  calculous  cholecystitis  when  the 
bladder  is  infected. 

Calculous  cholecystitis  shows  itself  in  different  forms.  In  the  first  and 
most  common  type  the  gall-bladder  diminishes  in  size  ;  it  may  even  be 
reduced  to  "  a  calculous  stump."  This  condition  is  due  to  atrophying 
sclerosis  of  the  walls.  The  fibrous  walls  are  sclerosed  and  retracted  on  to 
the  calculi.  On  the  inside,  the  gall-bladder  is  furrowed  with  folds  and  bands, 
dividing  it  into  partitions,  and  giving  it  the  look  of  a  beehive.  In  the 
alveoli  of  the  hive  larger  or  smaller  calculi  are  embedded  in  a  purulent 
cavity,  and  are  sometimes  very  difficult  to  enucleate.  An  infiltration  of 
embryonic  cells  is  found  in  all  the  layers  of  the  gall-bladder,  and  numerous 


982  TEXT-BOOK  OF  MEDICINE 

micro-organisms  are  also  found.  No  tumour  is  found,  the  gall-bladder  being 
retracted  under  the  liver.  As  it  does  not  reach  below  the  lower  edge  of  the 
liver,  and  as  it  cannot  be  felt  on  exploring  the  region,  it  gives  no  aid  in  the 
diagnosis. 

In  the  second  type  of  cholecystitis,  which  is  less  common,  a  tumour  is 
found.  The  walls  of  the  gall-bladder  are  "  as  hard  as  a  cardboard  shell," 
much  hypertrophied  and  thickened,  and  the  cavity  is  enlarged.  The  size 
of  the  cystic  tumour  is  not  due  to  the  fluid,  which  is  only  present  in  small 
quantities  ;  it  results  chiefly  from  the  enormous  thickness  of  the  walls. 
These  cases  of  calculous  cholecystitis  make  a  large  projection  under  the  liver  ; 
the  tumour  can  be  felt  on  examining  the  lower  edge  of  the  organ. 

Besides  the  two  preceding  types,  represented  by  sclero-atrophic  chole- 
cystitis, which  is  very  common,  and  by  sclero-hypertrophic  cholecystitis, 
which  is  very  rare,  a  third  type  is  found  ;  it  is  characterized  by  great  dilata- 
tion of  the  gall-bladder,  with  thinning  of  the  walls  and  accumulation  of  much 
fluid  in  the  cavity.  This  dropsy  of  the  gall-bladder  is  generally  associated 
with  obliteration  of  the  cystic  duct.  The  liquid  is  colourless,  shreddy, 
or  tinged  with  bile.  The  mucosa  of  the  gall-bladder  is  not  alveolar,  as  in 
the  preceding  forms,  but  smooth,  Uke  a  true  cyst  wall  (Schwartz).  The 
tumour  may  be  pedunculated,  and  the  obliterated  cystic  duct  forms  part 
of  the  pedicle  ;  the  tumour  descends  into  the  abdomen,  and  simulates  other 
abdominal  swellings. 

The  infection  of  the  gall-bladder  is  caused  by  the  inechanism  referred 
to  above,  whether  the  obliteration  is  in  the  common  duct  or  in  the  cystic 
duct ;  cases  have  been  recorded  where  the  gall-bladder  became  infected 
in  the  absence  of  any  obliteration.  The  lesions  of  calculous  cholecystitis 
are  not  always  identical  in  these  different  forms.  The  liquid  in  the  infected 
gall-bladder  is  generally  scanty.  It  may  be  scarcely  clouded  with 
mucus,  or  it  may  be  purulent,  sanious,  foetid,  and  coloured  or  not  by  bile 
(empyema  of  the  gall-bladder).  The  gall-bladder  is  the  more  distended,  the 
more  its  walls  are  thinned  and  the  less  they  are  sclerosed.  Miliary  abscesses 
are  often  found  in  the  walls. 

The  different  forms  of  cholecystitis  just  described  are  often  followed  by 
pericholecystitis.  Adhesions  form  between  the  bladder  and  the  neighbouring 
organs  (intestine,  pylorus,  cystic  duct,  etc.)  ;  ulcerations,  perforation,  and 
fisti^lee  appear,  and  are  followed  by  passage  of  large  calculi  into  the  intestine 
and  intestinal  occlusion,  calculous  peritonitis,  stenosis  of  the  pylorus,  etc. 

Symptoms  and  Diagnosis. — Let  us  take  the  simplest  case  first.  A 
patient  has  suffered  for  several  years  from  hepatic  colic,  verified  by  the 
presence  of  gall-stones  in  the  stools.  The  pains  have  later  lost  the  classical 
characteristics  of  hepatic  colic.  The  region  of  the  liver  has  become  painful. 
Sudden  movements,  jolts,  or  tight  clothing  cause  pain  in  the  hypochon- 


DISEASES  OF  THE  LIVER  983 

drium.  The  digestive  functions  are  disturbed.  Sometimes  vomiting  of  bile 
and  bilious  diarrhcEa  are  seen.  Jaundice  is  absent,  and  the  urine  does  not 
contain  bile.  Fever,  with  or  without  rigors,  is  common  ;  the  tongue  is 
dry  and  the  appetite  lost.  At  certain  times  attacks  of  pain  resembling 
hepatic  colic  occur,  and  the  patient  says  :  "  A  swelling  is  forming  under  the 
hver." 

The  patient  is  examined  in  the  erect  and  supine  positions.  I  would 
specially  recommend  the  erect  position,  because  it  is  very  favourable  for 
the  discovery  of  tumours  and  deformities  of  the  abdomen.  A  tumour 
appreciable  to  sight  and  touch,  and  painful  on  pressure,  is  sometimes  seen 
under  the  edge  of  the  ribs,  external  to  the  rectus  muscle,  at  the  tenth  costal 
cartilage. 

In  such  a  case  it  is  reasonable  to  diagnose  calculous  cholecystitis — a 
diagnosis  that  may  be  confirmed  by  radiography.  During  the  last  few  years 
I  have  seen  three  similar  cases  :  one  with  Pinard,  in  a  recently  confined 
woman,  successfully  operated  on  by  Hartmann ;  another  in  a  woman  suc- 
cessfully operated  on  by  Delbet ;  and  a  third  in  a  woman  successfully 
operated  on  by  Hartmann.  In  the  three  cases  the  inflamed  gall-bladder 
formed  a  tumour  below  the  liver.  The  diagnosis  of  calculous  cholecystitis 
is  not  always  as  easy  as  in  the  preceding  cases.  For  example,  a  patient 
complains  of  sharp  pains  in  the  hypochondrium,  vomiting,  anorexia, 
fever,  and  loss  of  flesh.  The  liver  is  not  enlarged  ;  the  lower  edge  of  the 
organ  is  painful  on  pressure,  but  neither  bulging  nor  tumour  in  the  gall- 
bladder region  is  found,  because  the  gall-bladder  is  hidden  under  the  liver, 
and  is  consequently  inaccessible  to  exploration.  Doubt  exists  as  to  the 
nature  of  the  disease.  We  may,  however,  arrive  at  a  diagnosis  if  we  find 
a  history  of  hepatic  colic,  as  it  is,  then,  probable  that  we  have  to  deal  with  a 
case  of  calculous  cholecystitis.  Pellereau  and  myself  were  thus  able  to 
make  a  diagnosis  in  the  case  of  a  woman  who  was  successfully  operated  on 
by  Tuffier.  The  calculus  was  as  large  as  a  walnut,  and  the  gall-bladder  was 
hidden  under  the  liver.  Finally,  the  diagnosis  of  calculous  cholecystitis 
presents  difficulties  of  another  kind,  when  the  gall-bladder,  by  its  size  or 
by  its  displacement,  simulates  hydatid  cyst,  cancer  of  the  liver,  tumours 
of  the  peritoneum  or  of  the  kidneys,  or  an  aberrant  lobe  of  the  liver.  All 
these  mistakes  in  diagnosis  have  been  made.  If  the  reader  will  refer  to  the 
section  on  Aberrant  Lol)e  of  the  Liver,  he  will  find  the  difliculty  in 
diagnosis  discussed. 

Calculous  cholecystitis  may  become  the  cause  of  a  series  of  complications, 
such  as  passage  of  large  calculi  into  the  intestine  and  intestinal  occlusion ; 
obliteration  of  the  pyloric  orifice  ;  perforation  of  the  diaphragm,  and  rejec- 
tion of  the  biliary  contents  through  the  bronchi ;  superacute  peritonitis, 
pyelitis,  endocarditis,  etc. 


984  TEXT-BOOK  OF  MEDICINE 

Finally,  there  is  quite  a  new  side  to  the  question — viz.,  the  association 
of  cholecystitis  with  appendicitis,  to  which  a  special  section  will  be 
devoted. 

Pericholecystitis  and  Adhesions. — For  fuller  details,  I  would  refer  the 
reader  to  Section  XXIII.,  on  Cholecystitis  in  General. 

Treatment. — When  the  diagnosis  of  calculous  cholecystitis  has  been 
made,  recourse  must  be  had  to  surgical  intervention.  The  many  com- 
plications already  described  show  the  danger  of  undue  delay.  I  need  not 
discuss  what  kind  of  operation  should  be  undertaken.  The  progress  made 
in  this  direction  during  recent  years  has  been  considerable.  Cholecystotomy 
is  sometimes  performed,  and  consists  in  opening  the  gall-bladder,  removing 
the  calculi,  and  establishing  an  external  biliary  fistula,  which  closes  later. 
Sometimes  cholecystectomy  is  performed ;  this  operation  consists  in  resection 
of  the  gall-bladder.  In  other  cases  cholecystenterostomy  is  performed 
(especially  in  the  obliteration  of  the  common  duct)  ;  it  consists  in  joining 
the  gall-bladder  directly  to  the  duodenum  or  the  ileum. 

Pylephlebitis — Aneurisms. — Calculous  obstruction  of  the  biliary  pas- 
sages and  the  lesions  of  angiocholitis  which  it  causes  are  sometimes  accom- 
panied by  pylephlebitis  (infection  of  the  portal  vessels).  Pylephlebitis  may 
attack  the  trunk  of  the  portal  vein  or  the  secondary  branches.  The  close 
relation  of  the  branches  of  the  portal  vein  to  the  biliary  canals  explains  the 
possibility  of  portal  phlebitis,  consecutive  to  peri-angiocholitis.  In  the  same 
way,  the  inflammation  of  the  portal  trunk,  secondary' to  the  lesions  of  the 
common  duct,  may  be  explained. 

Pylephlebitis  may  be  obliterating  or  suppurative.  Obliterating  phlebitis 
is  very  much  the  rarer ;  when  it  affects  the  portal  trunk,  we  find  ascites, 
swelling  of  the  spleen,  and  collateral  circulation  of  the  abdomen.  When  the 
pylephlebitis  is  suppurative,  it  is  accompanied  by  attacks  of  intermittent 
fever,  and  multiple  abscesses  of  the  liver  are  found  post  mortem. 

In  some  cases  the  arteries  of  the  neighbourhood  may  be  affected  by 
enlargement  and  ulceration,  causing  fatal  attacks  of  haemorrhage  (hsema- 
temesis  and  mela^na). 

Biliary  Endocarditis.— As  I  have  already  said,  bihary  lithiasis  favours 
the  infection  of  the  bihary  passages,  with  or  without  suppuration.  This  fact 
explains  angiocholitis,  pylephlebitis,  cholecystitis,  and  hepatitis.  The 
pathological  agents  being  readily  transported  into  the  heart,  endocarditis 
is  a  common  result.  The  left  side  of  the  heart  is  usually  affected,  especially 
at  the  mitral  and  aortic  valves.  Endocarditis  fairly  often  assumes  the 
ulcerative  forms.  The  symptoms  of  biliary  endocarditis  are  generally  in- 
definite ;  the  fever  and  the  jaundice  that  accompany  it,  indicate  the  onset 
of  the  lesions,  which,  through  lack  of  attention,  may  pass  unnoticed. 


DISEASES  OF  THE  LIVER  985 


5.  Peritonitis — Biliary  Fistulae. 

Let  us  now  consider  cases  of  partial  and  general  peritonitis,  due  to 
perforation  of  the  gall-bladder  and  bile-ducts  and  to  the  passage  of  micro- 
organisms into  the  peritoneum. 

Peritonitis. — The  varieties  of  peritonitis,  which  for  short  I  call  calculous 
peritonitis,  are  of  diverse  kinds.  We  find  partial  peritonitis,  which  is 
Umited  by  adhesions,  uniting  the  gall-bladder  to  the  stomach,  duodenum, 
omentum,  colon,  and  abdominal  wall.  Purulent  cloacae,  which  may  fuse 
later,  are  thus  formed.  The  diagnosis  is  very  difficult  in  these  cases.  The 
adhesions  are  sometimes  so  thick  that  they  form  a  tumour  around  the  gall- 
bladder. Chnically  speaking,  these  cases  of  partial  peritonitis  are  much  less 
serious  than  acute  general  peritonitis,  which  will  now  occupy  our  attention. 
Trousseau  has  reported  three  cases  : 

A  rich  shopkeeper  of  Tours,  under  Bretonneau's  care,  was  suddenly  taken  ill  during 
an  attack  of  hepatic  colic  which  had  lasted  for  six  days,  with  imcontrollable  vomiting, 
and  every  sign  of  acute  peritonitis,  which  proved  fatal  in  twenty-four  hours.  The 
autopsy  revealed  a  gall-stone  as  large  as  a  -v^-alnut  in  the  peritoneal  cavity,  and  in  the 
common  duct  was  the  perforation  by  which  the  stone  and  a  certain  quantity  of  bile 
had  made  their  exit. 

"  About  eight  years  ago,"  says  Trousseau,  "  I  was  attending  an  old  notary,  who 
had  been  subject  to  attacks  of  hepatic  cohc  for  some  time.  I  was  called  in  one  day 
because  the  symptoms  were  more  severe  than  usual.  He  was  vomiting  incessantly, 
the  belly  was  distended,  the  urine  was  entirely  suppressed,  the  pulse  was  scarcely 
perceptible,  and  the  temperature  was  subnormal.  He  had,  in  fact,  all  the  symptoms  of 
superacute  peritonitis.  I  considered  the  case  hopeless,  and,  as  a  matter  of  fact,  the 
patient  succumbed  next  day.  Although  no  post-mortem  examination  was  allowed,  I 
feel  justified  in  stating  that  it  was  a  case  of  peritonitis,  caused  by  effusion  into  the 
peritoneum,  following  rupture  of  the  gall-bladder,  or  of  one  of  the  bile-ducts." 

Werner's  case  :  "  I  was  called,"  says  he,  "  to  a  patient  who  had  extremely  acute 
hepetic  cohc.  I  diagnosed  gall-stones,  and  ordered  treatment.  Next  day,  as  the  jmins 
were  worse,  and  peritonitis  had  set  in,  I  suspected  a  rupture  of  the  gall-bladder.  The 
patient  died  two  days  later,  and  at  the  post-mortem  examination  I  found  twentv-live 
stones  as  large  as  hazel-nuts  in  the  gall-bladder  ;  the  bladder  was  perforated,  and  the 
bile  had  Howed  into  the  peritoneum.  A  calculus  larger  than  the  others  blocked  the 
common  duct." 

Calculous  peritonitis  is  a  most  treacherous  complication.  It  is  due  to 
perforation  of  the  large  bile-ducts,  and  especially  to  perforation  of  the 
gall-bladder.  It  may  come  on  during  an  attack  of  hepatic  colic,  and  as 
the  symptoms  in  each  case  are  similar  (violent  pain  and  vomiting),  it  may 
cause  serious  mistakes.  More  frequently  it  appears  during  the  cour.se  of 
obvious,  suspected,  or  latent  cholecystitis.  The  prognosis  is  fatal,  unless 
speedy  laparotomy  can  be  performed.  Tlic  patliogonosis  of  these  compli- 
cations has  yet  to  be  studied.  The  peritonitis  is  due  to  infection  by  the  bile, 
fluid,  or  calculi ;  the  Bacillus  coli  is  the  most  common  and  most  active  agent 


986  TEXT-BOOK  OF  MEDICINE 

in  this  affection.  How  does  the  peritoneum  become  infected  ?  Is  there 
always  a  rupture  of  the  bihary  passages  ?  and  if  so,  how  is  this  rupture 
caused  ?  It  might  be  supposed  that  if  the  gall-bladder  is  affected  with 
calculous  cholecystitis  and  ruptures,  it  is  because  its  cavity  is  greatly  dis- 
tended and  its  walls  are  very  thin.  Examination  of  cases  proves,  on  the 
contrary,  that  the  gall-bladder  is  habitually  contracted,  and  that  its  walls 
are  thickened,  hypertrophied,  and  brawny.  The  mucosa  of  the  gall-bladder, 
however,  presents  numerous  alveoli,  formed  by  hypertrophied  fibro-muscular 
bands.  In  these  alveoli,  which  are  of  various  forms  and  sizes,  we  often  find 
large  or  small  calculi  that  are  difficult  to  enucleate,  and  are,  as  it  were,  let 
into  the  wall.  The  alveoli  also  contain  septic  fluid  ;  they  are,  therefore,  an 
excellent  culture  medium  for  micro-organisms.  The  result  is  an  ulcerative 
process  which  may  lead  to  perforation  and  peritonitis.  Seuvre  and  Bouchard 
have  described  this  ulcerative  process  in  the  alveoli  of  the  mucosa,  but  we 
now  understand  the  mechanism  better,  through  bacteriological  researches. 
The  Bacillus  coli  is  the  essential  agent  in  the  ulcerative  process,  and  in  certain 
cases,  just  as  in  appendicitis,  the  organisms  imprisoned  in  these  closed 
alveoli  pass  through  the  walls  of  the  gall-bladder,  and  spread  afar  the 
peritoneal  infection,  previous  perforation  of  the  walls  not  being  absolutely 
necessary. 

Biliary  Fistulse. — The  process  which  has  favoured  adhesions  between 
the  gall-bladder  and  the  neighbouring  organs  frequently  terminates  in 
ulceration  and  perforation,  and  gives  rise  to  fistulas  which  give  exit  to  the 
contents  of  the  bladder  and  to  the  calculi.  These  fistulas  may  be  external 
or  internal,  and  either  spontaneous  or  secondary  to  surgical  intervention. 
In  Murchison's  statistics  we  find  eighty-nine  cutaneous  fistulse,  thirty-six 
duodenal  fistulse,  nine  colic  fistulse,  and  twelve  gastric  fistulse ;  in  addition 
to  the  foregoing  varieties,  renal,  vaginal,  pleuro- pulmonary,  and  hepato- 
bronchial  fistulse  have  been  found. 

Hepato-bronchial  and  cystico-bronchial  fistulse  explain  the  rejection, 
through  the  bronchi,  of  bile,  pus,  and  calculi.  The  close  proximity  of  the 
pleura  explains  bihary  pleurisy  (Gilbert  and  Lereboullet). 

The  cutaneous  fistulse  have  a  fairly  long,  anfractuous,  and  irregular 
course  ;  they  usually  occur  in  the  umbilical  region  and  the  right  hypochon- 
drium.  The  formation  of  the  cutaneous  opening  is  usually  preceded  by 
cellulitis  of  the  wall,  and  the  orifice  gives  exit  to  bile,  pus,  and  often  to 
calculi.     These  fistulse  generally  heal. 

The  cystico-duodenal  are  more  frequent  than  the  cystico-coHc  fistulse, 
and  it  may  be  said  that  many  large  gall-stones  found  in  the  stools  have 
passed  through  intestinal  fistulse.  The  calculi  are  sometimes  so  large  that 
they  provoke  symptoms  of  intestinal  occlusion.  The  cystico-gastric  fistulse 
explain  how  gall-stones  may  be  vomited.     It  is,  however,  not  impossible  for 


DISEASES  OF  THE  LIVER  987 

a  calculus  to  pass  back  into  the  stomach  during  an  attack  of  hepatic  colic, 
and  to  be  vomited  later.  In  the  celebrated  case  of  Ignatius  de  Loyola  there 
was  a  communication  between  the  common  duct  and  the  portal  vein. 

XXI.  PERMANENT  OBLITERATION  OF  THE  CO.ABION  DUCT- 
DIAGNOSIS  OF  THE  CAUSE  OF  THE  OBLITERATION. 
In  permanent  obliteration  of  the  common  duct  it  is  essential  to  diagnose 
the  cause  of  the  obliteration.  Prognosis  and  treatment  are  equally  con- 
cerned. If  the  duct  is  obHterated  by  a  calculus,  an  operation  is  indicated, 
and  recovery  may  be  expected.  If  it  is  obliterated  by  cancer,  the  prognosis 
is  hopeless,  in  spite  of  the  temporary  improvement  that  may  follow  an 
operation.  By  what  signs  and  sjTnptoms  can  we  make  this  pathogenic 
diagnosis  ?  How  are  we  to  recognize  the  nature  of  the  obliteration  ?  I 
shall  attempt  to  answer  these  questions,  utilizing  two  clinical  lectures 
which  I  have  devoted  to  this  subject.* 

In  the  first  place,  every  permanent  obliteration  of  the  common  duct 
shows  itself  by  an  invariable  syndrome,  no  matter  whether  the  obliteration 
is  due  to  calculus,  to  cancer  of  the  bihary  passages,  of  Vater's  ampulla,  or 
of  the  head  of  the  pancreas,  or  to  compression  by  a  neighbouring  tumour. 
This  syndrome  includes  jaundice,  the  presence  of  much  bile  pigment  in  the 
urine,  and  clay-coloured  faeces.  The  jaundice  may  be  accompanied  by 
intolerable  itching. 

Of  the  lesions  causing  permanent  obHteration  of  the  common  duct,  some 
are  rare,  others  are  common.  Amongst  the  former,  let  me  mention  hydatid 
cyst.s  of  the  liver,  hypertrophy  of  the  glands  of  the  hilum,  cicatrix  of  an  ulcer 
of  the  duodenum,  bands  and  adhesions  in  the  neighbourhood,  which  all 
cause  retention  of  bile.  The  most  frequent  causes  are  prolonged  catarrhal 
icterus,  cancer  of  Vater's  ampulla,  and  primary  cancer  of  the  biliary  pas- 
sages. Of  all  these  causes,  the  most  common  are  cancer  of  the  head  of  the 
pancreas  and  chronic  pancreatitis. 

In  the  pathogenic  diagnosis  we  must  first  eliminate  hypertrophic  biliary 
cirrhosis  (Hanot's  disease)  and  chronic  icterus,  with  enlarged  liver  and 
enlarged  spleen,  which  is  distinguished  from  the  syndrome  that  we  are  dis- 
cussing, by  the  coloratioii  of  the  faeces  and  by  the  uninterrupted  flow  of 
bile  into  the  intestine. 

Permanent  Obliteration  of  the  Common  Duct  by  Prolonged  Catarrhal 
Icterus.-^I  have  given  the  name  of  "prolonged  catarrhal  icterus"  to  a 
vaiiety  of  infective  icterus  (with  or  without  remissions),  which  may  last 
two  or  three  months.     In  prolonged  catarrhal  icterus  we  must  not  forget 

♦  "  ()l)lit«  ration  Pormannnto  du  Canal  aioledoquo  "  (Clintque  Medicale  de  V Hotel- 
Dieu,  1898,  11''^' et  l^'""  109003). 


988  TEXT-BOOK  OF  MEDICINE 

that,  besides  the  icteric  syndrome  common  to  every  permanent  obliteration  of 
the  large  bile-ducts  (hepatic  and  common),  we  may  also  find  anorexia,  loss  of 
flesh,  and  swelling  of  the  liver,  and  that  the  disease,  in  spite  of  its  threatening 
appearance,  generally  ends  in  recovery.  The  diagnosis  is  sometimes  very 
difficult.  When  we  see  a  patient  who  has  been  ill  for  two  months  or  more 
with  jaundice,  urobiUnuria,  clay-coloured  stools,  enlargement  of  the  liver, 
and  rapid  loss  of  flesh,  we  naturally  think  of  obstruction  of  the  common  duct, 
due  to  cancer  of  Vater's  ampulla  or  of  the  head  of  the  pancreas.  I  have 
often  been  anxious  in  cases  of  this  kind  as  to  the  outcome  of  the  disease. 

Permanent  Obliteration  of  the  Common  Duct  by  Cancer  of  Vater's 
Ampulla. — The  small  cancer  of  Vater's  ampulla,  already  described,  may 
cause  permanent  obliteration  of  the  common  duct.  The  growth  remains 
limited  to  the  ampulla,  has  no  invading  tendency,  and  soon  betrays  its 
presence  by  the  "  icteric  syndrome."  It  may  even  be  said  that  jaundice  is 
the  first  apparent  symptom,  and  is  due  to  obstruction  of  the  orifice  of  the 
common  duct  by  the  epitheliomatous  tumour.  It  has  all  the  attributes  of 
icterus  due  to  permanent  obliteration  :  yellowish  or  olive  colour  of  the  skin, 
bile-stained  urine,  and  colourless  faeces.  At  times  the  faecal  matter  may 
regain  its  colour  and  the  jaundice  become  paler,  proving  that  the  orifice  of 
the  common  duct  recovers  its  permeabOity  for  the  moment.  The  liver  is 
enlarged ;  the  gall-bladder,  though  greatly  distended,  cannot  always  be  felt 
through  the  abdominal  walls.  Pain,  either  spontaneous  or  provoked,  is  a 
rare  symptom  ;  it  is,  however,  seen  in  some  cases.  Rendu's  patient  had  acute 
attacks  of  pain  in  the  right  hypochondrium  and  the  epigastrium.  Palpation 
was  so  painful  at  the  pit  of  the  stomach  and  over  the  left  lobe  of  the  liver 
that  a  calcuhis  was  thought  to  be  impacted  in  the  common  duct.  The  post- 
mortem examination  showed  the'  absence  of  calculi  and  the  existence  of  a 
cancer  of  Vater's  ampulla. 

In  such  a  case  the  icteric  syndrome  (permanent  jaundice,  bile  in  the  urine, 
and  clay-coloured  stools,  with  enlarged  liver)  may  persist  for  months.  How, 
then,  are  we  to  diagnose  the  cause  of  the  obliteration  in  the  common  duct  ? 
The  diagnosis  is  very  difficult.  It  may  be  said  that  in  the  case  of  cancer  of 
Vater's  ampulla  icterus  and  decoloration  of  the  stools  sometimes  undergo 
remissions,  but  the  transient  remissions  are  of  no  value  in  the  diagnosis, 
for  they  are  met  with  in  other  cases  of  obliteration.  On  the  other  hand, 
it  may  be  said  that  pain  is  an  especial  feature  in  gall-stones  ;  but  cancer  of 
Vater's  ampulla  may  also  provoke  pain  similar  to  that  of  gall-stones,  as  in 
Rendu's  case.  It  has  been  said  that  diarrhoea  is  in  favour  of  cancer,  but 
in  reality  this  symptom  is  of  no  more  value  than  the  preceding  ones ;  it 
allows  us  neither  to  accept  nor  to  reject  the  hypothesis  of  cancer  of  Vater's 
ampulla.  Intestinal  haemorrhage  is  of  more  value.  When  the  growth 
blocks  Wirsung's  duct,  stearrhoea  and  examination  of  the  faeces  by  Gaultier's 
method  give  useful  information  {vide  Section  VII.,  Diseases  of  the  Pancreas). 


DISEASES  OF  THE  LIVER  989 

Permanent  Obliteration  of  the  Common  Duet  by  Primary  Cancer  of  the 
Biliary  Passages. — A  small  gro\vth  in  the  hepatic  or  common  duct  may  block 
the  canal  and  give  rise  to  mtense  and  prolonged  jaundice,  bile  in  the  urine, 
colourless  faeces,  rapid  loss  of  flesh,  and  sometimes  pain.  Primary  cancer  of 
the  gall-bladder  only,  causes  the  syndrome  in  question  when  it  spreads  to 
the  large  bile-ducts  or  to  the  adjacent  glands,  and  thus  obstructs  the  flow  of 
bile ;  as  primary  cancer  of  the  gall-bladder  is  associated  with  the  formation 
of  gall-stones,  the  result  is  that  in  three-fourths  of  the  cases  true  hepatic 
colic  may  be  associated  with  the  icteric  syndrome — a  fact  that  greatly 
complicates  the  diagnosis. 

Primary  epithelioma  of  the  common  or  of  the  hepatic  duct  is  not  rare. 
In  x3ither  case  the  icteric  syndrome  is  present,  but  the  condition  of  the  gall- 
bladder differs.  If  the  cancer  is  in  the  common  duct,  the  accumulation  of 
bile  in  the  gall-bladder  may  cause  considerable  distension ;  if  the  growth  is 
in  the  hepatic  duct  (Claisse),  the  gall-bladder  is  not  dilated.  In  primary 
cancer  of  the  biliary  canals  jaundice  is  sometimes  preceded  by  loss  of  flesh. 
The  appearance  of  jaundice  is  sometimes  sudden,  sometimes  progressive  ; 
when  it  has  appeared,  it  does  not  recede,  or,  at  least,  the  remissions  are 
momentary.  The  skin  assumes  a  deep  yellow  or  greenish  tint.  As  a  rule 
pain  is  absent,  but  I  have  seen  a  case  of  primary  cancer  of  the  biliary  passages 
wliere  the  pain  led  me  to  believe  in  obstruction  by  gall-stone  ;  my  mistake 
was  revealed  at  the  post-mortem  examination.  The  liver  is  practically 
normal  in  size,  and  secondary  cancer  never  attacks  it.  Anorexia  is  constant, 
digestive  troubles  are  frequent,  and  the  patient  grows  rapidly  thin,  and 
dies  in  eight  to  ten  months.  The  pathogenic  diagnosis  of  the  obliterating 
cause  is  for  several  months  a  matter  of  conjecture. 

Permanent  Obliteration  of  the  Common  Duct  by  Cancer  of  the  Head  of 
the  Pancreas.  - -Cancer  of  the  head  of  the  pancreas  is  one  of  tlic  most  frequent 
cau.ses  of  permanent  obliteration  of  the  common  duct.  The  following  cases 
will  give  an  idea  of  its  evolution  : 

1  \\a8  called  to  an  elderly  lady  suffering  from  jaundice,  which  had  commenced  a 
few  (lays  previously,  but  Avas  not  very  marked,  though  the  urine  contained  bile,  and 
the  fa'ces  were  (juito  colourless.  The  diagnosis  of  obliteration  of  the  common  duct  by 
a  calculus  was,  in  my  opinion,  very  improbable,  because  the  i)aticnt  had  never  luid  any 
sign  of  hepatic  colic  ;  the  jaundice  had  come  on  without  ]iain,  and  the  n-gion  of  the 
gall-bladder  was  absolutely  painless.  Althougii  tlio  i)atient  had  had  no  vomiting,  no 
diarrhn'a,  and  no  cohc,  I  nevertheless  tiiought  of  simj)le  catarrhal  jaundice,  and  pre- 
scribt^l  mild  jmrgatives,  large  cnemata  of  cold  water,  and  ingestion  of  oil  ;  the  patient 
was  put  on  milk  diet.  Tiireo  weeks  j)assed  Avithout  any  improvement  iji  the  symptoms, 
and  intolerable  itching  also  appeared.  The  jiaticnt  did  not  consider  her.scif  ill,  and  fol- 
lowed her  usual  habits.  Her  ai)petite,  however,  grew  less.  The  obstinacy  of  the  jaundice 
made  me  anxious,  but  I  tried  to  fall  back  on  the  hypothesis  of  j)rolonged  catarrhal 
jaundice.  E.xamination  of  the  abdomen  and  of  the  liver  gave  no  information.  Other 
remedies  were  tried  with  no  better  result,  and  after  six  weeks  the  )jatient,  who  had 
grown  thin  and  had  a  distaste  for  food,  decided  to  leave  lor  one  of  the  Mediterranean 
towns. 


990  TEXT-BOOK  OF  MEDICINE 

During  the  five  months  of  her  residence  in  the  South  the  symptoms  were  unchanged. 
She  wrote  that  her  colour  had  now  become  a  brownish  yellow,  the  loss  of  flesh  was 
making  rapid  progress,  and  several  times  a  week,  without  ajiparent  cause,  she  had 
acute  attacks  of  fever,  with  a  temperature  of  102°  to  104°  P.  These  attacks  com- 
menced with  a  rigor,  and  ran  through  three  stages — cold,  hot,  and  sweating,  just  as  in 
malaria.  Quiaine  had  no  effect.  Between  these  irregular  attacks  of  fever  the  tem- 
perature was  normal. 

When  the  patient  returned  to  Paris  I  was  immediately  sent  for.  In  six  months  she 
had  lost  nearly  50  poimds  in  weight,  and  was  hterally  reduced  to  a  skeleton.  I 
examined  her.  The  anorexia  was  complete  :  she  could  scarcely  drink  a  cup  of  milk. 
The  faeces  were  clay-coloured,  but  at  times  they  showed  a  shght  tint,  proving  that  a 
small  quantity  of  bile  reached  the  intestine.  The  extreme  thinness  of  the  patient  made 
the  exploration  of  the  abdomen  very  easy,  but  nothing  abnormal  could  be  felt.  The  Uver 
was  of  normal  size,  and  the  gall-bladder  could  not  be  found.  It  was  certainly  a  case 
of  cancer  in  the  bile-ducts,  Vater's  ampulla,  or  the  head  of  the  pancreas,  imless,  by  some 
happy  exception,  a  large  gall-stone  had  become  impacted  in  the  common  duct  without 
causing  pain.  In  any  case  an  exploratory  laparotomy  was  absolutely  indicated,  and 
Routier,  who  was  called  in,  expressed  the  same  opinion. 

The  operation  was,  therefore,  performed.  No  calculus  was  found.  The  gall-bladder, 
which  was  deep-seated  and  only  sHghtly  apparent  at  first  sight,  though  much  distended, 
contained  about  10  ounces  of  bile,  removed  by  aspiration.  There  was  no  cholecystitis. 
The  fiver  was  almost  normal  in  size.  We  were  convinced,  after  careful  examination, 
that  the  obstruction  of  the  common  duct  was  due  to  cancer  of  the  head  of  the  pancreas, 
and  the  operation  was  concluded  by  anastomosing  the  gall-bladder  with  a  coil  of  small 
intestine.  A  few  days  after  the  operation  the  jaimdice  diminished,  the  faeces  became 
coloured,  the  urine  was  clear  and  Hmpid,  and  the  patient  was  able  to  take  Hght  nourish- 
ment. The  improvement,  however,  was  not  of  long  duration^  and  three  months  later 
the  patient  succumbed  to  cachexia. 

This  case  gives  an  idea  of  obliteration  of  the  common  duct  by  cancer  of 
the  head  of  the  pancreas,  and  corresponds  to  the  classical  description.  In 
their  description  of  cancer  of  the  head  of  the  pancreas,  Bard  and  Picq  thus 
sum  up  the  question  :  "  The  characteristic  symptoms  of  primary  cancer 
of  the  head  of  the  pancreas  are  progressive  jaundice,  enormous  dilatation  of 
the  gall-bladder,  loss  of  flesh,  and  rapid  cachexia,  without  notable  enlarge- 
ment of  the  liver.  The  last  of  these  four  signs,  though  purely  negative  in 
character,  is  just  as  important  as  the  other  three  ;  their  union  constitutes 
the  special  characteristic  of  the  disease."  These  conclusions  hold  good  in 
most  cases,  but  the  exceptions,  which  are  far  from  being  rare,  must  be  taken 
into  account.  These  exceptions  show  us  that  the  jaundice  may  not  be  pro- 
gressive, the  gall-bladder  may  not  be  dilated,  and  the  hver  may  be  consider- 
ably enlarged. 

I  said  previously  that  the  jaundice  may  not  always  be  progressive,  and 
in  proof  thereof  I  quote  the  following  case,  published  by  Legrand  : 

A  man  who  was  admitted  for  chronic  jaundice  had  cancer  of  the  head  of  the  pancreas, 
proved  at  the  post-mortem  examination.  On  admission  we  foimd  very  deep  icterus, 
bile  in  the  urine,  and  colourless  faeces.  Furthermore,  the  gall-bladder  was  enormous 
and  easily  felt.  One  day  a  flow  of  bile  occurred  ;  the  faeces  were  of  a  deep  green  colour, 
and  the  tumour  formed  by  the  gall-bladder  diminished.     Dutil  has  pubhshed  a  similar 


DISEASES  OF  THE  LIVER  991 

case  :  A  patient  was  admitted  to  hospital  with  jaimdice,  biUous  urine,  and  colourless 
faeces.  On  several  occasions,  however,  it  was  noticed  that  bile  was  present  in  the  stools, 
and  the  post-mortem  examination  revealed  cancer  of  the  head  of  the  pancreas. 

The  following  case  shows  stiU  better  how  the  symptoms  of  cancer  of  the 
head  of  the  pancreas  may  differ  from  the  classical  type  : 

A  man,  thirty-six  years  of  age,  was  taken  ill  in  September,  1891,  with  digestive 
troubles  and  pain,  that  was  especially  severe  after  meals.  The  pain  was  most  severe 
in  the  epigastrium  and  left  hypochondrium,  but  thd  not  exactly  show  the  characteristics 
of  hepatic  coUc.  It  persisted  for  several  months.  In  February,  1892,  progressive 
jaimdice  supervened,  with  increasing  loss  of  fiesh,  great  weakness,  and  intolerable 
itching.  These  symptoms  made  progress  in  March,  April,  and  Ma3\  At  this  date 
Dr.  Ferras  de  Macedo  sent  the  patient  to  Paris.  The  condition  was  as  follows  :  Very 
intense  jaundice,  continual  itching,  colourless  foul-smelUng  fseces,  and  urine  containing 
bile  and  albumin.  The  liver  was  enormous,  measuring  9  inches  in  the  median  line  and 
11  inches  in  the  nipple  line  ;  the  surface  was  regular,  of  normal  resistance,  without 
fluctuation,  and  the  organ  formed  a  marked  bulging  in  the  epigastrium.  The  edge  was 
soft,  and  palpation  did  not  reveal  the  gall-bladder.  The  spleen  was  normal,  and  the 
principal  viscera  were  healthy.  The  appetite  was  good,  but  digestion  was  painful,  and 
accompanied  by  a  feehng  of  heaviness  and  by  pain  racUating  into  the  left  hypo- 
chondrium. 

It  was  clearly  a  case  of  jaundice  from  obliteration  of  the  common  duct.  Was  the 
obliteration  due  to  cancer  or  to  a  gall-stone  ?  The  pathogenic  diagnosis  was  most 
difficult.  Bouchard  and  Terrier  favoured  the  diagnosis  of  cancer  of  the  pancreas,  an 
opinion  shared  by  Ferras  de  Macedo.  Hanot  and  myself  favoured  the  diagnosis  of  a 
calculus.  Reclus,  Perier,  and  Oettinger  concluded,  and  tliis  was  also  my  opinion,  that 
it  was  necessary  to  perform  exploratory  laparotomy,  followed  by  choledochotomy  or 
biliary  enterostomy.  The  patient,  wishing  for  further  advice,  went  to  Germany,  and 
finally  returned  to  Paris.  Reclus  performed  the  operation.  The  Uver  was  enormous, 
and  of  a  very  deep  brown,  colour.  Under  its  soft  edge  the  gall-bladder  was  found  ;  in 
size  it  was  larger  than  two  fists.  The  gall-bladder  and  the  cystic  duct  were  free,  but 
the  common  duct,  near  the  head  of  the  pancreas,  was  obhterated  by  a  hard  body,  as 
large  as  a  walnut,  so  firmly  and  deeply  set  that  its  extraction  seemed  impossible.  The 
gall-bladder  was  united  to  an  intestinal  coil  (bifiary  enterostomy). 

The  operation  was  followed  by  marked  improvement,  and  the  patient  got  up  on  the 
fourteenth  day.  The  appetite  returned,  and  on  the  seventh  day  the  fiver  measured  but 
7  inches  in  the  nipple  fine.  Three  months  later  the  patient  was  in  perfect  health,  but  a 
short  time  after,  as  the  pain  and  other  symptoms  returned,  he  came  back  to  Paris. 
Ho  underwent  another  operation,  performed  by  Reclus,  who  discovered  that  the  hard 
body  found  at  the  first  operation  was  a  cancer  of  the  head  of  the  pancreas.  The  fact 
was  verified  at  the  post-mortem  examination.  This  case  proves,  contrary  to  the 
conclusions  arrived  at  by  certain  writers,  that  the  Uver  may  become  much  enlarged  in 
obstruction  of  the  common  duct  by  cancer  of  the  head  of  the  pancreas.  It  also  sliows 
that  the  icteric  syndrome  due  to  the  obstruction  of  the  common  duct  by  cancer  of  the 
head  of  the  pancreas  may  be  accompanied  by  jmin  that  is  not  always  easily  dis- 
tinguished from  that  due  to  obUteration  of  the  duct  by  a  gall-stone. 

Permanent  Obliteration  of  the  Common  Duct  by  a  Calculus. — We  have 
still  to  make  tlu;  pathogenic  diagnosis  hetwccu  ohlilcratioii  of  the  duct  by 
cancer  of  the  head  of  the  pancreas  and  by  gall-stones.  The  diagnosis  is  singu- 
larly simplified  if  the  (j])]iteration  lias  been  ])recedcd  by  classical  hepatic 
colic.     In  such  a  case  the  cause  of  the  obUteration  is  obvious.    In  other  cases. 


992  TEXT-BOOK  OF  MEDICINE 

however,  the  pains  due  to  impaction  of  a  stone  are  very  difficult  to  distin- 
guish from  those  due  to  cancer  of  the  pancreas.  Moreover,  permanent 
obliteration  by  a  stone  may  cause  considerable  loss  of  flesh,  thus  resembling 
the  cachexia  of  cancer,  and  rendering  the  diagnosis  doubtful.  The  following 
case  will  illustrate  this  point : 

On  August  25,  1897,  a  woman,  sixty-three  years  of  age,  was  admitted  for  chronic 
jaundice,  involving  the  skin  and  the  mucous  membranes.  The  urine,  which  had  an  oily 
look,  was  of  a  deep  mahogany  colour,  and  contained  much  bile  pigment  and  traces  of 
albumin.  On  the  other  hand,  the  faeces  were  clay-coloured.  The  contrast  between 
the  deep  jaundice  of  the  skin  and  of  the  urine  and  the  whiteness  of  the  faeces  clearly 
pointed  to  obstiiictive  jaundice  ;  the  bile,  being  arrested  in  its  course,  could  no  longer 
flow  into  the  intestine. 

The  patient  told  us  that  she  had  been  yellov/  for  a  year.  The  jaimchce  had  been 
preceded  by  pain,  that  came  on  about  three  hours  after  breakfast.  The  jjain  started  in 
the  epigastric  region,  and  rachated  over  the  belly,  into  the  back,  and  between  the 
shoulder-blades  ;  it  was  sometimes  followed  by  fainting-fits.  The  pain  was  frequently 
accompanied  by  vomiting  of  bile.  After  the  jaundice  had  appeared  the  faeces  became 
whitish.  The  patient  still  continued  to  work  in  spite  of  the  pain.  She  had  been  unwell 
for  nearly  a  year,  and  although  she  no  longer  had  the  attacks  of  pain  with  which  the 
disease  began,  the  pain  was,  nevertheless,  almost  continuous,  with  exacerbations  and 
vomiting  of  bile.  The  jaundice  increased  or  diminished  at  intervals,  but  never  dis- 
api^eared.  On  several  occasions  she  had  severe  attacks  of  fever,  preceded  by  rigors, 
and  followed  by  profuse  sweating.  Pruritus  was  constant.  The  appetite  had  failed, 
and  the  stomach  had  become  so  intolerant  that  she  could  only  take  milk  in  small 
quantities.  Her  strength  had  gradually  diminished,  and  she  had  lost  over  30  pounds  in 
weight,  and  therefore  when  I  saw  this  feeble  old  woman  t\^ith  cachexia,  chronic 
jaundice,  and  a-dema  of  the  legs,  I  could  not  at  first  set  aside  the  idea  of  cancer. 

Examination  of  the  patient  gave  the  following  results  :  The  belly  was  sUghtly 
distended,  but  there  was  no  trace  of  collateral  circulation  ;  ascites  and  tumour  were 
absent.  The  hver  reached  three  fingers'  breadth  below  the  costal  margin,  and  was 
very  painful  on  palpation.  The  gall-bladder,  however,  was  not  enlarged,  and,  even 
supposing  that  it  had  been,  it  was  deeply  hidden,  and  could  not  be  felt.  The  spleen, 
heart,  and  lungs  were  normal.  There  was  no  tricuspid  murmur,  and  the  pulse -rate  was 
75.     The  urine  contained  some  albumin,  but  not  a  trace  of  sugar — an  important  point. 

Such  was  the  condition  on  admission.  It  was  now  a  question  of  making  a  diagnosis, 
and  it  was  necessary  to  find  out  the  lesion  preventing  the  passage  of  bile  into  the 
intestine.  Was  it  a  calculus,  or  was  it  cancer  ?  Although  she  was  old  and  very  thin — 
both  points  in  favour  of  cancer — I  was  compelled  to  consider  the  nature  of  the  pains  at 
the  onset  of  the  disease  in  making  a  diagnosis.  These  pains  appeared  to  me  to  be  in 
favour  of  hepatic  colic,  rather  than  of  cancer  of  the  pancreas.  In  consequence,  I  decided 
in  favour  of  obhteration  of  the  common  duct  by  a  calculus. 

The  question  of  treatment  remained.  As  I  felt  that  the  obstruction  was  due  to  a 
calculus,  and  as  it  had  already  lasted  a  year,  I  thought  of  surgical  intervention. 
Nevertheless,  as  I  wished  to  observe  the  case  closety,  I  prescribed  milk,  with  bicarbonate 
of  soda,  capsules  of  ether  and  turpentine  (Durnade's  remedy),  and  sahne  purgatives. 
I  tried  to  reheve  the  itching  by  baths  of  starch  and  gelatine,  alcohol  rubs,  and  inunction 
of  a  bromide  ointment.  From  this  date  the  disease  ran  the  following  course  :  The 
icteric  syndi'ome  (icterus,  bilious  urine,  and  colourless  faeces)  was  not  always  regular. 
At  times  a  small  ciuantity  of  bile  made  its  way  into  the  intestine,  the  faeces  became 
sUghtly  tinged,  the  colour  of  the  urine  and  of  the  skin  ^^'as  not  quite  so  deep,  and  the 
itching  was  less  troublesome.  In  vicAv  of  these  shght  remissions,  I  asked  myself  whether 
the  obhteration  might  not  yield  spontaneously.    The  faeces  were  strained  tluough  a  sieve 


DISEASES  OF  THE  LIVER 


993 


and  examined  for  gall-stones,  without  success.  Evidently  the  bile  under  pressure  was 
able  at  times  to  force  the  barrier,  which  was  not  quite  insurmountable,  but  the 
obhterating  body  was  not  dislodged. 

The  hver  extended  below  the  ribs.  The  patient  had  no  ajjpetite,  and  took  only  a 
few  spoonfuls  of  soup  or  milk.  At  times  she  complained  of  sharp  epigastric  and 
hepatic  pains,  and  vomited  fluid  containing  a  small  quantity  of  bile,  a  further  proof 
that  the  bile  was  able  to  pass  through  the  obstructed  ducts.  Suddenly  severe  attacks 
of  fever  appeared,  ^ith  violent  rigors,  rise  of  temperature  to  104°  F.,  and  profuse 
sweating.  Apart  from  these  severe  attacks  of  fever,  which  for  some  months  past  had 
appeared  at  iiTegular  intervals  once  or  t\\-ice  a  week,  the  temi^erature  was  practically 
normal,  as  the  following  chart  shows. 


Sepferhber 


Date 


Fxu.  60. — Temperature  Chart  in  Obstruction  of  the  Common 
Bile-Duct. 


I  shall  return  later  to  these  severe  attacks  of  fever,  and  shall  try  to  indicate  their 
cause.  When  fever  supervenes  in  a  patient  suffering  from  obhteration  of  the  bile-ducts, 
wo  think  of  cholecystitis  or  hepatic  abscesses,  but  yet  I  ehminated  the  idea  of  infective 
fever.  The  patient  continued  to  lose  flesh,  the  pain  did  not  diminish,  the  itching  was 
intolerable,  the  nausea  was  permanent,  and  it  was  time  to  intervene.  The  patient 
readily  consented  to  an  operation. 

Du[)lay  diagnosed  obhteration  of  the  common  duct  by  a  gall-stone.  The  belly 
was  opened,  and  the  anterior  edge  of  the  hver  was  pushed  upwards,  so  as  to  expose  ita 
lower  surface.  The  gall-bladder  was  not  distended  ;  indeed,  it  could  not  be  felt  in  the 
cystic  fossa.  After  the  hver  had  been  tilted  backwarrls,  Duplay  succeeded  in  feeling 
near  the  hilum  a  deep-seated  tumour  as  large  as  a  hazel-nut,  of  stony  hardness,  and 
covered  by  a  fairly  thick  soft  wall.  It  was  impossible  to  state  precisely  whether  the 
tumour  involved  the  common  or  the  cystic  duct,  but  it  appeared  rather  to  be  at  the 
junction  of  the  cystic  and  hepatic  ducts  with  the  common  duct.  Digital  exploration 
of  the  common  duct  along  the  free  edge  of  the  gastro-hepatic  omentum  and  in  its 
retroduodcnal  portion  showed  that  the  common  duct  contained  no  calculi  in  (liis 
portion  of  its  course.  The  soft  parts  covering  the  hard  tumour  were  then  incised,  and 
the  curette  brought  out  some  small  fragments,  and  then  a  largo  calculus  weighing 
j^  ounce. 

The  diagnosis  was  therefore  verified.  The  result  of  tlie  operation  was  excellent. 
The  icteric  syndrome  disafipearod,  the  ffeces  became  colounid,  the  urine  gradually 
regained  its  normal  tint,  in  a  fortnight  the  jaundice  had  entirely  disappeared,  and  in 
three  weeks  the  wound  had  healed.     The  itching  ceased  as  soon  as  the  bik^  (lowed  into 

63 


994  TEXT-BOOK  OF  MEDICINE 

the  intestine  ;  there  was  no  recurrence  of  pain  or  vomiting.  The  fever  disappeared  as 
soon  as  the  bile  took  its  normal  course,  proving  that  it  was  not  due  to  hepatic  infection. 
In  less  than  three  months  the  patient  regained  her  normal  weight  and  appetite.  A 
year  later  she  was  in  perfect  health. 

Analysis  of  the  Symptoms. — The  patient  had  cachectic  oedema  and  rapid 
loss  of  weight.  Such  wasting  in  permanent  obhteration  of  the  common  duct 
might  lead  to  error  and  cause  belief  in  cancer,  and  yet  we  have  just  seen  that 
marked  loss  of  flesh  is  of  small  importance  in  the  diagnosis  of  the  cause  of 
the  obliteration  of  the  common  duct ;  this  fact  I  have  noticed  on  several 
occasions. 

There  is  another  point  deserving  of  notice.  Even  before  admission  to 
hospital,  the  patient  had  suffered  from  attacks  of  fever  that  commenced 
with  a  violent  rigor,  and  reached  104°  F. 

In  order  to  discuss  the  cause  and  the  value  of  febrile  attacks  in  patients 
with  biliary  retention,  let  us  consider  the  question  as  a  whole. 

The  migration  of  gall-stones  during  hepatic  colic  is  sometimes  accom- 
panied by  attacks  of  fever  (Charcot's  heptalgic  fever).  I  have  discussed  this 
point  under  the  Satellite  Symptoms  of  Hepatic  Cohc.  In  this  case,  however, 
the  attacks  of  fever  could  not  be  attributed  to  migration  of  calculi,  because 
an  enormous  calculus  was  impacted  in  the  common  duct,  and  prevented  any 
migration.  On  the  other  hand,  the  attacks  could  not  be  attributed  to  infec- 
tion of  the  bile-ducts  (angiocholitis,  hepatitis,  cholecystitis),  because  the  fever 
ceased  when  the  flow  of  bile  became  normal.  How,  then,  are  we  to  explain 
the  thirty  or  forty  attacks  of  fever  which  the  patient  had  within  a  few 
months  ?  I  have  no  intention  of  formulating  a  theory,  but,  seeing  that  the 
attacks  lasted  as  long  as  the  biliary  retention,  and  that  they  ceased  as  soon 
as  the  biliary  retention  ceased,  it  is  quite  logical  to  attribute  them  to  the 
retention  and  absorption  of  bile.  Is  the  bile  altered  in  consequence  of  long 
retention  ?  I  do  not  know,  but  the  great  clinical  fact  is  that  in  patients 
suflering  from  permanent  obliteration  of  the  common  duct  severe  and 
repeated  attacks  of  fever  may  occur  without  appreciable  infection  of  the 
bihary  passages. 

Similar  attacks  of  fever  were  present  in  a  case  that  I  saw  with  Charrier  on 
July  7,  1895.  The  patient  was  suffering  from  bihary  retention  due  to  permanent  obhtera- 
tion of  the  common  duct  by  a  stone.  The  obstruction  had  already  lasted  seven  months. 
The  gall-bladder  could  not  be  felt,  but  the  Hver  was  enlarged  and  painful.  We 
recommended  an  operation,  and  the  patient  was  taken  to  the  Necker  Hospital,  where 
Routier  operated.  The  gall-bladder  was  of  small  size,  and  was  not  infected  ;  it  contained 
seven  calcuH,  whilst  two  others  were  impacted  in  the  common  duct,  blocking  it  com- 
pletely.    No  pus  was  foimd.     The  operation  was  a  complete  success. 

In  this  case  the  attacks  of  fever  could  not  be  attributed  to  an  infection  of  the  bihary 
passages,  as  the  operator  did  not  find  any  trace  thereof,  and  as  the  attacks  yielded  as 
soon  as  the  operation  had  re-established  the  normal  flow  of  the  bile.  The  retention 
and  absorption  of  bile  cause  these  attacks  of  fever.  I  have  also  noticed  similar  attacks 
of  fever  in  obhteration  of  the  common  duct  by  cancer  of  the  head  of  the  pancreas.     I 


DISEASES  OF  THE  LIVER  995 

have  already  mentioned  a  case  of  jaundice  of  eight  months'  duration  following  on  cancer 
of  the  head  of  the  pancreas.  The  patient  had  also  had  attacks  of  fever,  Avith  a  rise  of 
temperature  to  104°  F.  ;  the  attacks  lasted  for  several  months.  In  this  case  also  an 
operation  revealed  no  trace  of  suppuration  ;  the  gall-bladder  was  not  infected,  and  the 
attacks  of  fever  ceased  as  soon  as  the  obstacle  to  the  flow  of  bile  had  been  removed. 

The  object  of  this  digression  is  to  emphasize  certain  varieties  of  fever  in 
cases  of  jaundice.  First  variety  :  so-called  heptalgic  fever  (satelUte  fever), 
associated  with  the  migration  of  calculi  and  hepatic  colic.  Second  variety  : 
so-called  bilio-septic  fever,  the  result  of  infection  of  the  bihary  passages 
(angiochoUtis,  cholecystitis,  abscesses).  Third  variety  :  fever  resulting  from 
the  permanent  retention  of  bile.  In  these  three  varieties  the  fever  occurs 
in  attacks,  with  this  difference  however  :  that  the  attacks  are  distinct  and 
separated  by  longer  or  shorter  periods  of  ajjyrexia  in  the  first  and  third 
varieties,  whereas  they  are  part  of  a  more  continuous  febrile  condition  in 
infection  or  suppuration  of  the  biliary  passages. 

Diagnosis. — Let  us  now  consider  the  diagnosis  of  the  cause  of  the  oblitera- 
tion. In  general  terms  cancerous  obstruction  of  the  common  duct  causes 
dilatation  of  the  gall-bladder,  while  obstruction  by  a  stone  causes  atrophy. 
This  rule  holds  in  many  cases,  but  as  exceptions  we  find  the  cases  of  Cruveil- 
hier,  Sabourin,  Billroth,  Jalaguier,  Hanot,  Griffon,  etc.,  in  which  the  gall- 
bladder showed  enormous  dilatation,  consequent  on  obliteration  of  the 
terminal  portion  of  the  common  duct  by  a  calculus,  cancer  being  absent. 
I  agree,  therefore,  with  Reclus  that  "  dilatation  of  the  gall-bladder  is  in 
favour  of  cancer,  because  atrophy  of  the  bladder  is  much  more  frequent 
than  enlargement  in  gall-stones."  This  sign  is,  however,  not  absolute,  and 
cannot  jper  se  decide  the  question  without  reckoning  on  the  fact  that  it 
is  not  easy  to  make  out  dilatation  of  the  gall-bladder,  since  there  are  cases 
in  which,  though  it  is  dilated,  it  is  so  deeply  seated  that  it  cannot  be 
examined. 

Enlargement  of  the  liver,  formerly  considered  to  be  special  to  calculous 
obliteration,  may  exist  in  the  case  of  cancerous  obliteration,  as  is  shown  by 
the  enormous  size  of  the  liver  in  the  patient  I  saw  with  Reclus.   i 

Rapid  loss  of  flesh  and  cachexia  are  in  favour  of  cancer.  And  yet  calcu- 
lous obliteration  of  the  common  duct  may  be  followed  by  considerable  loss 
of  flesh  and  cachexia,  as  was  seen  in  my  patient,  who  had  lost  over  30  pounds 
in  a  few  months. 

The  comparative  analysis  of  the  faoces  will  be  described  under  Pan- 
creatitis. 

Glycosuria  has  been  given  as  a  sign  of  cancer  of  the  pancreas,  but  this 
sign  is  only  of  slight  value.  Glycosuria  is  found  in  about  a  third  of  the  cases, 
and  even  then,  according  to  Bard  and  Vm[,  it  is  a  secondary  symptom, 
due  not  to  cancer,  but  to  concomitant  sclerosis  of  the  pancreas. 

03— 2 


996  TEXT-BOOK  OF  MEDICINE 

Summary :  The  pain  furnishes  the  most  important  support  in  the  diag- 
nosis of  the  cause  of  the  obHteration,  and  even  then  it  is  necessary  to  define 
clearly  the  character  of  the  pain.  Cancer  of  Vater's  ampulla  may  cause  pain 
and  simulate  hepatic  colic,  as  in  Rendu' s  case.  Cancer  of  the  head  of  the 
pancreas  is  even  more  painful ;  this  fact  led  to  an  erroneous  belief  in 
calculous  obliteration.  Pain  is  a  valuable  sign  only  when  it  appears  in  the 
form  of  classical  hepatic  colic,  which  at  more  or  less  distant  periods  has 
preceded  or  accompanied  the  definite  obliteration  of  the  common  duct. 

I  have  intentionally  omitted  in  this  section  obliteration  of  the  common 
duct  consecutive  to  pancreatitis.  This  question  is  so  important  that  I  shall 
deal  with  it  in  a  special  section  under  Diseases  of  the  Pancreas. 

Treatment. — Operative  interference  becomes  necessary  at  some  stage  of 
obliteration  of  the  common  duct,  even  in  the  absence  of  an  exact  diagnosis 
as  to  the  cause.  Even  in  cases  of  cancer  an  operation  is  proper  because  it 
re-establishes  the  flow  of  bile,  relieving  the  itching  and  giving  the  patient 
some  months  of  hope. 

In  obliteration  by  a  gall-stone  an  operation  leads  to  recovery.  As  my 
experience  has  increased,  I  feel  sure  that  surgical  treatment  is  to  be  preferred 
m  obhteration  of  the  bile-ducts  by  a  gall-stone,  because  the  obliteration  is 
so  often  accompanied  by  cholecystitis.  The  operation  re-establishes  the  flow 
of  bile,  and  removes  the  gall-bladder,  which  may  give  rise  to  complications. 
It  has  the  further  advantage  of  preventing  the  onset  of' severe  pancreatitis. 
I  know  that  the  objection  will  be  raised  that  obhteration  by  a  calculus  of 
several  months'  duration  may  yield  to  treatment  at  Vittel,  Vichy,  Contrexe- 
ville,  Carlsbad,  etc.  ;  it  is,  however,  proper  to  add  that  many  of  these  cases 
are  liable  to  relapses,  to  hepatic  colic,  cholecystitis,  pancreatitis,  and  other 
well-known  comphcations. 

We  must  be  ready  to  decide,  for  it  is  better  to  intervene  early  rather 
than  late.  In  the  case  above  quoted  a  late  operation  did  not  prevent 
recovery  ;  the  passage  of  small  amounts  of  bile,  however,  saved  the  situation. 
I  feel,  however,  that  more  prompt  decision  is  needed.  In  permanent  ob- 
literation of  the  common  duct  by  a  calculus,  the  most  favourable  time  for 
operation  is  within  the  first  two  months  {vide  Section  VII.,  Diseases  of  the 
Pancreas). 

Cases  recently  pubished  by  Lejars  and  Morestin  are  in  favour  of  this 
view,  and  a  case  under  my  care  at  the  Hotel-Dieu  sums  up  the  situation  : 

A  woman  was  admitted  into  my  wards  on  May  7,  1907.  She  had  suffered  from 
attacks  of  hepatic  coHc  for  four  years,  and  the  present  attack  was  of  seven  weeks' 
duration,  the  icteric  syndrome  being  complete.  I  made  a  diagnosis  of  permanent 
obliteration  of  the  common  duct  by  a  calculus.  As  medical  treatment  failed,  I  asked 
Terrier  and  Gosset  to  operate.  The  atrophied  gall-bladder  was  excised,  and  the 
common  duct  was  catheterized,  revealing  a  rounded  stone,  as  large  as  a  small  nut, 
near  Vater's  amijulla.     The  hepatic  duct  was  drained.     Complete  recovery  followed. 


DISEASES  OF  THE  LIVER  997 

XXII.  ANGIOCHOLITIS— CHOLECYSTITIS. 

Pathogenesis. — Angiocholitis  and  cholecystitis  are  always  due  to  microbic 
toxi- infections.  The  infectious  process  is  sometimes  favoured  by  stagnation 
of  bile  due  to  compression  or  obstruction  of  the  bile-ducts  ;  at  other  times 
the  invasion  of  the  bile-ducts  by  microbes  takes  place,  without  previous 
obstruction.  Biliary  calculi  realize  the  tj'pe  of  the  obstructive  infection ; 
typhoid  infection  realizes  the  type  of  infection  without  previous  obstruction. 
I  would  therefore  refer  the  reader  to  the  sections  on  Biliary  Lithiasis  and  on 
Typhoid  Fever. 

In  the  normal  state  the  bile,  the  gall-bladder,  and  the  bile-ducts  are 
aseptic,  the  only  exception  being  the  lower  portion  of  the  common  duct  on 
account  of  its  proximity  to  the  duodenum,  in  which  coli  bacilh,  strepto- 
cocci, and  staphylococci  are  normally  present.  In  pathological  conditions, 
however,  these  microbes  enter  the  bile-ducts.  Many  other  agents,  such  as 
the  pneumococcus,  the  Bacillus  typhosus,  the  cholera  bacillus,  diplococci, 
and  liquefying  saprogenic  bacilli  may  also  infect  the  biliary  passages.  In 
some  cases  the  organisms  may  even  live  in  a  latent  state  in  the  bile,  which 
has  not  the  bactericidal  properties  formerly  attributed  to  it. 

The  micro-organisms  come  mo^t  frequently  from  the  infected  intestine. 
Why,  however,  do  the  biliary  passages  allow  themselves  to  be  invaded  ? 
What  cause  governs  the  emigration  of  microbes  from  an  infected  intestine 
to  the  aseptic  biliary  passages  ?  The  virulence  of  the  intestinal  microbes 
may  be  a  sufficient  cause  for  the  emigration,  but  most  frequently  this  migra- 
tion towards  the  biliary  passages  is  favoured  by  pathological  conditions  of 
these  passages  from  obstruction  and  injury  due  to  calculi,  by  retention 
of  the  bile  in  the  intra-  and  extrahepatic  ducts,  or  by  some  previous  change 
in  the  hepatic  cell  (alcoholism,  gout,  or  syphilis).  In  other  words,  the 
microbes  rush  in  when  the  breach  is  practicable.  When  the  organ  is  in  a 
condition  of  morlnd  receptivity,  the  microbes  and  their  toxines  accomplish 
their  work. 

When  the  biliary  infection  is  established,  whether  the  migration  of  the 
organisms  takes  place  with  or  without  the  previous  assistance  of  trauma- 
tism, of  obstruction,  or  of  biliary  retention,  how  does  the  infection  reveal 
itsolf  ?     The  answer  involves  the  study  of  angiocholitis  and  cholecystitis. 

Angiocholitis. — Angiocholitis,  or  inflammation  of  the  bile-ducts,  affects 
both  the  lal-ge  and  small  ducts  (extra-  or  intrahepatic),  just  as  bronchitis 
affects  the  large  and  small  Inonchi. 

Angiocholitis  of  the  large  ducts,  and  especially  of  the  common  duct,  Ls 
usually  due  to  gall-stones,  but  inllammation  of  the  common  duct  (chole- 
dochitis)  is  not  always  due  to  a  calculus.  Longuet  mentions  three  cases, 
reported  by  Terrier,  Helierich,  and  fVhlfeld,  in  which  the  common  duct  con- 


998  TEXT-BOOK  OF  MEDICINE 

tained  no  stone,  but  yet  it  was  enormously  distended,  and  contained  greenish 
viscid  or  suppurating  fluid. 

Angiocholitis  of  the  small  ducts  is  so  closely  allied  to  the  calculous  form 
that  I  would  refer  the  reader  to  the  section  on  Gall- Stones.  It  may  give  rise 
to  the  areolar  abscesses  of  the  liver  described  by  Chauffard,  and  also  to  enor- 
mous intrahepatic  enlargements  of  the  ducts,  simulating  large  abscesses  of 
the  liver.  Longuet  quotes  an  absolutely  characteristic  case.  Intra- 
hepatic angiocholitis  may  be  accompanied  by  jaundice,  without  decolora- 
tion of  the  faeces  ;  swelling  and  pain  in  the  liver  are  frequent  but  inconstant 
symptoms.  Fever  is  seldom  absent ;  it  has  been  called  intermittent  hepatic 
fever  (Charcot),  or  intermittent  bilio-septic  fever  (Chauffard).  It  exactly 
resembles  malarial  fever,  with  this  difference,  that  the  attack  is  generally 
vesperal  and  irregular  in  type. 

In  some  cases  the  infection  affects  the  liver  and  the  blood,  spreading  from 
the  ducts  to  the  portal  and  hepatic  veins,  and  producing  infective  endo- 
carditis of  the  right  side  of  the  heart,  suppurating  infarcts  in  the  lungs  and 
pleura,  infective  endocarditis  of  the  left  side  of  the  heart,  suppurative 
meningitis,  etc. 

Cholecystitis. — I  would  ask  the  reader  to  refer  to  the  section  on  Calculous 
Cholecystitis,  where  certain  sides  of  this  question  have  been  treated  in 
detail. 

The  pathogenesis  of  the  infection  of  the  bile-ducts  is,  applicable  to  infec- 
tion of  the  gall-bladder  (cholecystitis).  As  regards  its  evolution,  however, 
cholecystitis  may  be  divided  into  certain  varieties — cholecystitis,  para- 
cholecystitis,  and  pericholecystitis. 

1.  Cholecystitis,  whether  it  is  or  is  not  due  to  gall-stones,  follows  biliary 
infection.  In  both  forms  there  may  be  obstruction  of  the  excretory  canals, 
either  by  calculi  or  "  because  the  inflamed  mucosa  has  formed  a  plug  in  the 
fine  cysto-choledochic  ducts."  The  infected  gall-bladder  may  or  may  not 
contain  fluid  ;  the  fluid  may  be  serous  (hydrocholecystitis),  sero-purulent 
(pyocholecystitis),  or  haemorrhagic  (hsemocholecystitis). 

Cholecystitis  with  effusion  causes  more  or  less  enlargement,  so  that  the 
gall-bladder  may  resemble  a  cyst  with  thin  and  distended  walls,  or  a  tumour 
with  thick,  hypertrophied  walls.  In  non-calculous  cholecj^stitis  the  gall- 
bladder is  usually  distended  ;  in  calculous  cholecystitis  it  is  always  con- 
tracted and  shrunken  (Terrier). 

2.  In  pericholecystitis  the  inflammation  is  localized  around  the  gall- 
bladder, and  does  not  extend  to  remote  organs.  It  may  be  calculous  or  non- 
calculous,  suppurative  or  fibrinous.  Pericholecystitis  is  most  frequently 
suppurative  in  the  case  of  calculous  cholecystitis  ;  it  is  often  fibrous  and 
rich  in  adhesions,  whether  it  is  or  is  not  due  to  gall-stones. 

3.  Paracholecystitis  must    be  reserved  for  suppuration  more   or  less 


DISEASES  OF  THE  LIVER  999 

distant  from  the  infected  gall-bladder.  Longuet  divides  the  abscesses  into 
four  types  :  '■  Some,  anterior  and  inferior,  invade  the  abdominal  wall  (flank 
and  right  hypochondrium),  and  give  rise  to  fistulse.  Others  spread  upwards 
over  the  upper  surface  of  the  liver,  between  the  diaphragm  and  the  false  ribs 
on  the  one  side  and  the  liver  on  the  other ;  they  form  the  antero-superior 
type.  If,  however,  they  continue  their  course  as  far  as  the  posterior  wall  of 
the  abdomen,  they  become  postero-superior.  Finally,  the  postero-inferior 
abscesses  leave  the  roof  of  the  abdominal  cavity,  in  order  to  reach  the 
posterior  wall  of  the  abdomen  and  the  renal  and  lumbar  regions."  These 
remote  abscesses  are  more  commonly  seen  in  non-calculous  than  in  calculous 
cholecystitis  ;  they  are  comparable  with  the  remote  abscesses  of  appendicitis. 
The  symptoms  of  cholecystitis  have  been  described  elsewhere.  Non- 
calculous  cholecystitis,  as  often  as  calculous  cholecystitis,  is  complicated 
by  adhesive  pericholecystitis.  These  adhesions  may  cause  very  acute  pain — 
a  common  symptom  when  adhesions  are  formed  in  the  abdominal  cavity. 
Often,  indeed,  the  other  symptoms  pass  unnoticed,  or  are  of  minor  impor- 
tance, and  a  patient  suffering  from  adhesive  cholecystitis  is  seized,  just  as  in 
hepatic  colic,  with  acute  pain  and  vomiting.  The  attacks  of  pain  recur  ;  the 
diagnosis  of  hepatic  colic  or  of  calculous  cholecystitis  is  made,  and  an  opera- 
tion is  decided  on.  No  calculus  is, met  with,  but,  on  the  contrary,  adhesions 
due  to  pericholecystitis  are  found.  The  adhesions  are  removed,  and  the 
patient  recovers  from  the  so-called  hepatic  colic.  He  has  really  been  suffer- 
ing from  hepatic  pseudo-colic.  Fraenkel  and  Terrier  have  reported  cases  of 
this  kind. 

Kummel  mentions  a  woman  who  was  subject  to  hepatic  colic  with  icterus,  and 
passed  gall-stones  in  the  stools.  As  the  pains  grew  worse,  an  operation  was  per- 
formed. The  gall-bladder  contained  no  calculi,  but  had  become  adlierent  to  the 
omentum  and  to  the  cystic  and  common  ducts.  The  adhesions  were  the  cause  of  the 
pains. 

I  have  seen  two  similar  cases.  The  adhesions  were  removed,  and  the 
pains,  which  had  been  agonizing,  ceased  completely. 


XXIII.  ASSOCIATION  OF  APPENDICITIS  AND  CHOLECYSTITIS. 

My  communication  to  the  Academie  de  Medecine,*  on  the  association  of  appendicitis 
with  cholecystitis,  is,  I  believe,  the  first  work  published  in  France  on  this  subject.  I 
iiavo  since  discussed  the  question  in  a  cUnical  locture.f  This  association,  which  is 
fairly  frequent,  is  not  the  result  of  a  fortuitous  coexistence  ;  the  two  infections  are 
associated,  the  one  causing  the  other.  Appendicitis  and  diolecystitis  enter  into  com- 
bination, and  from  this  coml)ination,  wbicli  may  bo  sudden  and  acute  or  slow  and 
jtrogressiv  e  in  its  onset,  a  complex  condition  results.     The  |)n!sent  description  is  founded 

*  Academie  de  Medecine,  stance  du  17  Juin,  1903. 

f  Dieulafoy,  Clinique  Medicate  de  VHvtel-Dieu,  190G,  7'"'  lo^on. 


1000  TEXT-BOOK  OF  MEDICINE 

on  about  thirty  cases  ;  it  is  of  importance,  because  it  has  as  its  immediate  corollary,  to 
state,  as  precisely  as  possible,  the  indications  for  surgical  intervention. 

Clinical  Cases.— On  September  25,  1902,  Achard  asked  me  to  see  an  old  lady,  seventy- 
eight  years  of  age,  who  had  been  taken  ill  two  days  before  with  abdominal  pain,  nausea, 
and  sliglit  fever.  On  examining  the  patient,  Achard  had  chscovered  a  painful  spot 
over  the  gall-bladder.  There  was  no  muscular  resistance,  and  the  belly  was  not 
distended.  Although  there  was  no  history  of  gall-stones  or  of  hepatic  cohc,  the 
location  of  the  pain  led  him  to  suspect  cholecystitis.  The  pain  grew  worse,  and  the 
fever  was  more  severe  on  the  following  day. 

When  we  examined  the  patient  two  days  later,  the  clinical  picture  was  complete. 
'  he  belly  was  distended ;  the  situation  of  the  pain  had  changed,  acute  pain,  with 
muscular  resistance,  being  present  over  the  appendix.  We,  then,  diagnosed  acute  appendi- 
citis, and  as  the  condition  of  the  patient  grew  rapidly  worse,  we  recommended  immediate 
operation.  Segond  was  then  called  in.  He  also  diagnosed  acute  api^enchcitis,  and 
operated  at  11  p.m. 

Before  anaesthesia  was  induced,  the  pain  and  the  muscular  resistance  had  not  allowed 
us  to  ascertain  certain  details.  As  soon  as  the  abdominal  wall  was  relaxed,  Segond 
found  induration  over  the  appendix,  and  a  tumour  in  the  region  of  the  gall-bladder.  He 
therefore  made  a  rather  high  incision,  and  foimd  two  lesions,  appendicitis  and  chole- 
cystitis. Exudate  matted  together  the  gall-bladder,  the  colon,  the  caecum,  and  the 
appendix.  The  gall-bladder  Avas  pushed  down,  and  formed  a  violet  and  distended 
tumour  ;  it  contained  a  turbid  and  biUous  fluid,  as  well  as  several  calcuU.  Cholecyst- 
ostomy  was  performed.  The  appenchx  of  the  ascending  type  was  adherent  and  swollen. 
It  was  then  resected.  The  operation  was  followed  by  complete  relief.  During  the  next 
few  days  the  biliary  fistula  gave  issue  to  bile  and  to  two  calcuh.  Two  months  later 
the  patient  left  for  Nice  in  excellent  health.  She  no  longer  vomited,  and  had  only  a 
small  biUary  fistula,  which  was  cicatrizing. 

This  case  shows  the  benefit  of  prompt  operation,  because  imqaediate  relief  followed. 
If  the  operation  had  been  postponed,  the  double  infection  in  the  appendix  and  the  gall- 
bladder would  very  probably  have  proved  fatal. 

In  December,  1902, 1  was  called  with  Segond  to  see  a  man  of  about  thirty  years  of  age. 
Two  days  previously  the  patient  had  felt  indisposed.  At  first  the  symptoms  of  gastric 
disturbance — loss  of  appetite,  malaise,  and  slight  fever — had  not  been  characteristic  ;  on 
the  following  day  the  abdominal  symptoms  were  more  marked,  the  pain  was  worse,  and 
a  painful  tumour  could  be  felt  in  the  region  of  the  gall-bladder.  The  patient's  physician 
had  diagnosed  cholecystitis.     The  temperature  had  been  over  104°  F.  on  two  occasions. 

Two  days  later,  when  I  examined  the  patient,  the  clinical  picture  had  changed. 
The  fever  persisted,  and  the  most  important  feature  was  not  the  pain  in  the  region  of 
the  gall-bladder,  but  a  sharp  and  characteristic  pain  -mth  miiscular  resistance  over  the 
appendix.  The  pain  was  most  marked  above  McBurney's  jDoint,  as  is  common  in 
cases  of  ascending  appendicitis.  Careful  examination  showed  that  the  pain  on  pressure 
decreased  in  proportion  as  we  ascended  towards  the  hver.  No  tumour  was  noticed  in 
the  region  of  the  gall-bladder.  These  signs  left  no  doubt  as  to  the  existence  of 
appendicitis.     Segond  formed  the  same  opinion.     The  urine  contained  albumin. 

The  symptoms  of  appendicitis,  therefore,  were  more  marked  than  those  of  chole- 
cystitis. The  rapid  course  of  the  disease,  the  temperature  rising  above  104°  F.,  and 
the  presence  of  albumin  gave  us  much  alarm. 

In  such  cases  a  decision  is  imperative.  Segond  and  myself  were  in  favour  of  im- 
mediate operation.  The  patient's  physician  did  not  agree  with  us.  As  we  shall  see, 
the  operation  was  the  more  indicated  in  that  it  revealed  peritonitis,  appendicitis,  and 
cholecystitis. 

The  operation  was  performed  at  10  p.m.,  Segond  first  attacking  the  appendix. 
On  opening  the  peritoneum  he  found  some  turbid  serous  fluid,  indicative  of  appendi- 


DISEASES  OF  THE  LIVER  1001 

citis  ;  a  larger  quantity  of  turbid  fluid  had  spread  into  the  pelvis.  Tlie  appendix,  -which 
was  inflamed,  and  which  reached  up  beliind  the  caecum,  was  excised.  Subsequent 
examination  by  Nattan-Larrier  revealed  ulcerative  appendicitis.  Below  a  plug  of 
fsecoidal  matter  were  two  large  ulcerations,  the  one  elongated,  the  other  oval.  At  the 
site  of  these  ulcerations  the  tissues  were  so  destroyed  that  they  were  transparent,  the 
wall  of  the  appendix  being  reduced  to  a  thin  sheet.  At  other  points  the  mucosa  was 
.swollen  ;  elsewhere  there  was  a  hanuorrhagic  stippling. 

Segond  next  turned  his  attention  to  the  gall-bladder.  The  incision  in  the  abdominal 
wall  was  prolonged  upwards,  and  by  means  of  digital  exploration  he  reached  the  gall- 
bladder, which  was  deeply  seated.  He  foimd  that  it  was  distended,  with  red  and  thick 
walls.  He  performed  cholecystostomy.  The  incision  gave  exit  to  a  yellowish  liquid, 
then  some  creamy  pus,  and  finally  to  some  tinted  pus  ;  no  gall-stones  were  present. 
The  neck  of  the  gall-bladder  appeared  to  be  obUterated. 

The  results  of  the  operation  were  remarkable.  In  spite  of  the  triple  infection,  two 
hours  after  operation  the  temperature  had  fallen  to  normal.     Speedy  recovery  followed. 

In  the  next  case  (Grant)  appendicitis  and  coexisting  cholecystitis  ended  in  perforation 
and  death.  A  man,  fifty-three  years  of  age,  was  said  to  have  previously  had  hepatic 
colic.  Violent  pains,  localized  to  the  region  of  the  gall-bladder,  suddenly  appeared 
one  night.  Grant  diagnosed  cholecystitis.  Two  hours  later  a  fresh  attack  of  pain 
with  vomiting  appeared.  Rupture  of  the  gall-bladder  was  diagnosed.  Next  morning 
intense  pain  over  the  appencbx  also  appeared.  Freeman  diagnosed  appendicitis  and 
cholecystitis.  The  operation  revealed  appendicitis  and  cholecystitis,  which  had  both 
ended  in  perforation.     The  patient  died  four  days  later  from  general  peritonitis. 

Adolf  Becker  has  recently  collected  some  thirty  cases  of  coexistent  appendicitis  and 
cholecystitis.  These  cases  fall  into  two  groups — in  the  first  group  the  appendicitis 
appears  to  have  preceded  the  cholecystitis,  and  in  the  second  and  larger  group  the 
cholecystitis  preceded  the  appendicitis. 

First  Group. — Kehrs  Case. — A  woman,  forty-six  years  of  age,  who  seemed  to  have 
had  previous  attacks  of  appendicitis,  was  taken  ill  with  acute  hepatic  colic.  Laparotomy 
was  performed.  The  ajDpendix  was  surrounded  by  adhesions,  and  fixed  to  the  back  of 
the  caecum  and  colon.  The  gall-bladder,  covered  with  membranes,  contained  turbid 
liquid  and  eight  gall-stones. 

Kehr's  Case. — In  the  case  of  a  man,  thirty-seven  years  of  age,  with  appendicitis 
cholecystitis  was  also  suspected.  The  operation  revealed  a  thickened  appendix, 
reaching  up  beliind  and  adherent  to  the  ca'cum  and  colon.  The  gall-bladder  was  com- 
pletely buried  in  adhesions.     The  gall-bladder  and  the  appendix  were  removed. 

Second  Group. — Mvllers  Case. — A  woman,  twenty-one  years  of  age,  had  three  attacks 
of  pain  in  the  right  hypochondrium  ;  the  pain  radiated  to  the  shoulders,  the  back,  and 
the  chest ;  jaundice  was  present,  and  gall-stones  were  not  present  in  the  stools.  The 
diagnosis  was  cholehthiasis.  Acute  pains  in  the  right  ileo-csecal  region  supervened 
several  days  later,  with  marked  tenderness  over  the  appendix.  Miiller  diagnosed 
cholelithiasis  and  apj)endicitis.  The  ojieration  revealed  cholecystitis,  with  an  adherent 
and  contracted  gall-bladder  containing  calculi,  and  apjiendicitis,  with  stenosis  of  the 
canal  at  the  mouth  of  the  caecum,  thickening  of  (lie  wall,  and  purulent  exudate. 

MaJleys  Case. — A  man,  forty-six  years  of  age,  had  for  several  years  j)ast  suffered  from 
hepatic  colic  with  jaundice,  but  no  calculi  had  ever  been  found  in  the  stools.  Later  a 
very  painful  tumour  was  noticed  in  the  ca-cal  region.  Miiller  diagnosed  chronic 
apiK!ndicitis,  for  which  he  operated.  He  found  the  appendix  surrounded  by  adhesions, 
and  dilated  in  the  shape  of  an  ampulla  in  its  lower  third.  In  spite  of  resection  of  the 
appendix  the  patient  still  continued  to  complain  of  violent  pain  in  the  right  hypo- 
cliondrinm.  A  very  painful  tumour  was  found  in  the  region  corresponding  to  the  gall- 
biaddcr.  A  scciond  operation  was  perfornK^d,  and  the  gall-bladder  was  found  to  bo 
surnmiKJcd  i)v  adhesions  and  to  contain  several  calculi. 


1002  TEXT-BOOK  OF  MEDICINE 

The  acute  or  clironic  lesions  in  these  cases  of  appendicitis  associated  with 
cholecystitis  are  of  every  kind  :  muco -purulent  or  haemorrhagic  fluid,  ulcer- 
ation of  the  walls  of  the  appendix,  stenosis,  dilatation,  perforation,  gangrene, 
adhesions,  pericsecal  suppuration,  peritonitis,  etc.  The  cholecystitis  may 
or  may  not  be  due  to  gall-stones,  and  the  gall-bladder  in  different  cases  is 
distended,  thickened,  retracted,  and  adherent,  and  contains  fluid  variable 
in  quantity  and  in  quality. 

Discussion. — We  must  now  consider  the  cause  of  this  double  infection 
of  the  appendix  and  the  gall-bladder.  Is  it  brought  about  simultaneously 
by  one  cause,  or  is  there  rather  a  superposition  of  the  two  infections,  the 
one  preparing  the  other  ?  And,  in  this  case,  which  is  the  earlier,  the  appen- 
dicitis or  the  cholecystitis  ? 

We  might  suppose  that  the  two  infections  are  due  to  a  calculous  process, 
causing  simultaneously  cholecystitis  and  appendicitis.  This  hypothesis  will 
not  hold  in  the  face  of  the  fact  that  in  this  double  infection,  calculi  are  very 
seldom  found  in  the  appendix,  and  are  sometimes  absent  in  the  gall-bladder. 
We  must  therefore  look  elsewhere  for  the  pathogenesis  of  the  double 
infection. 

Is  cholecystitis  the  result  of  appendicitis  ?  We  know  how  readily  ascend- 
ing infections  of  appendical  origin  occur.  In  Section  XIX.  we  saw  that  the 
infection  starts  from  the  appendix,  and  is  carried  to  the  liver  by  the  venous 
network  that  ends  in  the  portal  vein  and  in  the  liver.  This  infection  through 
the  veins  has,  however,  nothing  to  do  with  the  infection  of  the  gall-bladder. 
It  is  the  liver  that  is  attacked,  and  not  the  gall-bladder,  and  the  proof  is  that 
in  the  numerous  cases  of  appendicular  liver  the  gall-bladder  remains  healthy. 

We  may  also  ask  whether  the  infection,  starting  from  the  appendix, 
may  not  reach  the  gall-bladder  by  the  peritoneal  route,  through  the  adhesions 
"^^hich  so  often  unite  the  appendix,  the  intestine,  and  the  gall-bladder. 
This  ascending  infection  causes  subphrenic  empyema  and  pleurisy  in  appen- 
dicitis. This  question  has  been  discussed  under  Appendicular  Pleurisy.  In 
such  a  case  the  infection,  starting  from  the  frimum  movens  in  the  appendix, 
travels  up  along  the  csecum  and  colon,  reaches  the  hypochondrium,  often 
causing  subphrenic  empyema  ;  passes  through  the  diaphragm,  which  may 
or  may  not  be  perforated  ;  and  invades  the  pleural  cavity.  The  membranous 
and  purulent  tracks  stand  out  as  landmarks  along  the  route,  so  that  we  can 
follow  the  infection  from  its  modest  origin  in  the  appendix  to  its  intrathoracic 
expansion,  where  the  pleurisy  is  often  purulent  and  putrid.  On  referring, 
however,  to  the  numerous  cases  in  which  ascending  infection  has  led  to  sub- 
phrenic empyema  and  pleurisy,  it  will  be  seen  that  cholecystitis  was  not 
present,  the  infection  licking  the  walls  of  the  gall-bladder,  but  not  provoking 
cholecystitis. 

If  the  gall-bladder  escapes  the  broad  track  of  the  appendical  infection, 


DISEASES  OF  THE  LIVER  1003 

which,  as  it  ascends,  spreads  along  the  intestine,  around  and  above  the  liver, 
and  even  into  the  thoracic  cavity,  is  it  reasonable  to  suppose  that  it  can  be 
infected  by  the  small  track  which  in  the  present  case  joins  it  with  the 
appendix  ?  In  the  majority  of  cases  cholecystitis  causes  appendicitis,  the 
infection  taking  place  from  above  downwards.  Furthermore,  in  twenty- 
five  out  of  thirty  cases  the  earliest  symptoms  are  due  to  the  biliary  lesions, 
while  the  symptoms  of  appendicitis  appear  some  days,  weeks,  or  months 
later. 

A  patient,  for  example,  has  had  undoubted  signs  of  hepatic  colic  or  of 
cholecystitis,  especially  pains  in  the  right  hypochondrium  or  in  the  region  of 
the  gall-bladder,  the  diagnosis  of  cholelithiasis,  hepatic  colic,  or  cholecystitis 
being  made.  At  a  given  moment  pain  appears  in  the  right  iliac  fossa,  and 
is  accompanied  by  other  symptoms,  indicating  acute,  subacute,  or  chronic 
appendicitis.  As  a  rule,  especially  in  the  acute  form,  the  symptoms  of 
appendicitis,  with  or  without  peritonitis,  become  much  more  marked  than 
those  of  cholecystitis.  In  other  cases,  especially  in  the  subacute  forms,  the 
two  foci  (the  one  in  the  appendix  and  the  other  in  the  gall-bladder)  remain 
sufficiently  distinct  for  the  diagnosis  of  cholecystitis  and  appendicitis  to  be 
made. 

Many  mistakes  must  have  been  made  before  attention  was  called  to  the 
association  of  appendicitis  with  calculous  or  non-calculous  cholecystitis.  A 
physician,  having  seen  several  attacks  of  typical  hepatic  colic  in  a  patient, 
may  have  believed  in  a  fresh  attack  of  colic  when  the  appendicitis  broke 
out  in  a  subintrant  form.  Another  physician,  having  witnessed  the  onset  of 
acute  appendicitis,  may  not  suspect  the  previous  occurrence  of  cholecystitip 
if  the  symptoms  of  cholecystitis  are  effaced,  or  if  the  information  given  is 
insufficient. 

We  have,  then,  a  new  chapter  to  add  to  the  history  of  cholecystitis  and 
appendicitis  ;  the  possible  association  of  this  double  infection  must  keep  us 
constantly  on  the  alert. 

In  the  future,  therefore,  it  will  be  necessary  to  pay  attention  to  the 
coupling  of  these  two  infections.  The  infection  of  the  gall-bladder  is  cer- 
tainly serious,  but  the  toxi-infection  of  the  appendix  is  even  more  so. 
Failure  to  recognize  appendicitis,  and  to  fortify  oneself  on  the  ground  of 
cholecystitis  only,  is  a  grave  error,  because  it  may  falsify  the  therapeutic 
indications.  The  belief  that  we  have  to  fight  all  the  time  against  infection 
of  the  gall-bladder  leads  to  delay,  and  duiing  that  time  the  a])pendicitis, 
which  has  not  been  recognized,  may  rapidly  induce  toxi-infcctious  complica- 
tions, with  or  without  perforation  or  gangrene,  and  tlio  life  of  the  patient 
is  compromised  by  the  double  or  tri|tle  infection,  because  we  have  not  acted 
in  time. 

Pearly  surgical  intervention  is  especially  indicated  in  such  cases.     An 


1004  TEXT-BOOK  OF  MEDICINE 

operation  for  cholecystitis  alone  when  appendicitis  is  also  present  means 
leaving  the  appendicular  toxi- infection  to  do  its  worst.  Not  to  operate  on 
either  lesion,  and  to  advise  delay,  is  to  anticipate  the  most  dire  results. 

XXIV.  ABERRANT  LOBE  OF  THE  LIVER. 

In  certain  individuals  the  liver  has  an  extra  lobe,  which  has  been  called 
the  aberrant  or  erratic  lobe,  the  hepatic  tonguelet,  and  the  floating  lobe, 
as  it  has  a  certain  mobility.  The  aberrant  lobe  arises  on  the  under  surface 
of  the  liver,  close  to  the  quadrate  lobe.  It  is,  as  it  were,  hung  from  the  liver, 
which  is  not  depressed.  The  aberrant  lobe  is  sometimes  directly  continuous 
with  the  liver  substance  ;  at  other  times  it  is  attached  to  the  liver  by  a 
rudimentary  or  a  complete  pedicle.  The  size,  form,  and  length  of  the  aber- 
rant lobe  vary ;  it  may  reach  a  length  of  7  or  8  inches.  The  more  marked 
the  pedicle,  the  more  mobile  and  depressed  is  the  lobe  ;  it  simulated  a 
floating  kidney  in  the  cases  quoted  by  Pichevin  and  Faure. 

Symptoms. — The  floating  lobe  of  the  liver  may  remain  unnoticed.  It 
often  causes  sharp  pains  in  the  right  hypochondrium,  radiating  to  the  lumbar 
region  and  to  the  shoulder.  The  pains  simulate  the  crisis  seen  in  calculous 
cholecystitis  or  in  floating  kidney.  On  examining  the  belly,  the  tumour  is 
found.  The  liver  is  not  depressed.  The  aberrant  lobe  descends  more  or 
less  ;  it  is  smooth,  fairly  mobile,  and  sometimes  painful  on  pressure.  It 
follows  the  movements  of  the  liver,  unless  it  has  a  well-marked  pedicle.  The 
most  frequent  error  in  diagnosis  consists  in  mistaking  the  aberrant  lobe  for 
a  displaced  kidney.  Sometimes  a  mobile  lobe  is  found  with  a  mobile  kidney, 
and,  then,  the  diagnosis  is  complicated. 

An  interesting  feature  is  that  the  aberrant  lobe  of  the  liver  is  fairly  often  associated 
with  gall-stones  and  cholecystitis.  We  may  even  find  the  tumour  formed  by  the 
aberrant  lobe  and  the  tumour  due  to  cholecystitis  side  by  side.  The  question  was 
discussed  by  Riedel  (Berlin,  1888),  who  found  six  cases  of  aberrant  lobe  in  women 
suffering  from  cholecystitis,  with  or  without  cholehthiasis.  The  first  authentic  case, 
as  far  as  I  know,  was  reported  by  Trousseau.  A  woman  had  been  suffering  from 
hepatic  coUc  with  jaundice  and  fever.  A  tumour  was  felt  at  the  right  edge  of  the  Uver, 
and  was  taken  for  calculous  cholecystitis.  The  post-mortem  examination  revealed 
calculous  cholecystitis,  but  the  tumour  felt  during  Ufe  was  an  aberrant  lobe  of  the  liver 
masking  the  gall-bladder. 

This  description  of  the  aberrant  lobe  of  the  liver  shows  the  difficulties  in 
diagnosis,  especially  when  an  aberrant  lobe  and  cholecystitis  exist  in  the 
same  subject. 

XXV.  ICTERUS— JAUNDICE— CHOL^MIA. 

Description. — Under  certain  conditions,  the  bile  pigment,  elaborated  by 
the  liver,  is  reabsorbed  ;  it  passes  into  the  blood  and  circulates  in  the  plasma. 
The  organs,  tissues,  and  secretions  are  then  more  or  less  coloured  by  the  bile. 


DISEASES  OF  THE  LIVER  1005 

Icterus,  or  jaundice,  is  the  yellow  coloration  of  the  skin  and  of  the  mucosae 
by  the  bile  pigments.  Jaundice  appears  first  in  the  conjunctivae,  and  then 
spreads  over  the  face,  the  mucosa  of  the  mouth,  the  trunk,  and  the  hmbs. 
The  colour  of  the  skin  varies  from  the  palest  yellow  (subicteric  tint)  to  a  deep 
yellow,  which  is  generally  the  sign  of  icterus  from  retention.  A  golden- 
yellow  colour  is  especially  seen  in  acute  jaundice  ;  the  greenish,  olive,  or 
almost  black  tints  are  principally  seen  in  chronic  jaundice.  The  jaundice  is 
always  general,  and  there  is  no  such  thing  as  partial  jaundice,  but  it  is  more 
or  less  pronounced,  according  to  the  region.  The  colouring  matter  of  the  bile 
is  deposited  in  the  deep  layers  of  the  Malpighian  network,  and  the  jaundice 
does  not  completely  disappear  until  after  the  desquamation  of  the  coloured 
cells.  The  bile  pigment  is  chiefly  ehminated  by  the  kidneys,  whence  the 
characteristic  colour  of  the  urine  ;  but  it  is  also  eliminated  by  the  sweat  and 
sebaceous  glands,  which  explains  the  yellow  colour  of  the  linen  in  contact 
with  the  patient's  sweat.  As  the  milk  may  contain  bile  pigment,  a  child 
should  not  be  suckled  by  a  wet-nurse  suffering  from  chronic  jaundice.  In 
a  pregnant  woman  suffering  from  chronic  jaundice  the  yellow  colour  may  be 
communicated  to  the  foetus. 

When  the  skin  is  jaundiced,  the  urine  is  always  affected.  The  coloration 
oi  the  urine  precedes  by  some  hours  that  of  the  mucosae  and  of  the  skin. 
The  bile  pigment  is  eliminated  by  the  epitheUum  of  the  tubules  ;  the  kidneys 
are  greenish,  especially  in  the  cortical  region,  and  the  microscope  shows  the 
pigment  in  the  epithelium  of  the  tubules.  The  urine  is  of  high  specific 
gravity,  and  is  generally  less  copious  than  in  the  normal  condition  ;  its  colour 
varies  according  to  the  quantity  of  the  bile  pigment,  being  orange-yellow, 
greenish,  brownish,  or  almost  black.  The  green  tint  is  due  to  the  conversion 
of  bilii-ubin  into  biliverdin  by  oxidation.  The  urine  stains  the  linen,  and 
the  more  acid  it  is,  the  more  marked  is  the  green  colour. 

The  analysis  of  the  urine  should  be  made  in  the  following  manner  : 
Fuming  nitric  acid  is  poured  into  a  wineglass  (Gmelin's  reaction),  and  the 
urine  previously  filtered  is  slowly  added  by  means  of  a  pipette.  At  the 
junction  of  the  acid  and  the  urine  a  greenish  band  will  be  seen,  and  above  this 
green  zone  we  see,  from  below  upwards,  blue,  violet,  red,  and  yellow  rings. 
The  green  tint  predominates,  but  after  some  time  all  these  shades  are  blended 
ill  an  orange  colour. 

Effects  of  Jaundice. — I  shall  only  describe  the  symptoms  due  to  the 
impregnation  of  the  system  l)y  the  lule. 

1.  Gastro-intestinal  TrowW^'6'.^The  faeces  in  obstructive  jaundice  are  often 
clay-coloured,  foetid,  and  rich  in  fatty  matter — a  proof  that  the  bile  under 
normal  conditions  promotes  the  a})sorption  of  fat.  The  clay  colour  of  the 
fccccs  is  due  as  much  to  the  excess  of  fat  as  to  the  absence  of  bile.  In  obstruc- 
tive jaundice  we  must  carefully  look  for  a  return  of  colour  in  the  faeces,  because 


1006  TEXT-BOOK  OF  MEDICINE 

this  is  an  indication  that  the  obstruction  has  a  tendency  to  yield.  The 
patient  usually  has  a  distaste  for  food  ;  the  digestion  is  imperfect,  the  tongue 
is  coated,  and  there  is  a  bitter  taste  in  the  mouth.  According  to  Murchison, 
the  bitter  taste  is  due  to  the  passage  of  taurocholate  of  soda  into  the  blood. 
In  certain  patients  the  faeces  are  not  colourless,  and  there  may  even  be 
an  excess  of  bile  ;  the  faeces  are  greenish  and  liquid,  and  we  then  speak  of 
polychoHa  or  pleiochromia.  The  liver  secretes  an  excess  of  bile,  which  is 
partly  evacuated,  partly  absorbed. 

2.  Poisoning. — When  the  intestinal  digestion  is  deprived  of  bile,  less 
fatty  matter  is  absorbed,  and  the  patient  suffers  in  consequence.  He  may 
lose  flesh,  or  he  may  become  poisoned  by  the  products  of  fermentation 
absorbed  through  the  intestine,  and  by  the  bile  salts  absorbed  by  the  liver. 
This  double  cause  of  auto-intoxication  is  not  marked  in  most  cases,  because 
the  healthy  liver  cells  destroy  the  poison,  while  the  healthy  cells  in  the  kidney 
eliminate  it.  If,  however,  the  cells  of  the  liver  and  of  the  kidney  are  afEected, 
symptoms  of  intoxication  may  result.  In  chronic  jaundice  the  kidneys 
assume  a  greenish  colour ;  the  epithehum  of  the  canalicuU  becomes  pig- 
mented, and  sometimes  undergoes  fatty  degeneration. 

3.  Circidatory  Troubles. — The  pulse  is  generally  slow ;  it  may  fall  below 
30  a  minute.  Lowering  of  the  arterial  tension  is  also  noticed.  The  slowing 
of  the  heart-beats  and  of  the  pulse  is  due  to  the  action  of  the  bile  salts  in  the 
blood.  The  salts,  and  especially  the  colouring  matter  of  the  bile,  are  cardiac 
poisons.  I  have  described  elsewhere  the  mitral  and  tricuspid  murmurs 
which  sometimes  accompany  acute  and  chronic  jaundice.  Jaundice  often 
causes  epistaxis,  especially  from  the  right  nostril  (Galen). 

4.  Changes  in  the  Blood. — After  numerous  and  contradictory  experiments, 
the  following  conclusions  have  been  arrived  at :  Acute  jaundice  (I  am  not  re- 
ferring to  icterus  gravis)  causes  no  change  in  the  blood,  except  that  the  serum 
is  tinted  by  the  colouring  matter  of  the  bile.  Chronic  jaundice  causes  diminu- 
tion of  the  red  corpuscles  and  increase  of  the  fatty  matter  and  cholesterin. 
The  red  corpuscle,  in  order  to  resist  attack,  modifies  the  normal  conditions 
of  its  permeability. 

5.  Cutaneous  Troubles. — Jaundice  is  often  accompanied  by  pruritus. 
The  itching  is  particularly  severe  in  the  feet  and  in  the  hands,  and  is  some- 
times intolerable,  depriving  the  patient  of  sleep.  Urticaria  and  lichen  may 
also  occur  in  jaundice. 

In  chronic  jaundice  we  sometimes  notice  an  eruption  called  xanthelasma 
(from  ^av6o<i,  yellow ;  and  ixeXaafia,  a  black  spot),  a  name  that  is  preferable 
to  "  yellow  patches  on  the  eyelids,"  because  in  many  cases  the  eruption  is 
general.  Xanthelasma  confined  to  the  eyelids  often  exists  apart  from 
jaundice,  but  general  xanthelasma  is  almost  always  associated  with  chronic 
jaundice.     The  eruption  of  xanthelasma  shows  itself  in  the  shape  of  patches 


DISEASES  OF  THE  LIVER  1007 

of  the  colour  of  chamois-leather  (Rayer) ;  they  are  slightly  prominent,  but  non- 
indurated,  and  the  edges  are  clear  or  ii-regular.  Another  form — xanthelasma 
tuberosa — is  characterized  by  firm  reddish-yellow  nodules.  Xanthelasma 
commences  at  the  inner  canthus  of  the  eye,  extends  to  both  eyeUds,  and 
finally  spreads  over  the  palms  of  the  hands,  the  soles  of  the  feet,  the  elbows 
and  the  knees,  showing  a  well-marked  tendency  to  symmetry.  Xanth- 
elasma, from  the  anatomical  point  of  view,  is  characterized  by  chronic 
hyperplasia  of  the  derma,  with  fatty  infiltration  of  the  newly-formed 
elements  ;  there  is  no  tendency  to  ulceration. 

Pathogenesis — etiology. — Gubler  divided  jaundice  into  two  classes — 
haemapheic,  or  hsematogenous,  and  bilipheic,  or  hepatogenous.  We  shall  see 
the  meaning  of  these  two  varieties. 

Bihpheic  jaundice  is  due  to  retention  of  bile,  and  its  production  is  readily 
understood.  When  an  obstacle  is  opposed  to  the  free  flow  of  bile,  biliary 
stasis  in  the  liver  and  consequent  absorption  occur.  The  glands,  says 
Bernard,  are,  or  may  be,  organs  that  are  as  active  in  absorption  as  in  secre- 
tion. The  intrahepatic  absorption  of  bile  is  carried  out  by  the  lymphatics 
rather  than  by  the  veins.  The  obstacle  to  the  circulation  of  the  bile  may 
be  situated  in  the  Uver,  in  the  intrahepatic  canals  (catarrh  of  the  bile-ducts, 
cancer  of  the  liver,  cirrhosis,  abscess,  appendicular  liver,  etc.),  in  the  large  ex- 
cretory ducts,  and  at  the  duodenal  orifice.  To  this  last  category  belong  ob- 
struction by  calculi,  catarrh  of  the  common  duct,  worms,  hydatids,  cicatricial 
or  inflammatory  constrictions  of  the  common  duct  (ulcer  of  the  duodenum), 
primary  cancer  of  the  biliary  passages  or  the  head  of  the  pancreas,  aneurysms, 
and  tumours  situated  in  the  hilum  of  the  liver. 

In  obstructive  jaundice  the  colour  of  the  skin  is  very  pronounced,  and 
the  faeces  are  colourless  if  the  large  ducts  are  quite  blocked.  Furthermore, 
the  urine  contains  biliverdin,  as  shown  by  nitric  acid,  and  the  blood-serum 
assumes  a  greenish-yellow  tint. 

Such  are  the  characteristics  of  bilipheic  jaundice.  In  other  diseases, 
however,  the  skin  and  mucous  membranes  present  a  more  or  less  deep  sub- 
icteric  tint,  although  the  uriire  does  not  contain  bile  pigment.  We  may 
treat  this  urine  with  fuming  nitric  acid,  and  obtain  an  old  mahogany  tint, 
but  not  GmeUn's  reaction.  This  variety  is  Gubler's  hacmapheic  jaundice. 
His  explanation  is  as  follows  : 

In  the  normal  condition  the  rod  corpuscles  destroyed  in  the  system  give  rise  to  a 
su))stancc  called  hicmaphein,  which  is  converted  into  bile  pigment  in  tlio  liver.  If  the 
Uver,  in  conse(iuenco  of  lesions  or  functional  troubles,  can  no  longer  bring  about  this 
conversion,  or  if  the  destroyed  corpuscles  are  in  such  numbers  (pyrexia,  to.\;vmia)  tliat 
the  hver  caimot  convert  their  debris,  an  excess  of  luv>maphein  is  formed, and  is  eliminated 
by  tlie  kidneys,  giving  special  characters  to  the  urine.  So  far  tliere  is  no  colouring  of 
the  skin,  but  if  the  kidnc^ys  do  not  eliminate  the  colouring  matter,  the  tissues  take  on 
a  yellow  tint,  and  ha.'mapheic  jaundice  results. 


1008  TEXT-BOOK  OF  MEDICINE 

Gubler's  ingenious  theory  is  no  longer  accepted.  In  the  first  place, 
hsemaphein  has  never  been  isolated,  either  from  the  urine  or  from  the  serum. 
In  the  second  place,  the  blood  pigment  does  not  play  the  part  assigned  to  it 
by  this  theory  ;  the  chief  factor  is  the  liver  cell,  on  which  the  evolution  of  the 
haemoglobin  and  the  formation  of  the  pigments  depend.  The  colour 
reactions  in  the  so-called  hgemapheic  urine  are  due  to  urobilin  and  a  red- 
brown  pigment,  its  chromogene  (P.  Tessier).  Urobilin  (Jaffe)  belongs  to 
the  series  of  iron-free  pigments  derived  from  haemoglobin,  and  while  it  is 
not  found  in  normal  urine,  it  is  present  in  the  faeces,  which  owe  their  ordinary 
colour  to  it.  Hayeni,  who  has  carefully  studied  this  question,  found  that 
urobilin  dissolved  in  water  and  in  urine  gave  with  the  spectroscope  a  dark 
band  of  absorption  between  the  green  and  the  blue.  Urobilin,  according 
to  Hayem,  is  the  pigment  of  the  diseased  liver  :  when  the  liver  cell  is  attacked 
by  organic  and  physiological  decay,  it  elaborates  urobilin  and  other  modified 
pigments  instead  of  normal  bile  pigment. 

Urobilin  is  really  the  result  of  a  change  in  the  haemoglobin  ;  this  change 
takes  place  in  the  liver,  and  not  in  the  blood-serum.  Urobilin,  when 
reabsorbed,  gives  urobilinaemia,  and  its  excretion  by  the  kidney  causes 
urobilinuria. 

Urobilin,  however,  is  not  the  only  modified  pigment.  Winther  has 
isolated  a  red-brown  pigment  of  supreme  importance.  These  modified  pig- 
ments, which  are  sometimes  associated  with  the  normal  but  masked  bile 
pigments,  give  rise  to  the  so-called  haemapheic  jaundice.  These  various  kinds 
of  jaundice,  however,  are  not  absolutely  distinct ;  they  may  follow  one 
another  or  may  occur  together,  and  may  be  classified  in  the  following  manner 
(Hayem)  : 

1.  Bilipheic  jaundice,  with  normal  bile  pigments  in  the  urine  and  in  the 
serum  of  the  blood.  On  examining  the  urine,  we  obtain  Gmelin's  reaction. 
The  faeces  are  colourless  when  the  retention  of  the  bile  is  sufficient.  Uro- 
bilinuria may  or  may  not  be  associated  with  this  form  of  jaundice. 

2.  Gubler's  haemapheic  jaundice.  In  the  urine  presence  of  urobilin  and 
modified  bile  pigments  ;  absence  of  true  pigments.  In  the  serum,  bile 
pigments  and  a  trace  of  urobilin  ;  faeces  without  special  characters.  In 
reahty  haemapheic  jaundice  does  not  exist,  because  urobilin  has  an  ex- 
tremely feeble  staining  power.  It  is  therefore  more  correct  to  say  that 
there  are  varieties  of  jaundice,  with  urobilin  and  other  modified  pigments. 

3.  Slight  jaundice,  in  which  the  urine  contains  urobilin  alone,  whilst 
the  serum  contains  urobihn  and  bile  pigments. 

4.  Jaundice  in  which  the  urine  and  the  serum  contain  urobihn  alone. 
Custom  has  now  prevailed :  the  name  "  haemapheic  icterus "  has  been 
abandoned,  and  we  describe  two  varieties — true  or  bilipheic  jaundice,  and 
jaundice  with  urobilinuria.     These  ideas  are  of  much  importance  in  prog- 


DISEASES  OF  THE  LIVER  1009 

nosis ;  in  bilipheic  jaundice  the  hepatic  cell  is  healthy ;  in  urobilinuric 
jaundice  it  is  diseased  (Hanot,  Hayem).  Urobilinuria  and  jaundice  indicate 
degeneration  of  the  hepatic  cell. 

In  urobilinuric  jaundice  the  urine  stains  the  linen  with  salmon-coloured 
spots.  In  the  test-tube  the  colour  varies  from  amber-yellow  to  red-brown, 
but  the  greenish  sheen  observed  in  true  jaundice  does  not  occur.  Nitric 
acid  gives  an  old  mahogany  colour,  and  never  the  green  tint  due  to  bile 
pigment. 

The  spectroscope  is  indispensable  in  the  examination  of  the  urine, 
because  it  shows  whether  the  brown  colour  of  the  urine  is  due  to  true  bile 
pigment  or  to  urobilin.  The  use  of  the  small  hand  spectroscope  makes  this 
examination  easy,  even  at  the.  bedside  of  the  patient.  The  method  is  as 
follows  : 

We  commence  by  looking  through  the  spectroscope,  directing  its  extremity  towards 
the  light.  The  normal  solar  spectrum  is,  then,  seen,  the  colours  succeeding  one  another 
from  left  to  right  in  the  following  order  :  red,  orange,  yellow,  green,  blue,  indigo,  violet. 
The  instrument  must  be  carefully  focussed  until  the  edges  of  the  spectrum  are  clearly 
defined.  The  cleft  in  the  spectroscope  is,  then,  carefully  adjusted,  so  that  the  normal 
lines  of  the  spectrum  are  clear.  Two  Unes,  B  and  C,  are  seen  in  the  red  ;  one  hne,  D, 
in  the  orange  ;  one  Une,  E,  at  the  edge  of  the  yellow  and  the  green  ;  and  one  hne,  F, 
in  the  green. 

A  small  glass  reservoir,  containing  the  urine,  is  then  placed  between  the  hght  and 
the  end  of  the  spectroscope.  Normal  urine  does  not  affect  the  solar  spectrum  to  any 
appreciable  extent ;  such  is  not  the  case  when  the  urine  is  charged  with  bile  pigments 
or  with  urobilin.  Urine  containing  bile  pigments  blots  out  the  whole  right  side  of 
the  spectrum,  and  the  large  dark  band  commences  a  Httle  distance  to  the  right  of  the 
E  Une,  leaving  between  this  line  and  the  left  extremity  of  the  dark  zone  only  a  narrow 
luminous  band  of  greenish -yellow. 

Urine  charged  with  urobilin  gives  two  dark  bands  in  the  spectrum  :  the  first  one 
completely  obscures  the  violet  and  the  indigo,  and  darkens  the  right  part  of  the  blue  ; 
the  second  is  a  black  band,  situated  in  the  green,  and  completely  masking  the  F  hne. 
If  a  few  drops  of  aramoniacal  chloride  of  zinc  are  added  to  the  urine  containing  urobilin, 
it  becomes  dichroic,  rose-coloured  by  direct  hght,  and  green  by  reflected  light.  The 
dark  band  which  obscured  the  F  line  is  displaced  towards  tlie  left,  and  the  F  Hne  becomes 
visible  to  the  right  of  this  band.  This  displacement  of  tlie  band  of  ab.sorption  and  the 
reappearance  of  the  F  hne  on  addition  of  a  few  drops  of  ammoniacal  chloride  of  zinc 
are  characteristic  of  urobilin. 

The  distinctions  just  laid  down  in  the  pathogenesis  of  icterus  are  often 
met  with  clinically,  but  there  are  cases  (m  the  bUious  fevers,  for  example, 
in  malaria,  or  in  certain  intoxications  of  the  liver)  in  which  the  causes  and 
the  varieties  of  jaundice  are  as.sociated. 

Appendicitis  may  cause  either  variety.  In  Section  XtX.  I  have  de- 
scribed a  case  of  early  jaundice  with  urobilinuria  of  tOxic  origin,  and  a  case 
of  jaundice  associated  with  purulent  infection  of  the  liver.  These  cases  of 
appendicular  jaundice  arc  important  in  clinical  medicine. 

The  prognosis  must  always  be  reserved,  because  icterus  gravis  sometimes 

64 


1010  TEXT-BOOK  OF  MEDICINE 

commences  like  the  simple  catarrlial  form.  Jaundice  accompanied  by  fever 
or  by  adynamic  symptoms  must  be  looked  upon  with  suspicion.  We  shall 
see  in  the  following  section  that  pregnancy  is  a  grave  factor.  Chronic 
jaundice  is  often  the  index  of  formidable  lesions.  There  is  no  treatment  for 
jaundice  fer  se.  The  treatment  must  be  directed  to  the  causative  lesions. 
The  kidneys  must  be  watched ;  milk  diet  and  mild  diuretics  must  be  pre- 
scribed. 

Cholsemia. — ^In  addition  to  jaundice,  which  is  the  complete  chnical  ex- 
pression of  the  impregnation  of  the  organism  by  bile,  we  see  mild  attenuated 
bilious  conditions.  Sometimes  the  skin  is  slightly  jaundiced,  but  no  pigment 
is  found  in  the  urine  ;  this  condition  is  known  as  acholuric  jaundice.  Some- 
times the  skin  is  normal,  the  urine  contains  no  bile,  and  the  only  sign  of 
bihary  impregnation  is  the  presence  of  bile  pigments  in  the  blood ;  this 
condition  is  known  as  cholaemia.  This  morbid  syndrome  (cholsemia)  has 
recently  been  isolated  by  Gilbert  and  Lereboullet,  who  have  made  important 
contributions  to  the  subject. 

The  principal  symptom  of  cholaemia  is  furnished  by  the  examination  of 
the  serum,  which  generally  assumes  an  olive-yellow  tint  when  it  is  collected 
in  a  vessel.  With  the  spectroscope,  it  shows  absorption  bands  in  the  green 
part  of  the  spectrum  ;  with  nitric  acid  it  gives  Grnelin's  reaction.  The 
urine  contains  urobilin,  but  not  true  bile  pigments. 

According  to  the  authors  above  quoted,  cholsemia  m^y  be  accompanied 
by  dyspepsia,  pain  in  the  stomach,  and  diarrhoea ;  renal  troubles — albumin- 
uria and  hsemoglobinuria  ;  subacute  or  chronic  biliary  pseudo-rheumatism  ; 
cutaneous  troubles — erythema,  urticaria,  pruritus,  bullous  eruptions,  lentigo, 
xanthelasma,  pigmentation,  and  melanoderma ;  visceral  and  cutaneous 
haemorrhage  ;  cardio- arterial  phenomena,  intermittence,  and  hypotension  ; 
psychical  troubles — melancholia,  hypochondria,  and  neurasthenia.  The  pre- 
dominance of  these  troubles  in  a  given  case  will  allow  us  to  classify  the  forms 
as  dyspeptic,  hsemorrhagic,  or  nervous. 

Cholaemia  is  said  to  predispose  to  canaUcular  infections,  and  may  be 
complicated  with  acute  or  chronic  hepatic  troubles  (Uthiasis  and  biliary 
cirrhosis). 

Cholsemia  may  supervene  as  a  gymptom  in  many  j)rimary  and  secondary 
affections  of  the  liver  ;  it  may  also  exist  as  a  kind  of  idiopathic  disease — i.e., 
simple  cholaemia  and  family  cholaemia. 

The  anatomical  substratum,  variable  in  the  first  case,  seems  in  the  second 
case  to  be  a  discrete  and  perhaps  infective  angiocholitis.  The  diagnosis 
is  probable  when  abundance  of  urobilin  is  present  in  the  urine,  and  certain 
when  bile  pigments  are  found  in  the  serum.  The  treatment  is  practically 
identical  with  that  of  other  hepatic  affections. 


DISEASES  OF  THE  LIVER  iOii 

XXVI.  ICTERUS  GRAVIS— ICTERUS  AND  THE  PUERPERAL 

STATE. 

Nature  of  the  Disease— Pathogenesis. — Transient  icterus  is  in  itself  a 
benign  symptom.  Witli  few  exceptions,  tlie  tissues  may  be  impregnated  by 
bile  without  the  least  danger  resulting.  We  meet  people  who  have  hepatic 
colic  or  catarrh  of  the  biliary  passages,  with  temporary  obUteration  of  the 
common  bile-duct,  and  experience  no  serious  inconvenience  from  jaundice 
that  has  lasted  for  several  weeks.  We  also  see  people  sufiering  from  hyper- 
trophic biliary  cirrhosis  with  persistent  jaundice,  and  yet  they  preserve  their 
appetite,  their  strength,  and  their  appearance  of  health.  In  these  different 
cases  the  relative  benignity  of  the  icterus  arises,  on  the  one  hand,  from 
the  healthy  condition  of  the  kidneys,  which  eUminate  the  pigment  and  the 
bile  acids  (toxic  substances),  and,  on  the  other  hand,  from  the  capital  fact 
that  the  hepatic  cells  preserve  their  functional  activity.  The  danger  of 
certain  kinds  of  icterus,  then,  does  not  come  from  the  icterus  itself,  and 
here,  as  elsewhere,  the  icterus  is  little  more  than  a  symptom.  The  danger, 
as  we  shall  see  later,  conies  from  the  destruction  of  the  hepatic  cells,  and  the 
name  icterus  gravis  answers  to  a  somewhat  ill-defined  morbid  group,  the 
principal  characters  of  which  are.  as  follows  : 

An  individual  Ls  in  perfect  health.  After  a  few  days  of  fever,  lassitude, 
headache,  muscular  pains,  and  prostration,  symptoms  that  simulate  the 
invasion  of  influenza  or  typhoid  fever,  or  after  some  gastro-intestinal  trouble 
which  might  easily  be  taken  for  a  simple  catarrh  of  the  digestive  passages, 
slight  or  pronounced  icterus  supervenes.  The  fever  is  more  or  less  high. 
Epistaxis,  haemorrhage  from  the  gums,  hsematemesis,  mela^na,  haomaturia, 
purpura  or  ecchymoses,  then  appear,  and  are  accompanied  or  followed  by 
nervous  troubles,  such  as  vomiting,  hiccough,  dyspnoea,  dehriuni,  convul- 
sions, or  coma,  and  in  the  majority  of  cases  the  patient  is  carried  off  within 
two  to  three  weeks,  with  ataxo- adynamic  symptoms  and  hyperthermia  or 
hypothermia. 

In  the  foregoing  example  icterus  gravis  strikes  the  individual  in  the 
midst  of  good  health,  appearing  as  a  primary  disease,  resembling  typhus, 
yellow  fever,  or  some  other  infectious  disease,  and  breaking  out  at  times  in 
an  epidemic  state.  In  addition  to  primary  icterus  gravis,  we  find  a 
series  of  cas(\s  in  which  icterus  gravis  does  not  appear  as  a  morbid  entity, 
but  as  a  secondary  condition  in  the  course  of  some  otiier  disease  (maUgnant 
syphilis,  typhoid  fever,  or  pneumonia),  in  pregnancy,  or  in  the  course  of  a 
disease  of  the  liver.  Thus,  in  an  individual  suffering  from  cancer  of  the  liver, 
venous  or  biliary  cirrhosis,  gall-stones,  hepatic  tuberculosis,  or  hepatic 
s}q)hilis,  symptoms  of  icterus  gravis  appear,  and  the  icterus  in  such  a  case 
is  only  an  episode  in  the  course  of  the  hepatic  disease. 

64—2 


1012  TEXT-BOOK  OF  MEDICINE 

We  must  not  speak  of  one  but  of  several  forms  of  icterus  gravis  (Jaccoud) ; 
there  are  also  cases  in  which  the  syndrome  of  icterus  gravis  is  due  to  acute 
intoxication  (phosphorus),  and  in  this  section  we  shall  have  to  separate  each 
of  these  forms. 

Former  observers,  struck  by  the  course  and  the  symptoms  of  this  disease, 
gave  it  the  name  of  icterus  gravis  (Ozanam),  in  opposition  to  icterus 
benignus ;  this  name  implied  malignancy,  without  in  any  way  specifying  a 
distinct  morbid  entity.  On  the  other  hand,  the  predominance  of  certain 
symptoms  gave  the  disease  several  names  :  typhoid  icterus  (Lebert),  fatal 
icterus,  haemorrhagic  icterus  (Monneret). 

Later,  our  ideas  concerning  the  disease  were  modified.  Icterus  gravis 
was  no  longer  considered  a  syndrome,  and  writers  wished  to  make  it  a 
distinct  morbid  entity,  with  its  own  anatomical  character.  Rokitansky 
had  already  announced  that  icterus  gravis  was  the  result  of  acute  atrophy 
of  the  liver.  Frerichs  confirmed  his  researches,  and  several  writers  called 
it  acute  yellow  atrophy  of  the  liver.  Subsequent  researches  proved  that 
the  liver  is  not  always  atrophied,  that  the  lesions  of  the  cells  do  not  consist 
solely  in  atrophy  (Robin),  and  that  irritative  lesions  have  a  certain  part  in 
it,  and  the  disease  for  a  time  received  the  name  of  diffuse  parenchymatous 
hepatitis. 

It  may  be  said  that  the  nature  of  icterus  gravis  is  now  established. 
Icterus  gravis,  as  Bright,  Budd,  and  Trousseau  saw  it,  is- an  infective  disease 
which  in  some  features  resembles  yellow  fever.  It  has  its  origin  in  the  rapid 
anatomical  and  physiological  decay  of  the  cells  of  the  liver,  with  or  without 
atrophy  of  the  organ.  The  liver  is  not  only  attacked  in  its  histological 
elements,  but  also  in  the  chemical  constitution  of  its  parenchyma  (Quin- 
quaud) ;  the  hepatic  cell  may  be  physiologically  destroyed,  while  the  morpho- 
logical changes  appear  to  be  slight.  In  short,  the  multiple  and  important 
functions  of  the  liver  are  suppressed,  glycogenesis  is  abolished,  and,  as  a 
consequence,  there  is  rapid  decay  of  the  nervous,  vascular,  and  muscular 
systems.  The  hepatic  cell  is  no  longer  able  to  arrest  the  passage  of  the 
poisons  and  pepto-toxines  brought  by  the  portal  vein ;  the  products  of 
digestion  undergo  incomplete  elaboration ;  the  extractives,  in  the  form  of  urea, 
no  longer  undergo  their  final  oxidation ;  the  bile  acids  are  incompletely  elabor- 
ated, or,  in  a  word,  the  hepatic  function  tends  to  be  suppressed,  and  the 
liver  "is  no  longer  the  citadel  advanced  against  the  infection,"  but,  on  the 
contrary,  becomes  the  starting-point  of  secondary  infections.  To  these 
causes  of  infection  and  hepatic  intoxication  are  often  joined  causes  of 
ursemic  intoxication,  as  the  renal  epithelium  may  be  attacked. 

Another  question  now  arises  :  we  say  that  icterus  gravis  is  due  to  destnic- 
tion  of  the  hepatic  cells.  What  agent  produces  this  change  ?  Is  it  a  micro- 
organism or  a  toxic  substance  ?     Bacteriological  researches  have  shown 


DISEASES  OF  THE  LIVER  1013 

that  various  microbes  may  be  associated  with  the  lesions  and  symptoms  of 
icterus  gravis.  The  Staphylococcus  aureus  has  been  found  by  Legall  in  two 
cases  of  primary  icterus  gravis,  and  by  Girode  in  one  case  of  icterus  gravis 
during  pregnancy. 

In  the  cases  reported  by  Hanot  various  microbes  were  found.  A  yoimg  woman 
died  of  icterus  gravis.  Streptococci  were  found  in  the  small  ducts  and  veins  of  the  liver, 
and  in  the  serum  from  the  lung  and  the  spleen.  An  alcoholic  youth  was  carried  off  by 
icterus  gravis,  and  the  Bacillus  coli.was  found  in  the  hepatic  cells  and  capillaries.  A 
man  suffering  from  cancer  of  the  biliary  passages  died  of  icterus  gravis,  and  the 
Bacillus  coli  was  found  in  the  bile  and  in  the  blood  of  the  cardiac  cavities. 

Boix  reports  the  following  cases :  In  a  patient  suft'ering  from  icterus  gravis,  with 
hypothermia,  Hanot  and  Boix  found  the  Bacillus  coli  in  the  blood  and  in  tho  liver 
four  hours  after  death.  In  a  patient  suffering  from  icterus  gravis,  with  hyperthermia, 
the  same  authors  foimd  the  Staphylococcus  alhus  in  the  blood  twenty-four  hours  before 
death,  and  the  same  staphylococcus  in  the  hver  half  an  hour  after  death.  Babes  has 
published  four  cases  of  icterus  gravis  terininating  rapidly  in  death,  and  associated  with 
the  streptococcus.  Hanot  has  commimicated  two  cases  of  icterus  gravis  that  super- 
vened in  pneumonia  and  in  secondary  cancer  of  the  liver.  In  the  first  case  the  pneumo- 
coccus  was  found  in  the  liver,  and  in  the  second  case  the  pneumococcus  was  found  in 
the  blood  of  the  cephalic  vein  five  hours  before  death.  Achard  has  published  two  cases 
of  primary  cancer  of  the  liver  ending  in  icterus  gravis ;  in  each  case  the  Staphylococcus 
alhus  was  found  in  tho  liver  during  life.  Bar  and  Renon  have  reported  the  case  of  a 
new-bom  child  who  died  of  icterus  gravis  complicating  hepatic  syphihs.  The  Proteus 
vulgaris  was  foimd  in  a  pure  state  in  the  blood  of  the  umbilical  vein,  in  the  liver,  the 
spleen,  and  the  heart. 

This  enumeration  proves  that  icterus  gravis  may  be  associated  with  the 
Bacillus  coli,  streptococcus,  staphylococcus,  pneumococcus,  and  Proteus 
vulgaris.  There  can,  therefore,  be  no  question  of  a  specific  disease,  and  we 
have  proof  that  the  hepatic  cell,  under  certain  conditions  of  morbid  recep- 
tivity, may  be  attacked  by  various  pathogenic  agents,  and  undergo  changes 
which  produce  the  syndrome  of  icterus  gravis. 

The  hepatic  lesions  of  icterus  gravis  are,  however,  chiefly  due  to  the 
toxines.  The  poison  comes  in  some  cases,  perhaps,  from  ptomaines  absorbed 
by  the  liver.  This  hypothesis  of  a  poison  attacking  and  destroying  the 
hepatic  cell  is  realized  in  phopphorus-poisoning,  which  exactly  reproduces 
the  syndrome  of  icterus  gravis :  steatosis,  destmction  of  the  hepatic  cells, 
icterus,  haemorrhages,  nervous  symptoms,  and  hypothermia. 

Summary :  Whether  the  pathogenic  agent  acts  as  an  infective  or  as  a 
toxic  agent,  we  may  say  that  the  pathogenesis  of  icterus  gravis  is  being 
cleared  up.  The  only  difference  between  primary  and  secondary  icterus 
gravis  is  that  the  former  attacks  an  individual  whose  liver  is  apparently 
healthy,  whereas  the  latter  attacks  a  person  whose  liver  has  been  already 
damaged.  It  is  possible  that  the  difference  between  the  primary  and 
secondary  forms  is  not  so  pronounced,  for  it  is  not  proved  that  iji  the  so- 
callod  primary  forms  the  liver  has  not  been  surprised  in  a  condition  of 
morbid  imminence,  as  a  locus  mirwris  resistentiw.     The  varieties  of  icterus 


1014  TEXT-BOOK  OF  MEDICINE 

gravis  would  then  all  belong  to  one  class,  though  distinct  from  one  another, 
according  to  the  scale  of  gravity,  in  the  same  manner  as  cases  of  benign 
icterus  may  be  grouped  in  another  class,  having  only  the  scale  of  benignity  as 
their  distinctive  sign. 

The  so-called  primary  icterus  gravis,  which  so  closely  resembles  yellow 
fever  nostras,  must  not  be  completely  abandoned.  It  is  much  rarer  than 
secondary  icterus  gravis,  but  its  symptoms  are  more  clearly  pronounced, 
and  it  will  serve  best  as  a  type  for  our  description. 

Pathological  Anatomy.— In  icterus  gravis  the  Hver  is  generally  small ; 
the  atrophy  may  be  such  that  the  liver  may  weigh  only  15  to  20  ounces. 
GUsson's  capsule,  having  grown  too  large  for  the  atrophied  parenchyma,  is 
furrowed.  In  some  cases,  if  the  disease  is  very  rapid,  the  liver  remains  of 
normal  size,  and  the  lesions  are  only  appreciable  with  the  microscope.  The 
organ  is  hypertrophied  when  icterus  gravis  occurs  as  a  secondary  trouble  in 
a  person  whose  liver  was  already  enlarged  (malaria,  alcoholism,  or  hj^oer- 
trophic  cirrhosis).  Most  frequently  the  yellow  colour  of  the  liver  is  not 
uniform,  but  presents  mottlings  and  reddish  islands  (red  atrophy).  The 
parenchyma  is  softened,  friable,  or  sometimes  diffluent,  and  in  a  section 
the  lobular  appearance  is  no  longer  seen.  The  Uver  contains  but  little  blood 
and  bile,  and  there  is  also  but  Uttle  bile  in  the  gall-bladder  and  the  large 
bile-ducts. 

Under  the  microscope  the  following  lesions  are  seen  :  At  the  parts  most 
affected  the  liver  cells  have  disappeared,  and  are  replaced  by  an  amorphous 
veinstone,  infiltrated  with  embryonic  cells,  hsematoidin,  bile  pigment,  and 
fatty  granules.  Elsewhere  the  cells  remain,  but  have  undergone  complete 
disintegration ;  the  protoplasm  has  disappeared,  and  the  cell  is  infiltrated 
with  fatty  granules  and  bile  pigment.  "  The  cloudy  condition  of  the  cells 
and  the  infiltration  with  bile  is  the  first  phase  in  the  degeneration,  which 
ends  finally  in  fragmentation  and  destructive  softening  of  the  elements." 
This  destructive  process  has  been  explained  in  various  ways.  According 
to  some  writers,  it  is  simply  a  degenerative  process ;  according  to  others, 
it  is  an  irritative  one.  The  irritative  process  seems  at  times  to  be  limited 
to  the  cells,  passing  over  the  connective  tissue  (parenchymatous  hepatitis) ; 
at  other  times  the  connective  tissue  is  also  affected  (Frerichs).  The  hepa- 
titis is  both  parenchymatous  and  interstitial,  and  the  bloodvessels  participate 
in  the  process. 

In  certain  cases,  if  the  patient  dies  so  rapidly  that  the  lesions  have  not 
time  to  develop,  or  if,  for  other  reasons,  the  changes  in  the  Hver  are  less 
marked,  the  cells  show  cloudy  swelling,  and  the  parenchyma  encloses  a 
quantity  of  extractives.  Chemical  analyses  have  shown  that  in  some  cases 
the  extractives  have  increased  twofold.  The  bloodvessels,  and  especially 
the  hepatic  veins,  are  changed  ;  they  are  almost  bloodless,  and  contain  much 


DISEASES  OF  THE  LIVER  1015 

leucin  and  tyrosin.  The  bile-ducts  are  almost  always  involved;  we  find 
angiocliolitis  of  the  small  canals,  which  are  obliterated  by  cellular  detritus 
(Bamberger).  This  lesion  is  probably  the  cause  of  the  icterus,  unless  we 
admit,  with  Frerichs,  that  the  icterus  is  due  to  the  compression  of  the 
biliary  canaliculi  by  exudation  into  the  periphery  of  the  lobules.  Cornil,  in 
one  case,  found  the  interlobular  canaliculi  dilated  and  filled  with  cells,  and 
the  intralobular  network  abnormally  developed.  This  intra-acinous  net- 
work, which  has  been  noticed  by  other  authors,  is  said  to  appear  in  the  last 
stage,  when  the  fatty  detritus  of  the  parenchyma  is  absorbed.  It  is  probable 
that  the  bihary  canals  are  intact  in  the  very  rare  cases  in  which  icterus  is 
almost  absent.  The  kidneys  are  always  affected,  and  show  an  early  stage  of 
parenchymatous  nephritis.  Man}^  convoluted  tubes  are  blocked  by  large 
cloudy,  granular,  fatty,  and  deformed  cells.  A  certain  dependence  has  rightly 
been  found  between  the  lesions  of  the  kidneys  and  of  the  liver.  According 
to  some  writers,  the  lesion  of  the  kidneys,  following  that  of  the  liver,  is  said 
to  be  caused  by  the  icterus  and  by  the  ehmination  of  the  bile  ;  according 
to  others,  the  renal  and  hepatic  lesions  are  said  to  be  dependent  on  the  same 
cause.     Both  theories  are  accepted. 

The  blood  shows  the  abnormal  fluidity  found  in  cases  of  pyrexia  and 
in  the  infectious  diseases  (Vulpian).  It  has  tittle  tendency  to  coagulate, 
being  diffluent,  blackish,  and  tarry.  It  is  deficient  in  red  blood-corpuscles, 
and  is  loaded  with  leucin,  tyrosin,  and  xanthin,  due  to  incomplete  oxidation 
of  the  proteids.  According  to  some  writers,  it  is  said  to  contain  less  urea. 
The  hsemoglobin  affected  by  the  changes  in  the  extractives  is  said  to  absorb 
less  oxygen  than  in  the  normal  condition  (Quinquaud).  The  lungs,  pleura, 
capsule  of  the  liver,  spleen,  and  kidneys  may  show  haemorrhages.  The 
spleen  ls  usually  enlarged  and  softened.  The  heart  is  soft  and  fatty,  endo- 
perirarditis  being  common  (Jaccoud). 

Symptoms.  —  I  shall  first  describe  so-called  primary  icterus  gra\as, 
and  then  briefly  mention  the  secondary  forms.  The  onset  is,  as  a  rule, 
insidious.  The  disease  may  at  first  resemble  the  simple  catfirrhal  form, 
the  symptoms  of  icterus  gravis  appearing  a  few  days  later.  Sometimes  the 
disease  begins  with  a  violent  rigor,  accompanied  by  extreme  prostration, 
rachialgia,  and  vomiting  ;  but  this  sudden  and  acute  onset  which  recalls  the 
outburst  of  certain  pyrexias  is  more  rare  than  a  gradual  onset.  For  some 
days  the  patient  complains  of  lassitude,  pains  in  the  hmbs,  prostration,  and 
low  spirits,  resembling  the  invasion  of  influenza  or  of  typhoid  fever.  At 
other  times  gastro-intestinal  troubles  open  the  scene,  and  form  the  chief 
feature.  A  diagnosis  of  gastric  trouble  is  at  first  made.  The  malaise,  however, 
increases,  fever  appears,  and  from  the  third  to  the  eighth  day  icterus  sets  in. 
From  this  moment  three  classes  of  symptoms  dominate  the  situation — viz., 
icterus,  hajmorrhagc,  and  nervous  troulilcs. 


1016  TEXT-BOOK  OF  MEDICINE 

The  icterus  varies  from  the  lightest  yellow  colouring  of  the  conjunctivae 
and  of  the  sldn  to  a  green  or  bright  yellow  colour.  There  is,  however,  no 
relation  between  the  gravity  of  the  trouble  and  the  degree  of  the  icterus, 
and  if  I  insist  on  this  point,  it  is  because  an  old  theory  assigned  to  the  absorp- 
tion of  bile  an  important  part  in  the  production  of  the  trouble.  The  icterus 
is  due  to  divers  causes.  When  it  is  the  result  of  absorption  of  the  bile,  nitric 
acid  gives  the  well-known  green  reaction  in  the  urine ;  but  there  are  cases  in 
which  the  urine,  treated  with  nitric  acid,  does  not  reveal  pigment  of  hepatic 
origin,  and  is  coloured  a  dirty  brown.  Gubler  called  this  condition  haema- 
pheic  icterus.     These  two  forms  may  alternate  or  may  occur  together. 

As  the  disease  progresses,  the  icterus  may  disappear — a  bad  sign,  proving 
the  decay  of  the  hepatic  cell  (Jaccoud).  The  feeces  are  lighter  than  in  the 
normal  condition. 

Haemorrhages  are,  so  to  say,  constant,  appearing  in  the  course  of  the 
disease  or  in  its  last  stage.  Epistaxis,  which  may  be  seen  from  the  com- 
mencement, purpura,  haemorrhage  from  the  gums,  hsematemesis,  and  melsena, 
are  the  most  common  ;  haematuria,  haemoptysis,  and  metrorrhagia  are  much 
rarer.  These  haemorrhages  are  favoured  by  the  fluid  condition  of  the  blood. 
An  attempt  has  been  made  to  explain  them  by  the  passage  of  the  bile  into 
the  blood  ;  this  theory  must  be  abandoned.  Experiments  have  decided  the 
point ;  and,  furthermore,  the  same  haemorrhagic  diathesis  is  found  in  other 
diseases,  such  as  black  smallpox,  purpura,  and  typhoid  affections,  and  the 
explanation  does  not  require  the  presence  of  bile  in  the  blood.  The  haemor- 
rhages, as  in  phosphorus  -  poisoning,  depend  on  the  destruction  of  the 
hepatic  cell,  and  Galen  was  correct  in  saying,  Hepar  sanguifictmi.  The 
nervous  troubles  consist  in  phenomena  of  excitation :  slight  dehrium, 
dyspnoea,  hiccough,  insomnia,  tremor  of  the  Ups,  subsultus  tendinum,  con- 
vulsive movements  ;  and  in  phenomena  of  depression  :  sleepiness,  stupor, 
and  coma.  These  troubles  of  excitation  and  of  depression  occur  together, 
or  follow  one  another  without  a  fixed  rule.  The  symptoms  of  depression 
often  open  the  scene,  and  the  symptoms  of  excitation  appear  later,  being 
followed  by  coma. 

The  pulse  and  the  temperature  present  marked  variations.  The  pulse 
may  be  quick  or  slow.  The  temperature  may  rise  to  103°  or  104°  F.,  or 
else  it  is  lowered  from  the  commencement  of  the  disease,  and  remains  low 
until  its  last  stage  (Wunderlich).  There  is,  therefore,  no  fixed  relation, 
from  the  point  of  view  of  prognosis,  between  the  febrile  condition  and  the 
gravity  of  the  general  symptoms,  but  some  relation  may  be  estabhshed 
between  the  temperature  and  the  nature  of  the  infective  agents.  Recent 
researches  have  proved  that  the  Bacillus  coli  and  its  toxine  cause  hypo- 
thermia ( Dupre,  Netter,  Boix) ;  it  is  certain,  as  experiments  and  clinical 
medicine  prove,  that,  in  a  general  way,  the  intoxications  and  infections 


DISEASES  OF  THE  LIVER  1017 

caused  by  the  Bacillus  coli  produce  a  subnormal  temperature,  whilst  the 
infections  and  intoxications  of  other  microbes — streptococcus,  staphylococcus, 
or  pneumococcus — raise  the  temperature,  often  causing  considerable  hypo- 
thermia. These  same  distinctions  have  been  formulated  by  Hanot,  as 
regards  the  diseases  of  the  hver,  and  especially  of  icterus  gravis.  Boix  has 
collected  thirty-four  cases  of  icterus  gravis,  in  which  the  temperature,  curve, 
and  nature  of  the  pathogenic  microbe  are  indicated.  He  shows  that  in 
hepatic  infection  by  the  streptococcus,  staphylococcus,  or  pneumococcus, 
etc.,  the  temperature  rises  to  104°  or  105°  F.  (hyperthermia)  ;  on  the  other 
hand,  in  hepatic  infections  by  the  Bacillus  coli  the  temperature  is  lowered 
to  95°  F.  (hypothermia).  There  are,  of  course,  mixed  and  intermediate 
cases. 

The  two  morbid  types  of  icterus  gravis,  hyperthermic  and  h}'pothermic, 
are  seen,  as  Boix  has  pointed  out,  in  two  morbid  species  which  are  dissimilar 
as  regards  pathogenesis,  but  which  both  end  in  the  syndrome  of  icterus  gravis 
— i.e.,  yellow  fever,  with  its  high  temperature  (h^'perthermia) ;  and  phos- 
phorus-poisoning, with  its  low  temperature  (hypothermia). 

The  examination  of  the  urine  furnishes  information  of  great  value. 
The  urinary  secretion  is  generally  diminished.  Cases  have  even  been  quoted 
where  the  anuria  was  complete  for  several  days.  The  icteric  tint  of  the 
urine  is  more  or  less  pronounced.  It  is  generally  a  case  of  biUpheic  icterus  ; 
in  some  cases,  however,  the  reaction  of  the  so-called  haemapheic  icterus  has 
been  noticed.  The  urine  is  often  albuminous ;  it  contains  hardly  any  urea 
at  an  advanced  period  of  the  disease,  but,  on  the  other  hand,  leucin  and 
tyrosin  are  found  in  quantity  in  almost  all  cases.  The  urea  is  diminished 
because,  according  to  certain  writers,  the  liver  being  the  principal  producer 
of  urea,  this  salt  is  less  when  the  liver  is  destroyed,  or  when  its  functions 
are  suspended.  The  urine  contains  leucin  and  tyrosin,  because  the  Uver  no 
longer  fulfils  its  normal  functions ;  the  combustion  of  the  proteids  is  in- 
complete, and,  instead  of  producing  uric  acid  and  urea,  wliich  are  the  last 
stage  in  the  oxidation  of  the  proteids,  it  only  produces  less  oxidized  products, 
such  as  leucin,  tyrosin,  and  xanthin. 

The  examination  of  the  liver  does  not  always  cause  pain ;  it  reveals  the 
atrophy  of  the  organ.  The  spleen  is  enlarged.  The  skin  shows  such 
eruptions  as  erytlicnia,  roseola,  miliaria,  and  urticaria. 

Course,  Duration,  Prognosis. — I  have  already  dwelt  on  the  insidious  and 
variable  onset  of  icterus  gravis.  According  to  the  predominance  of  haemor- 
rhage or  of  adynamic  symptoms,  ha?niorrhagic  and  typhoid  forms  have 
been  described  ;  but  this  division  is  not,  in  my  opinion,  suitable,  the  mixed 
form  being  the  more  frequent.  The  prognosis  is  extremely  grave ;  in  some 
exceptional  cases  the  patient  succumbs  in  two  or  three  days,  and  the  course 
is  lightning-like.     The  final  symptoms  generally  supervene  from  the  sixth 


1018  TEXT-BOOK  OF  MEDICINE 

to  the  tenth  day.  However,  icterus  gravis  is  not  absolutely  fatal,  and  the 
name  of  fatal  icterus,  given  by  some  EngUsh  writers,  is,  happily,  not  justi- 
fied. There  are  some  undoubted  cases  of  cure,  and  they  are,  indeed,  more 
frequent  than  would  at  first  be  supposed,  considering  the  custom  of  looking 
upon  icterus  gravis  as  a  sentence  of  death.  In  truth,  it  may  well  be 
asked  why  this  so-called  essential  icterus  gravis,  or  yellow  fever  nostras, 
should  not  be  cured  hke  other  infectious  cases ;  therefore  I  do  not  see  why 
this  should  be  a  reason  for  making  a  special  variety,  and  for  grouping  the 
recoveries  under  the  name  of  icterus  pseudo-gravis.  Recovery  is  sometimes 
announced  by  a  crisis  of  polyuria,  increase  of  urea,  abundant  diaphoresis, 
and  profuse  diarrhoea.  The  urinary  toxicity,  which  is  very  much  lowered 
during  the  disease,  exceeds  its  normal  coefficient  at  the  moment  of  the  crisis. 
The  condition  of  the  kidneys  is  of  great  importance  in  the  prognosis ;  the 
danger  is  less  when  the  secretion  of  urine  is  free.  Parotiditis  (suppurative 
inflammation)  has  several  times  coincided  with  recovery. 

Diagnosis. — It  is  very  difficult  to  make  a  diagnosis  at  the  commencement 
of  the  disease  ;  later,  when  the  principal  symptoms  have  appeared,  icterus 
gravis  somewhat  resembles  other  diseases  accompanied  by  icterus,  such  as 
ulcerative  endocarditis,  purulent  infection,  poisoning  by  phosphorus,  and 
yellow  fever.  Icterus  is  very  rare  in  infective  endocarditis  ;  haemorrhage  is 
absent,  and  auscultation  of  the  heart  reveals  the  murmurs  of  endocarditis. 
Purulent  infection  originates  from  a  wound  or  injury,  and  is  characterized 
by  repeated  rigors,  by  violent  attacks  of  fever,  and  by  pain  in  the  hepatic 
region,  due  to  pysemic  abscesses  in  the  hver.  Poisoning  by  phosphorus 
resembles  icterus  gravis  so  closely  that,  in  the  absence  of  any  history  or  of 
traces  of  the  poison  in  the  vomit,  it  would  often  be  very  difficult  to  make 
a  diagnosis.  We  shall  see  later  the  complete  analogy  existing  between 
vomito  negro  and  icterus  gravis,  wliich  has  sometimes  been  called  yellow 
fever  nostras. 

Another  difficulty  presents  itself  :  for  some  few  days  a  patient  has  icterus 
supposed  to  be  catarrhal.  Fever  is  present,  repeated  epistaxis  occurs, 
and  purpura  appears.  How  are  we  to  know  whether  these  symptoms  are 
due  to  benign  or  grave  icterus  ?  The  analysis  of  the  urine,  the  discovery 
of  albumin,  and  the  cjuantity  of  urea  give  insufficient  information.  Diag- 
nosis and  prognosis  often  remain  in  doubt,  and  it  is  a  case  of  saying,  with 
Trousseau  :  "  In  icterus,  as  in  pleurisy,  we  never  know  how  it  may  end." 

etiology. — The  so-called  primary  icterus  gravis  is  far  less  common  than 
secondary  icterus  gravis.  It  sometimes  appears  suddenly  in  an  apparently 
healthy  subject ;  at  other  times  it  develops  tlirough  predisposing  causes, 
such  as  pregnancy,  alcoholism,  excesses  in  eating,  or  gastro-intestinal  auto- 
infection.  A  person,  although,  at  the  time  being,  in  good  health,  has  pre- 
viously suffered  from  hepatic  coUc,  symptoms  of  biliary  lithiasis,  or  jaundice, 


DISEASES  OF  THE  LIVER  1019 

and  the  affected  liver  has  not  quite  lost  all  traces  of  the  disease.  Another 
individual,  though,  for  the  time  being,  in  good  health,  has  some  hereditary 
predisposition,  and,  by  a  combination  of  circumstances  which  make  patho- 
logical heredity  a  very  complex  question,  an  organ,  such  as  the  brain,  the 
kidneys,  the  heart,  or  the  liver,  is  less  resistant  to  the  repeated  attacks  on 
life.  Under  the  influence  of  conditions  with  which  we  are  still  imperfectly 
acquainted,  icterus  gra\ns  has  been  epidemic,  but  it  must  be  stated  that  the 
epidemic  remains  limited.  The  focus  does  not  extend  beyond  a  bar- 
racks, prison,  or  ship.  It  is  not  rare  to  see  relatively  benign  cases  which 
resemble  catarrhal  icteras  during  the  same  epidemic  by  the  side  of  serious 
cases.    Kelsch  is  of  the  opinion  that  the  infective  agent  is  of  telluric  origin. 

Secondary  Icterus  Gravis. — This  form  supervenes  during  the  course  of 
some  disease  (typhoid  fever,  cholera,  or  pneumonia),  which  has  placed  the 
liver  in  a  condition  of  receptivity.  Pregnancy  has  this  effect,  because  it 
renders  the  Hver  hable  to  infection  by  steatosis  of  the  hepatic  cell.  Any 
disease  of  the  liver  may  be  complicated  by  the  hsemorrhagic  and  nervous 
troubles  of  icterus  gravis.  I  quote  as  such  :  alcoholic,  biliary,  cardiac,  and 
tubercular  cirrhosis  ;  cholelithiasis ;  cancer ;  permanent  obstruction  of  the 
biliary  canals  ;  hydatid  cysts  ;  and  hepatic  syphihs.  In  these  various  lesions 
the  door  is  opened  to  the  secondary  infections  and  toxines,  the  affected  liver 
cells  being  no  longer  in  a  state  of  defence.  Some  of  these  cases  refer  to 
patients  already  suffering  from  icterus,  and  in  them  the  disease  takes  the 
name  of  aggravated  icterus,  which  is  often  "  only  the  last  act  in  the  morbid 
process." 

The  symptomatic  picture  of  secondary  icterus  gravis  is  almost  the  same 
as  that  of  the  primary  form  ;  it  is,  however,  less  marked,  and  the  course  is 
less  rapid,  because  the  destruction  of  the  hepatic  cells  is  from  the  first  not 
so  general  as  in  essential  ictenis  gravis. 

The  course  and  gravity  of  the  trouble  depend  much  on  the  previous  con- 
dition of  the  patient.  Sometimes  the  complications  of  aggravated  icterus 
hasten  the  end  fairly  quickly  ;  at  other  times  they  follow  one  another  slowly 
in  a  snliacuto  form,  and  thoy  may  recover. 

Icterus  and  the  Puerperal  State. — As  I  have  already  remarked,  icterus 
due  to  gall-stones  is  not,  as  a  rule,  serious  in  a  pregnant  woman  ;  such  is  not 
the  case  in  the  other  varieties  comprised  under  the  term  of  "infective  icterus." 
Whatever  theory  is  put  forward  to  explain  the  changes  in  the  hepatic  cell 
matters  little  ;  as  soon  as  the  cell  participates  in  the  toxi-infectious  process, 
it  undergoes  an  adulteration  which,  under  other  conditions,  might  not 
have  serious  consequences,  but  which  in  the  gravid  condition  is  always  to 
be  feared.  When  icterus  appears  in  pregnancy,  it  is  always  of  serious 
import  (I  am  speaking  of  icterus  occurring  apart  from  hepatic  colic),  because 
it   indicates   a   hepatic    lesion   that    may   lead    to    insuificiency.     Hepatic 


1020  TEXT-BOOK  OF  MEDICINE 

insufficiency  is  sometimes  accompanied  by  albuminuria  and  renal  insuffi- 
ciency, the  epithelium  of  the  kidneys  being  directly  affected  by  the  toxi- 
infective  agent,  or  suffering  injury  from  the  elimination  of  poisonous  bile. 

Le  Masson  has  collected  thirty-nine  cases  of  icterus  during  pregnancy 
and  thirteen  cases  of  icterus  after  confinement.  The  thirty-nine  cases  show 
thirteen  recoveries  and  twenty-six  deaths.  The  thirteen  cases  occurring 
after  accouchement  show  three  recoveries  and  ten  deaths.  These  figures 
indicate  the  gravity  of  puerperal  icterus. 

The  icterus  of  pregnancy  appears  chiefly  after  the  third  month,  and  it 
is  generally  impossible  to  find  any  factors  other  than  the  gravid  condition. 
The  icterus  is  sometimes  preceded  by  nausea,  vomiting,  gastralgia,  and  coUc  ; 
in  other  cases  it  appears  without  any  previous  manifestation.  The  jaundice 
may  be  slight  or  intense,  from  a  subicteric  tint  to  deep  and  general  icterus. 
The  urine  contains  bile  pigment  and  urobilin  in  unequal  proportions ; 
albumin  is  often  found.  The  faeces  are  clay-coloured.  The  fever  is  slight 
or  severe.  The  liver  tends  to  be  enlarged,  and  is  sometimes  painful.  The 
other  symptoms  include  anorexia,  headache,  diarrhoea,  or  constipation, 
and  are  extremely  variable.  After  a  duration  of  a  fortnight  to  a  month, 
the  symptoms  improve,  the  icterus  disappears,  the  pregnancy  follows  its 
course,  and  the  patient  recovers,  without  further  disturbance.  This  is  the 
benign  form. 

In  other  cases,  if  the  hepatic  lesion  is  more  severe  or  more  prolonged, 
the  situation  becomes  serious,  and  the  disease  ends  in  miscarriage,  premature 
confinement,  or  even  in  the  death  of  the  mother.  Finally,  in  some  cases 
the  disease  assumes  the  characters  of  icterus  gravis,  with  haemorrhages, 
epistaxis,  purpura,  ecchymotic  patches,  violent  headache,  delirium,  restless- 
ness, dyspnoea,  and  tendency  to  coma.  "  In  these  grave  forms,  miscarriage, 
premature  confinement,  or  even  accouchement  at  term,  generally  occurs 
whilst  the  syndrome  is  at  its  height,  from  two  to  five  days  after  the  onset  of 
icterus,  and  very  often  on  the  second  day ;  but  there  is  occasion  to  insist 
on  their  suddenness.  Physicians  sometimes  discuss  the  question  of  inter- 
vention when  the  woman  is  about  to  be  confined,  as  if,  after  such  a  ter- 
mination, it  were  permissible  to  hope  for  recovery  !  The  relative  calm  and 
feeling  of  well-being  might  lead  us  to  form  a  favourable  prognosis.  This 
calm  is,  however,  deceptive,  and  the  amelioration  is  of  short  duration  ;  the 
symptoms  have  only  lulled,  to  reappear  some  hours  later,  when  they  cause 
death  with  terrible  rapidity  "  (Le  Masson). 

Icterus  appearing  after  the  confinement  is  much  more  often  grave  than 
benign,  since  in  thirteen  cases  it  was  followed  in  ten  by  death.  It  is, 
furthermore,  almost  always  associated  with  puerperal  infection.  Puerperal 
icterus  is  sometimes  epidemic.  The  following  summary  of  seven  epidemics 
is  taken  from  Le  Masson's  monograph  : 


DISEASES  OF  THE  LIVER  1021 

Epidemic  of  Liideuscheid  in  1879  ;  epidemic  of  Roubaix,  desciibcd  by  Carpentier ; 
epidemic  of  Saint -Pierre  de  la  Martinique  in  1858,  described  by  Rouillc  and  by  Saint- 
Vel  ("  out  of  tliirty  women  attacked  by  icterus,  twenty  succumbed  to  coma  after  mis- 
carriage, or  premature  confinement  ") ;  epidemic  of  Limoges,  described  by  Bardinet 
in  1860  ;  epidemic  of  the  Matemite  and  of  the  Hopital  des  CUniques  in  1870-1872, 
described  by  Hervieux,  Depaul,  and  Meunier  ;  epidemic  of  Saint-Paul  in  1873,  described 
by  Smith  ;  epidemic,  of  Neusenstamm  in  1876,  described  by  Vinay. 

In  1867  Hervieux  tried  to  explain  these  troubles  "  by  the  presence  of  a 
special  morbid  ferment  or  toxic  principle."  We  now  speak  of  toxi-infection, 
the  cause  of  which  it  is  often  possible  to  find.  In  short,  no  matter  what 
pathogenesis  is  invoked  to  explain  the  icterus  of  pregnancy  (leaving  aside 
icterus  due  to  gall-stones)  it  is  none  the  less  true  that  in  the  pregnant  woman 
the  Uver  cell  no  longer  has  the  same  antitoxic  properties,  so  that  toxi-infec- 
tions  readily  bring  about  decay.  The  gravity  of  this  condition,  of  which  the 
icterus  is  one  of  the  signs,  must  lead  us  to  reserve  our  prognosis. 

We  must  obviously  divide  icterus  occurring  in  pregnant  women  into 
two  great  classes.  If  it  Is  associated  with  cholelithiasis  or  occurs  with  hepatic 
colic,  the  prognosis  is  almost  always  good,  because  the  liver  cell  is  not 
affected.  If  the  pregnant  woman  has  neither  hepatic  colic  nor  gall-stones, 
or  if  the  icterus  supervenes  as  a  toxi-infection  of  the  liver,  with  or  without 
participation  of  the  kidney,  the  situation  may  become  perilous. 

Treatment. — Saline  purgatives  and  diuretics  must  be  administered  at 
the  commencement  of  icterus  gravis.  Milk  diet  is  absolutely  indicated.  I 
have  several  times  noted  the  utility  of  large  and  repeated  infections  of 
artificial  serum  ;  two  of  my  patients  recovered.  Intestinal  antisepsis  has 
been  recommended.  The  haemorrhages,  vomiting,  and  nervous  troubles 
demand  symptomatic  treatment.  Most  of  these  troubles  unfortunately 
resist  the  best-directed  measures. 


XXVII.  CATARRHAL  ICTERUS— PROLONGED  CATARRHAL 

ICTERUS. 

Pathogenesis. — Under  Icterus  Gravis  we  saw  that  there  was  a  scale  of 
gravity  in  its  various  forms,  and  so,  too,  benign  icterus  has  a  scale  of  be- 
nignity. Some  are  infectious,  others  are  not,  and  those  which  are  infectious 
are  not  in  the  same  class. 

Emotional  icterus,  for  example,  is  not  of  infective  origin.  It  does 
occur,  as  in  the  case  quoted  by  Potain,  of  a  man  about  to  be  shot ;  in  Rendu's 
case,  of  a  young  girl  excited  by  catheterLsm  ;  and  in  ChaufEard's  case,  of  a  man 
seized  with  a  violent  fit  of  temper.  Emotional  icterus,  which  may  appear  in 
less  than  an  hour,  Ls  proljably  due  to  an  excess  of  biliary  secretion  and  to 
its  absorption. 

Under  Angiocholitis  I  quoted  several  varieties  of  benign  icterus,  such  as 


1022  TEXT-BOOK  OF  MEDICINE 

syphiKtic  icterus  of  the  secondary  period,  icterus  from  pigmentary  hyper- 
cliolia  in  the  newly-born,  and  icterus  associated  with  angiocholitis  of  biliary 
origin.  These  various  kinds  of  icterus,  which  are  generally  benign,  have 
already  been  described.  I  shall  now  especially  deal  with  the  condition 
described  as  catarrhal  icterus. 

Primary  catarrh  of  the  biliary  passages,  still  called  simple  catarrhal 
icterus,  because  the  icterus  is  the  most  apparent  symptom,  may  invade  the 
intrahepatic  and  also  the  extrahepatic  bile-ducts.  If  the  catarrh  attacks  the 
intrahepatic  canals  alone,  icterus  appears,  because  the  bile  is  absorbed  in 
situ,  from  the  obhterated  canals ;  but  the  stools  are  not  colourless,  because  suffi- 
cient bile  continues  to  pass  into  the  intestine.  On  the  contrary,  if  the  catarrh 
attacks  the  common  bile-duct,  so  that  it  is  obstructed  by  the  inflammatory 
products,  obstructive  icterus  occurs,  and  is  associated  with  more  or  less 
complete  decoloration  of  the  faeces.  This  last  form  is  the  type  of  so-called 
catarrhal  icterus. 

In  the  very  rare  cases  where  a  patient  with  catarrhal  icterus  has  suc- 
cumbed to  an  intercurrent  disease,  inflammation  of  the  conmion  duct  has 
been  found  post  mortem  ;  the  inflammation  may  be  limited  to  the  intestinal 
portion  and  to  the  duodenal  orifice  of  the  duct  (Virchow).  The  walls  of  this 
portion  of  the  common  duct,  the  connective  tissues  around  it,  and  Vater's 
ampulla,  show  oedematous  swelling,  which  constricts  or  blocks  the  orifice. 
"  It  will  readily  be  understood  that  this  oedematous  swelhng  may  obstruct 
the  flow  of  the  bile  and  produce  icterus,  when  we  remember  that  coryza 
prevents  nasal  respiration  in  consequence  of  the  swelling  of  the  mucosa." 
Moreover,  the  common  duct  at  this  level  is  blocked  by  a  mass  of  epithehal 
cells,  forming  a  kind  of  plug,  which,  unstained  by  the  bile,  completes  the 
obstruction  of  the  duct  and  opposes  the  passage  of  the  bile  into  the  intestine 
(Vulpian). 

In  a  post-mortem  examination  performed  by  Miiller  the  common  duct 
was  obstructed,  the  mucosa  being  swollen  and  covered  with  petechise  ; 
catarrhal  obstruction  of  Wirsung's  canal  was  also  present. 

The  affected  parts  of  the  common  duct  preserve  their  normal  dimensions 
(about  6  millimetres  in  diameter),  and  are  not  impregnated  with  bile,  whilst 
the  biliary  passages  above  the  obstacle  are  dilated.  This  obstacle  to  the 
flow  of  the  bile  causes  icterus  by  retention,  the  constant  and  prominent 
symptom  of  catarrh  of  the  biliary  passages.  Such  is,  in  general  terms,  the 
chief  lesion  in  catarrhal  icterus.  How  is  this  lesion  produced  ?  According  to 
an  old  theory,  angiochohtis  of  the  common  duct  was  said  to  be  associated 
with  gastro-intestinal  catarrh,  and,  in  consequence,  connected  with  the  causes 
of  this  catarrh  (high  living,  chill).  Some  individuals,  it  is  true,  suffer  from 
gastro-intestinal  troubles  and  icterus,  following  on  orgies,  acute  alcoholism 
(and  we  know  the  influence  of  alcohol  on  the  liver),  or  drunkenness,  whence 


DISEASES  OF  THE  LIVER  1023 

the  old  name  of  icterus  a  crapula.  This  theory  only  takes  account  of  a  local 
process  ;  it  is  founded  on  the  spread  of  the  catarrh  from  the  duodenum  to  the 
common  duct,  with  obliteration  of  the  lumen. 

Other  theories  are  opposed  to,  or  associated  mth,  this  theory  of  the 
disease.  Catarrhal  icterus  is  considered  to  be  an  infectious  disease,  due  to 
internal  or  external  infection.  That  catarrhal  icterus  is  frequently  a  general 
disease,  or  a  variety  of  bilious  fever  chiefly  limited  to  the  biliary  canaLs, 
follows  from  the  careful  study  of  cases.  It  will  thus  be  perceived,  as 
Chauffard  points  out,  that  the  disease  commences  wth  pre-icteric  symptoms 
of  fever,  lassitude,  anorexia,  vomiting,  epistaxis,  insomnia,  albuminuria,  labial 
herpes,  and  sometimes  with  foetid  bilious  diarrhoea,  indicating  hypersecretion 
of  the  hver.  The  icterus  appears  three  or  four  days  after  this  period  of 
invasion,  and  is  soon  followed  by  decoloration  of  the  faeces.  "  The  secre- 
tion of  the  urine  and  the  excretion  of  the  urea  run  a  parallel  course."  In 
the  first  phase  the  urine  is  scanty,  bilious,  and  poor  in  urea  ;  in  the  second 
phase  at  the  moment  of  the  crisis  the  urine  is  abundant  and  rich  in  urea. 
In  this  form  catarrhal  icterus  has  the  aspect  of  a  general  disease,  and  takes 
this  aspect  from  its  mode  of  appearance.  Catarrhal  icterus,  as  a  matter  of 
fact,  is  often,  like  certain  fevers,  a  disease  of  certain  seasons,  whence  the  old 
name  of  vernal  or  autumnal  ifcterus.  It  is  epidemic,  and  attacks  two, 
three,  or  more  persons  in  the  same  house  or  in  the  same  locality.  These  cases 
have  been  frequently  noticed  in  the  army. 

Through  these  considerations,  certain  forms  of  catarrhal  icterus  are 
classed  with  general  infective  diseases,  and  side  by  side  with  icterus  gravis, 
of  which  they  are  sometimes  an  attenuated  form.  The  discord,  however, 
arises  when  it  becomes  a  question  of  stating  the  cause  of  the  infection. 

Chauffard  is  of  the  opinion  that  catarrhal  icterus  has  its  origin  in  the 
putrid  poisons  formed  in  the  intestine.  These  poisons,  or  ptomaines, 
normally  absorbed  m  situ  in  order  to  be  eliminated  by  the  liver,  may,  under 
certain  conditions,  increase  their  noxious  properties  and  cause  auto-infec- 
tion, according  to  the  expression  of  Jaccoud.  Kelsch  does  not  consider  the 
ptomaines  as  the  cause  of  the  evil.  "  Is  chemistry  going  to  take  us  back 
to  the  humoral  theories  which  time  and  experiments  seemed  to  have  killed, 
and  which,  besides,  are  so  little  encouraging  to  ])rophylaxis  ?"  The  infec- 
tive agent  is  said  to  be  exterior.  "  The  ground  appears  to  us  to  be  the 
generating  focus  par  excellence  of  this  agent.  The  shmy  bottom  of  ditches 
or  of  ponds  seems  to  be  the  most  favourable  medium  for  the  preservation 
and  the  multiplication  of  this  agent."  All  these  views  are  acceptable — a 
proof  that  infective  icterus  may  result  from  multiple  causes,  and  show 
slightly  different  aspects. 

Symptoms. — In  some  cases  the  disease  cominenccs  with  gastro-diiodcnal 
catarrh.     The  patient  suffers  for  three  or  four  days  from  loss  ot  appetite, 


1024  TEXT-BOOK  OF  MEDICINE 

nausea,  vomiting,  constipation,  furred  tongue,  pain  in  tlie  epigastrium, 
prostration,  headache,  and  fever.  At  this  moment  icterus  appears.  The 
yellowish  tint  first  affects  the  conjunctivae,  forehead,  and  neck.  Within  a 
day  or  two  the  faeces  become  clay-coloured,  and  the  icteric  tint  grows  deeper 
and  extends  over  the  whole  body.  The  urine,  ricli  in  bile  pigment,  takes  on 
a  saffron  colour,  and  on  the  addition  of  nitric  acid  the  characteristic  greenish 
tint  appears.  In  other  cases  the  gastro-intestinal  catarrh  attracts  less 
attention,  and  the  disease  from  the  first  presents  symptoms  more  like  those 
of  general  disease.  Lassitude,  aching  of  the  muscles,  prostration,  epistaxis, 
fever,  bilious  diarrhoea,  scanty  and  albuminous  urine,  are  the  symptoms  of 
the  period  of  invasion,  and  recall  the  commencement  of  typhoid  fever. 
Even  when  the  icterus  appears  we  are  far  from  being  assured  as  to  the  prog- 
nosis ;  we  wonder  whether  we  are  not  face  to  face  with  a  case  of  icterus 
gravis,  and  we  recall  the  phrase  of  Trousseau  :  "  In  icterus,  as  in  pleurisy, 
we  never  know  how  it  may  end." 

Finally,  in  some  patients  icterus  is,  from  the  first,  the  chief  symptom  of 
the  disease ;  the  urine  contains  bile  and  the  faeces  are  colourless,  but  the 
patient  has  neither  fever  nor  distaste  for  food.  Catarrhal  icterus  may, 
therefore,  present  itself  in  various  forms. 

The  clay-coloured  stools  are  caused,  on  the  one  hand,  by  the  absence  of 
bile  pigments,  and,  on  the  other,  by  the  accumulation  of  fat  in  the  intestine 
(steatorrhoea).  As  in  the  absence  of  bile  the  fat  is  no  Jonger  emulsified  and 
does  not  pass  into  the  lacteals,  the  faeces  take  on  their  putty-hke  appearance. 
As  obhteration  of  the  pancreatic  duct  accompanies  that  of  the  common  duct, 
it  has  been  maintained  that  the  steatorrhoea  is  due  to  the  absence  of  the 
pancreatic  juice.  MiiUer  does  not  hold  this  view ;  he  admits  that  the  pan- 
creatic juice  alters  the  quahty  but  not  the  quantity  of  the  fat  in  the  faeces, 
and  it  seems  impossible  to  take  sides  for  or  against  the  bile  or  the  pancreatic 
juice. 

The  liver  is  often  enlarged,  the  hypertrophy  being  considerable  if  the 
disease  is  of  long  duration. 

Prolonged  Catarrhal  Icterus. — In  catarrhal  icterus  the  common  duct 
generally  becomes  permeable  in  the  second  or  tliird  week.  The  appearance 
of  bile  in  the  intestine  indicates  recovery  ;  the  faeces  regain  their  colour  ;  the 
urine  increases  in  quantity,  and  gradually  loses  its  bile  pigment.  There  is 
often  a  crisis  of  pol}n.iria  and  azoturia  (Chauffard) ;  the  toxicity,  previously 
normal,  rises  suddenly  (Roger),  but  the  coloration  of  the  skin  lasts  for  two 
or  three  weeks,  until  the  renewal  of  the  epidermis.  The  pulse  is  slow  during 
the  entire  disease. 

Such  is  the  usual  course  of  catarrhal  icterus,  but  numerous  exceptions 
occur.  In  several  cases  I  have  seen  an  attack  of  catarrhal  icterus  last  more  than 
two  months,  and  I  have,  therefore,  called  this  variety  prolonged  catarrhal 


DISEASES  OF  THE  LIVER  1025 

icterus ;  *  it  must  be  recognized  in  order  to  avoid  mistakes  in  diagnosis.  Wt  en 
we  see  prolonged  catarrhal  icterus  and  an  enlarged  liver  in  an  elderly  man, 
we  are  always  tempted  to  think  of  cancer.  We  find  analogous  cases  in  the 
writings  of  various  authors.  According  to  Niemeyer,  the  "  disease  may 
drag  on  for  weeks  and  months.  The  icterus  becomes  intense,  the  patient 
grows  very  thin,  and  the  hver  shows  e^'ident  sweUing."  According  to 
Frerichs,  catarrhal  icterus  may  last  two  or  three  months.  Amongst  the 
cases  which  I  have  seen,  two  occurred  simultaneously  in  two  members  of  the 
same  family,  and  I  attributed  them  to  the  ingestion  of  high  game.  The 
disease  was  marked  by  successive  outbursts  :  the  icterus,  decoloration  of 
the  fseces,  and  yellow  colour  of  the  urine  improved,  and  reappeared  on  several 
occasions,  and  the  Hver  became  very  much  enlarged.  In  one  patient  the 
disease  lasted  two  months,  and  in  the  other  three  months,  with  epistaxis, 
while  the  hver  remained  enlarged  for  a  long  time,  and  only  became  normal 
after  a  season  at  Vichy.  I  saw  at  the  Necker  Hospital  a  case  of  prolonged 
catarrhal  icterus  lasting  for  seven  weeks.  These  cases  of  relapsing  catarrhal 
icterus  have  been  designated  by  the  name  of  Weil's  disease. 

Diagnosis. — The  diagnosis  of  catarrhal  icterus  is  easy  if  the  disease 
announces  itself  with  symptoms  of,  simple  gastro-intestinal  catarrh,  followed 
by  icterus  and  clay-coloured  stooLs.  If,  however,  the  general  symptoms 
are  severe  from  the  first,  loss  of  strength,  epistaxis,  albuminuria,  and  fever 
being  the  symptoms  of  invasion  in  the  midst  of  which  icterus  appears,  we 
naturally  think  of  the  possibility  of  typhoid  fever  or  of  icterus  gravis.  The 
diagnosis  and  the  prognosis  must,  for  the  time  being,  be  reserved. 

Cholelithiasis  also  provokes  obstruction  of  the  common  duct,  accom- 
panied by  symptoms  of  icterus,  bihous  urine,  and  colourless  faces,  greatly 
resembling  those  of  catarrhal  icterus.  But  the  patient  with  chole- 
lithiasis in  most  cases  suddenly  feels  the  more  or  less  sharp  pain  of  hepatic 
colic,  with  bilious  vomiting,  vertigo,  and  rigors  that  so  often  accompany 
the  passage  of  the  calculi.  On  the  other  hand,  he  has  not,  as  a  rule,  the 
symptoms  which  in  catarrhal  icterus  form  the  pre-icteric  phase. 

Syphilis,  in  its  secondary  stage,  sometimes  causes  catarrhal  icterus ; 
the  patliogeuic  diagnosis  has  been  given  under  SyphiUs  of  the  Liver. 

When  catarrhal  icterus  is  prolonged  and  the  hver  is  enlarged,  the  diagnosis 
is  especially  difficult.  We  must  diflferentiate  it  from  hypertrojjhic-  biliary 
cirrhosis,  cancer  of  the  liver,  and  cancer  of  the  head  of  the  pancreas,  com- 
pressing the  common  duct.  Hypertrophic  biliary  cirrhosis  and  prolonged 
catarrhal  icterus  have,  as  common  symptonis,  persistent  icterus  and  an 
enlargement  of  the  liver,  but  the  decoloration  of  the  fasces  seen  in  catarrhal 
icterus  is  not  met  with  in  hypertrophic  biliary  cirrhosis;  at  least,  if  it  is 

*   Dieulafoy,    "  De    I'ictcro    Catarrhal    Prolong6"    {Semaine    Mcdiealc,    July    11, 

1888). 

65 


1026  TEXT-BOOK  OF  MEDICINE 

observed,  it  is  not  so  marked  or  so  persistent  as  in  catarrhal    icterus. 
Furthermore,  the  spleen  is  not  hypertrophied  in  the  case  of  catarrhal  icterus. 

Secondary  cancer  of  the  hver  and  prolonged  catarrhal  icterus  may 
present,  as  common  symptoms,  icterus  and  enlargement  of  the  hver, 
and  even  decoloration  of  the  fasces,  if  the  common  duct  is  compressed 
by  the  cancer  (glands  of  the  hilum) ;  but  the  swelHng  of  the  hver  is 
uniform  in  the  case  of  catarrhal  icterus,  while  it  is  accompanied  by 
nodules,  and  often  by  ascites,  in  secondary  cancer.  I  am  not  speaking 
here  of  massive  cancer  of  the  liver,  because  icterus  is  absent  in  this 
variety. 

The  diagnosis  between  prolonged  catarrhal  icterus  and  cancer  of  the 
head  of  the  pancreas,  compressing  the  common  duct,  is,  in  my  opinion,  a 
most  difficult  problem.  In  both  cases  we  find  persistent  icterus,  enlarged 
liver  (bihary  plethora),  and  decoloration  of  the  faeces  and  stearrhoea. 
Theoretically,  it  might  be  thought  that  the  obstruction  of  the  common  duct 
by  cancer  of  the  head  of  the  pancreas  would  be  gradual  and  much  slower 
than  the  obstruction  of  the  duct  in  the  case  of  catarrhal  icterus  ;  practically 
it  is  not  always  so,  and,  to  quote  examples,  in  three  patients  in  my  wards 
the  cancerous  obstruction  of  the  duct  was  almost  immediate,  and  at  an 
advanced  stage  of  the  disease  a  copious  flow  of  bile  followed  a  long  period 
of  retention.  It  might  hkewise  be  supposed  that  the  examination  of  the 
fatty  matter  in  the  intestine  might  give  useful  information  as  to  the  absence 
of  the  pancreatic  juice,  but  we  have  abeady  seen  that,  according  to  Miiller, 
the  diagnosis  cannot  be  based  on  the  study  of  stearrhoea ;  and,  again,  the 
pancreatic  duct  may  be  obhterated  in  both  cases.  Rapid  loss  of  flesh  and 
sugar  in  the  urine  are  not  constant  in  pancreatic  cancer ;  diarrhoea  and 
cutaneous  pigmentation  are  in  favour  of  cancer.  According  to  Salhi,  salol, 
which  is  a  combination  of  sahcyUc  acid  and  phenol,  is  decomposed  in  the 
intestine  into  its  two  elements  by  the  pancreatic  juice.  If,  therefore,  salol 
is  given  to  a  patient  whose  pancreas  is  healthy,  sahcyhc  acid  and  phenol 
vnR  appear  in  the  urine.  If  they  are  not  found,  the  salol  has  not  been  de- 
composed, because  there  is  no  pancreatic  juice  in  the  intestine.  This  pro- 
cedure, supposing  it  were  exact,  would  not  be  enough  in  the  present  case  to 
make  the  diagnosis  positive,  because  Wirsung's  duct  may  also  be  obhterated 
in  catarrhal  icterus.  It  is  only  the  course  of  the  disease  which  will  remove 
the  doubts  and  permit  us  to  affirm  the  existence  of  prolonged  catarrhal 
icterus. 

The  diagnosis  between  prolonged  catarrhal  icterus  and  cancer  of  Vater's 
ampulla  presents  for  several  weeks  the  greatest  difficulties.     The  prognosis 
of  catarrhal  icterus  is  generally  benign,  but  yet  in  the  presence  of  icterus, 
even  of  the  most  simple  kind,  we  must  always  make  some  reserves,  because. 
icterus  gravis  may  commence  hke  benign  infective  icterus ;  and  we  see  in  the 


DISEASES  OF  THE  LIVER  1027 

same  epidemic  very  benign  cases  of  catarrhal  icterus,  terrible  cases  of  icterus 
gravis,  and  mixed  or  intermediate  cases. 

Treatment. — When  angiochoHtis  is  associated  with  gastro-intestinal 
catarrh,  we  should  first  prescribe  a  sahne  purgative.  The  patient  is  dieted 
and  is  given  bitters,  extract  of  quinine,  sweetened  with  syrup  of  orange-peel 
(Jaccoud),  alkaline  beverages,  and  Vichy  water. 

Some  years  ago  Kriill  employed  a  new  method  of  treatment  for  catarrhal 
icterus.  He  gave  daily  a  cold  enema  of  water  at  a  temperature  of  60°  to 
65°  F.  After  a  few  enemata,  the  bile  generally  appeared  in  the  intestine, 
the  duct  became  permeable,  and  recovery  took  place  in  a  few  days.  I  have 
not  obtained  such  good  results.  The  ingestion  of  large  doses  of  oil  has 
likewise  been  extolled,  but  few  patients  are  wiUing  to  submit  to  this  treat- 
ment, the  results  of  which,  by  the  way,  are  open  to  discussion. 


65—2 


CHAPTER  VIII 
DISEASES  OF  THE  PANCREAS 

I.  GENERAL  SURVEY  OF  THE  DISEASES  OF  THE  PANCREAS. 

The  pancreas  may  be  the  seat  of  irritative,  destructive,  or  neoplastic  changes 
that  interfere  with  the  normal  functions  of  the  gland.  The  resulting  symp- 
toms in  some  cases  indicate  the  lesion.  The  physical  signs  here  are  of  small 
importance,  as  the  pancreas  is  too  deeply  seated  for  palpation  to  be  possible  ; 
only  large  tumours  of  pancreatic  origin  can  be  felt.  Nevertheless,  in  certain 
affections  of  the  pancreas  the  epigastrium  is  very  sensitive  to  pressure,  and 
acute  pains  of  a  neuralgic  kind  are  sometimes  felt.  Miralhe,  who  has  care- 
fully studied  these  pains,  attributes  them  to  neuralgia  of  the  coehac  plexus, 
which  is  in  direct  contact  with  the  upper  edge  of  the  pancreas. 

As  physiologists  have  proved  the  importance  of  the  pancreatic  secretion 
in  intestinal  digestion,  it  might  reasonably  be  thought  that  changes  in 
the  pancreas  would  induce  characteristic  digestive  troubles.  Nothing  of 
the  kind  is  the  case.  The  distaste  for  fatty  and  proteid  substances, 
the  difficulty  of  digesting  fats,  and  intestinal  meteorism,  are  banal 
symptoms. 

Pancreatic  vomiting  is  said  to  supervene  several  hours  after  meals,  and 
to  consist  of  viscous  and  thready  hquid.  Pancreatic  diarrhoea  is  said  to  be 
characterized  by  drops  of  fat  which  has  not  undergone  emulsion  ;  these  httle 
drops  are  whitish  and  soluble  in  ether  (stearrhoea).  Diabetes  is  an  important 
symptom  of  extensive  changes  in  the  pancreas.  Removal  or  experimental 
destruction  of  the  whole  pancreas  causes  severe  glycosuria  (Mering  and 
Minkowski).  As  a  matter  of  fact,  the  pancreas  pours  into  the  blood  an 
internal  secretion,  which  prevents  glycaemia  (glycol}i;ic  ferment,  Lepine). 
The  preservation  of  a  small  fragment  of  the  pancreas  suffices  to  prevent 
glycosuria.  Pancreatic  diabetes  (Lancereaux)  has  some  special  charactei-- 
istics — viz.,  sudden  onset,  acute  course,  loss  of  flesh,  and  rapid  cachexia. 
The  termination  by  galloping  consumption  is  frequent  in  pancreatic  dia- 
betes, but  even  in  the  absence  of  this  comphcation,  the  disease  is  of  short 
duration,  and  the  patient  dies  in  five  or  six  months  from  cachexia  or  diabetic 
coma.     Diabetes  may  also  be  due  to  syphihs  of  the  pancreas. 

1028 


DISEASES  OF  THE  PANCREAS  1029 


II.  CANCER  OF  THE  PANCREAS. 


Tlie  pancreas  may  be  invaded  by  cancer  in  a  neighbouring  organ.  More 
often  it  is  a  case  of  primary  cancer  of  the  head,  body,  or  tail  of  the  pancreas. 
Cancer  of  the  head  of  the  pancreas  is  the  most  common  form,  and  is  also  the 
easiest  to  diagnose. 

The  relations  between  the  common  duct  and  the  head  of  the  pancreas 
explain  the  obhteration  of  this  canal  by  cancer.  As  I  have  discussed  this 
question  in  detail,  I  shall  merely  mention  in  this  section  cancer  of  the  pan- 
creas, which  is  not  accompanied  by  icterus,  the  explanation  being  that  the 
neoplasm  is  in  the  body  or  the  tail  of  the  organ. 

In  such  a  case  the  s3miptomatology  is  very  obscure  :  loss  of  flesh  and 
of  appetite,  distaste  for  fatty  substances,  and  dyspeptic  troubles.  Obstruc- 
tion or  ascending  infection  of  the  excretory  ducts  of  the  pancreas  may  c^use 
fibrosis  and  diabetes.  When  the  growth  involves  the  solar  plexus,  it  causes 
a  bronze  coloration  of  the  skin.  Cancer  of  the  pancreas  may  invade  the 
prevertebral  glands,  the  vena  cava,  the  portal  vein,  and  the  superior  mesen- 
teric artery.  When  it  obstructs  the  vena  cava,  it  causes  cyanotic  cedema 
of  the  subdiaphragmatic  half  of  the  body ;  when  it  compresses  the  portal 
vein,  it  causes  ascites  and  collateral  circulation.  Thrombosis  of  the  superior 
mesenteric  artery  brings  about  intestinal  infarcts,  followed  by  bloody  diar- 
rhoea and  fatal  peritonitis. 

The  disease  usually  spreads  to  the  liver.  The  cancerous  nodules  are 
multiple,  lenticular,  and  transparent,  like  grease-spots.  Sometimes  they 
form  large  white  nodules,  softened  in  the  centre,  which  Gilbert  calls  cocoa- 
nut  cancer. 

The  duration  of  cancer  of  the  pancreas  is  short,  and  death  generally 
supervenes  in  five  or  six  months ;  I  have,  however,  seen  a  patient  in  whom 
the  affection  lasted  twenty-one  months.*  In  Section  VII.  we  shall  see  that 
hypertrophic  pancreatitis  may  simulate  cancer. 

III.  CYSTS  OF  THE  PANCREAS. 

I  do  not  refer  here  to  dilatation  of  the  pancreatic  canaliculi  met  with  in 
chronic  pancreatitis  and  hthiasis,  nor  to  cysts  consequent  on  the  encystment 
of  an  intraglandular  hsemorrhage.  I  shall  only  discuss  the  large  cysts,  which 
may  reveal  themselves  clinically.  These  cysts  are  sometimes  multiple,  and 
constitute  cystic  disease  of  the  pancreas.  Sometimes  (and,  indeed,  most 
often)  a  large  unilocular  cyst  develops,  and  exceeds  in  size  the  head  of  an 
adult.  It  is  formed  of  a  fibrous  wall,  smooth  externally,  irregular  and  an- 
fractuous internally,  and  filled  witli  a  limpid  and  colourless  fluid. 
*  Clinique  Medicate  de  riluld-Dieu,  1897-1898,  p.  212. 


1030  TEXT-BOOK  OF  MEDICINE 

As  the  cvst  starts  from  the  pancreatic  region  behind  the  stomach,  it 
can  only  grow  by  insinuating  itself  between  the  organs  situated  in  front  of  it. 
Sometimes  it  develops  between  the  stomach  and  the  Hver,  pushing  the 
stomach  downwards  and  coming  in  contact  with  the  anterior  abdominal 
wall ;  it  is  covered  by  the  distended  gastro-hepatic  omentum.  More  com- 
monly it  pushes  the  stomach  upwards  and  the  transverse  colon  downwards, 
lodging  in  the  large  omentum,  which  it  doubles  up  as  it  grows.  In  some 
rare  cases,  adhesions  of  the  large  omentum  prevent  the  doubUng-up,  and  the 
cyst  can  only  grow  by  insinuating  itself  under  the  colon. 

The  cyst,  on  account  of  its  situation,  produces  early  troubles  of  com- 
pression— viz.,  uncontrollable  vomiting,  acute  paroxysmal  pain  in  the  epi- 
gastrium, and  intermittent  intestinal  obstruction.  These  troubles  have 
nothing  characteristic,  and  it  is  only  when  the  tumour  is  present  that  we 
can  make  a  diagnosis.  When  the  cyst  develops  downwards  (subcoHc  type)  it 
may  readily  be  taken  for  a  cyst  of  the  mesentery  or  of  the  ovary.  In  cysts 
which  grow  upwards  the  special  prominence  formed  by  the  cyst  above  the 
umbihcus  sometimes  permits  of  a  diagnosis.  The  tumour  pulsates,  because 
the  aortic  pulsations  are  transmitted  to  it,  but  is  not  expansile.  It  is  gener- 
ally separated  from  the  hver  by  a  resonant  zone.  The  only  treatment  is 
surgical  intervention.  Puncture  of  the  cyst  gives  deplorable  results. 
Laparotomy,  on  the  contrary,  cures  the  patient  in  most  of  the  cases.  In 
many  cases  adhesions  necessitate  incision  and  marsupiaUzation. 

IV.  HAEMORRHAGE  OF  THE  PANCREAS. 

The  rarity  of  haemorrhage  is  so  great  that  we  do  not  think  of  it.  It 
presents,  however,  a  fairly  constant  symptomatology.  In  most  cases  the 
patient  is  alcoholic  or  a  sufferer  from  gall-stones.  Without  any  appreciable 
cause,  he  is  seized  with  sharp  epigastric  pain  and  rigors,  and  he  has  an  anxious 
look.  Examination  at  this  moment  would  furnish  no  explanation  for  this 
condition,  except  tenderness  of  the  epigastrium  on  deep  pressure.  The 
following  day  the  condition  becomes  worse  ;  the  facies  is  peritoneal,  the 
pulse  is  small  and  frequent,  the  belly  is  tender  in  the  upper  part,  and  nausea 
or  vomiting  occurs.  The  extremities  grow  cold,  the  temperature  falls, 
the  voice  is  lost,  and  the  patient  dies  of  collapse  twenty-four  to  forty-eight 
hours  after  the  onset  of  symptoms. 

At  the  post-mortem  examination  blackish  blood  is  found  behind  the 
omenta  and  around  the  pancreas,  which  is  partially  or  entirely  transformed 
into  a  blackish  diffluent  mass,  having  the  look  of  a  clot  of  blood.  There  is 
difficulty  in  recognizing  the  lobules  pushed  aside  by  the  blood.  In  some 
places  the  blood  is  brownish,  as  if  digested,  and  this  transformation  seems, 
indeed,  to  be  the  result  of  auto-digestion  by  the  pancreas.     This  auto- 


DISEASES  OF  THE  PANCREAS  1031 

digestion  may  go  so  far  that  the  organ  becomes  apparently  gangrenous. 
Auto-digestion  has  also  been  noted  when  haemorrhage  was  the  result  of 
epigastric  traumatism.  The  haemorrhage  is  often  associated  with  cyto- 
steatonecrosis  {vide  Section  VII.). 


V.  PANCREATITIS. 

Most  of  the  infectious  diseases  and  of  the  intoxications  may  cause  pan- 
creatitis. The  acinous  structure  of  the  pancreas  is  then  destroyed ;  the 
epithehal  cells  are  destroyed,  and  affected  with  cloudy  swelling,  necrosis, 
and  fatty  degeneration ;  bands  of  interlobular  or  intralobular  fibrous  tissue 
break  up  the  parenchyma.  These  lesions  are  found  in  typhoid  fever, 
pneumonia,  dysentery,  diphtheria,  malaria,  and,  \vith  some  variants,  in 
poisoning  by  phosphorus,  mercury,  and  alcohol.  Changes  in  the  pancreas 
may  also  be  found  in  diseases  of  the  kidneys,  the  hver,  the  heart,  and  the 
stomach.  Infective  and  toxic  pancreatitis  have  been  reproduced  experi- 
mentally. 

The  lesioas  of  pancreatitis  only  acquire  an  interest  when  they  are  suffi- 
ciently acute  to  cause  suppuration,  or  deep  enough  to  produce  the  entire 
degeneration  of  the  pancreas  and  fibrosis  of  the  gland. 

Suppurative  Pancreatitis— Abscess  of  the  Pancreas.— Abscesses  of  the 
pancreas  may  be  the  result  of  infection  through  the  blood,  as  in  Macaigne's 
case,  where  several  pneumococcal  abscesses  developed  in  the  pancreas  after 
bronchopneumonia.  The  condition  is  more  frequently  a  local  trouble  due 
to  infection  of  intestinal  origin,  which  spreads  along  the  canahculi.  This 
infection  is  favoured  by  lesions  of  the  excretory  canals  of  the  pancreas. 
Suppurative  pancreatitis  is  frequently  seen  as  a  complication  of  neoplasms 
of  the  head  of  the  pancreas  and  of  pancreatic  calculi.  Pancreatitis  is  often 
caused  by  perinopliritic  abscess. 

Sclerous  Pancreatitis— Sclerosis  of  the  Pancreas.— In  certain  cases  of 
pancreatic  diabetes  we  find  at  the  post-mortem  examination  that  the 
pancreas  is  atrophied  and  indurated. 

VI.  PANCREATIC  CALCULI. 

We  may  find  in  the  excretory  canals  of  the  pancreas  concretions  of  car- 
bonate of  lime,  rounded  like  a  pea  or  elongated  like  a  grain  of  wheat.  They 
are  often  multiple.  They  induce  secondary  dilatation  of  the  pancreatic 
duct  and  the  formation  of  small  retention  cysts.  They  are  one  of  the  prin- 
cipal causes  of  suppuration  in  the  pancreas  and  of  ]Kincreatic  fibro.sis.  They 
cau.se  crises  of  epigastric  pain  (pancreatic  c<ili('),  which  is  very  difficult  to 
diagno.se  and  to  ascribe  to  its  true  cause. 


1032  TEXT-BOOK  OF  MEDICINE 

Pancreatic  colic  exists  in  three  out  of  four  cases  of  pancreatic  calculi. 
It  is  accompanied  by  vomiting,  and  in  some  cases  by  a  tendency  to  syncope. 
The  pains  radiate  towards  the  first  lumbar  vertebra,  between  the  shoulders, 
to  the  groins,  and  into  the  deep  parts  of  the  abdomen. 

Diabetes  is  very  common,  having  been  found  in  thirty-six  out  of  eighty 
cases  of  pancreatic  calculi.  The  quantity  of  sugar  varies  from  a  few  grains 
up  to  15  ounces  in  the  twenty-four  hours.  It  is,  as  a  rule,  permanent,  but 
it  may  be  intermittent,  occurring  only  during  the  attacks  of  colic.  Lazarus 
quotes  two  cases,  in  which  the  glycosuria  was  alimentary  and  not  sponta- 
neous. 

Eickhorst  has  often  noticed  indicanuria,  which  he  considers  an  indication 
that  the  diabetes  arises  from  calculi  in  the  pancreas. 

Examination  of  the  fgeces  shows  excess  of  fatty  matter,  intact  muscular 
fibres,  and  much  fatty  acid  in  crystals,  all  pointing  to  pancreatic  insufficiency. 

Pancreatic  calculi  have  been  found  in  the  stools.  The  stones  may  be 
rounded,  coral-hke,  or  prickly.  They  vary  in  size  from  a  pin's  head  to  a  pea  ; 
they  are  friable,  and  readily  dissolve  in  water.  Their  weight  varies  from 
3  to  30  grains.  Their  chemical  composition  is  :  carbonate  and  phosphate  of 
lime,  72  parts  to  magnesia,  4 ;  and  organic  matter,  3.  Dieckhoff  has  found 
the  Bacillus  coli  and  streptococci  in  the  centre  of  the  calcuh. 

X-ray  photographs  of  these  calcuh  have  been  made  by  Lazarus.  They 
are  not  transparent  to  the  rays  and  give  a  clear  shadow. , 

VII.  RELATION  BETWEEN  PANCREATITIS  AND  GALL-STONES 

—  PANCREATICO-BILIARY  SYNDROME  —  CYTOSTEATONECROSIS 

AND  PANCREATICO-PERITONEAL  HEMORRHAGE. 

This  section  deals  with  the  relations  that  may  exist  between  pancreatitis 
and  gall-stones.  This  question  is  of  great  importance  in  medicine  and 
surgery,  and  we  shall  see  that  pancreatitis  is  beginning  to  occupy  a  most 
important  situation.  Much  of  the  matter  in  this  section  is  taken  from  ten 
of  my  clinical  lectures  on  this  question  at  the  Hotel-Dieu. 

Those  who  suffer  from  gall-stones  may  be  attacked  by  the  following 
complications  :  acute  and  chronic  pancreatitis  ;  fibrous  pancreatitis,  com- 
pressing the  common  bile-duct  and  Wirsung's  duct ;  cirrhosis  of  the  pancreas, 
with  overgrowth  of  tissue,  simulating  cancer  of  that  organ  ;  suppuration 
and  gangrene  of  the  pancreas  ;  pancreatitis  simulating  acute  peritonitis 
and  perforation  of  the  abdominal  viscera ;  sudden  onset  of  cytosteatonecrosis 
and  pancreatico-peritoneal  haemorrhage. 

I  have  thought  it  better  to  discuss  this  question  under  Diseases  of  the 
Pancreas,  and  not  under  Gall-Stones,  first  giving  a  resume  of  a  case  at  the 
Hotel-Dieu  : 


DISEASES  OF  THE  PANCREAS  1033 

On  April  3,  1906,  a  man  was  admitted  for  severe  jaundice  of  some  six  weeks' 
duration.  The  lu-ine  was  of  an  orange  colour,  and  nitric  acid  gave  the  characteristic 
reaction  of  bile  pigment.  The  faeces  were  quite  colourless,  and  contained  much  fatty 
matter. 

Fever  was  absent,  itching  severe.  The  hver  was  sUghtly  enlarged,  but  was  not  pain- 
ful. Neither  tumour  nor  pain  over  the  gall-bladder.  Examination  of  the  supra- 
umbilical  region,  above  and  external  to  the  navel — the  area  corresponding  to  the  head 
of  the  pancreas  and  the  course  of  the  common  duct — revealed  no  swelling,  induration, 
or  pain.  The  patient  had  been  suffering  from  obstructive  jaundice  for  six  weeks.  It 
remained  to  find  out  the  cause  of  the  obstruction ;  everything  pointed  to  a  gall-stone 
in  the  common  duct. 

The  patient  had  suffered  during  the  past  eighteen  months  from  typical  hepatic  coKc, 
and  on  February  15,  1906,  the  jaundice  had  appeared.  On  March  15,  1906,  after  a 
very  bad  attack  of  colic,  Dr.  Silvy  found  a  cylindrical  gaU-stone,  which  must,  from  its 
shape,  have  increased  in  size  while  in  the  common  duct.  IMoreover,  cylindrical  calculi 
in  the  common  duct  are  fairly  common,  because  Jordan  has  collected  some  fifty  cases. 
Millard  has  found  several  specimens,  and  Chauffard  has  ^vritten  an  interesting  mono- 
graph on  "  Litliiasis  of  the  Common  Duct."  He  found,  on  making  a  median  longitudinal 
section  of  a  calculus,  a  series  of  concentric  and  ascending  stratifications  of  cholesterin, 
showing  the  growth  of  the  calculus  at  the  upper  part. 

The  patient  had  obviously  been  suffering  from  jaundice,  caused  by  a  gall-stone 
in  the  common  duct.  The  problem  was  to  explain  the  persistence  of  the  jaundice 
after  the  stone  had  been  passed  two  weeks  previously.  Either  the  duct  contained  other 
gall-stones,  or  else  it  was  compressed  by  fibrous  pancreatitis,  which  is  often  associated 
with  gaU-stones. 

The  javmdice  showed  no  change  for  some  weeks  after  the  patient's  admission  under 
my  care ;  the  stools  were  colourless,  and  the  urine  contained  bile  pigment.  As  the 
patient  lost  nearly  2  stones  in  weight,  I  began  to  doubt  the  diagnosis  of  chronic  pancrea- 
titis ;  and  if  I  had  not  seen  the  gall-stone,  I  shouid  have  suspected  cancer  of  the  head  of 
the  pancreas.     I  handed  the  patient  over  to  Terrier  for  operation. 

Gosset  operated  on  April  2.3.  At  this  date  the  jaundice  had  lasted  for  sixty-seven 
days  (thirty-seven  days  after  the  expulsion  of  the  gall-stone).  The  abdomen  was  opened 
by  Kehr's  bayonet  incision.  The  liver  was  pulled  upwards  and  backwards,  in  order  to 
examine  the  gall-bladder.  It  was  small,  retracted  under  the  liver,  and  partly  hidden 
Jjy  omental  adhesions ;  no  calculi  were  present.     Cholecystectomy  was  then  performed. 

The  common  duct  was  explored,  first  with  a  No.  10  olivary  bougii^  and  then  with 
a  curette,  which  passed  over  an  obstacle  at  the  ampulla  of  Vater  into  the  duodenum. 
The  duct  and  the  ampulla  contained  no  calculus. 

The  hepatic  duct  was  next  examined  by  a  lateral  incision  in  the  common  duct  up 
to  the  hepatic  duct.     No  stone  was  found. 

Examination  of  the  head  of  the  pancreas  showed  marked  induration  in  Desjardin's 
triangle  of  infection  ;  the  tissue  was  so  hard  that  there  was  a  question  of  the  presence 
of  a  calculus.  Puncture  with  a  needle  showed  no  calculus,  but  fibrous  pancreatitis. 
The  hepatic  duct  was  drained. 

In  a  fortnight  the  bile  found  its  way  into  the  bowel ;  the  jaundice  disappeared  ; 
the  urine  and  the  stools  became  of  normal  colour.  Six  weeks  after  the  operation,  the 
patient  having  gained  some  30  pounds  in  weight,  left  the  hospital  cured. 

It  is  easy  to  reconstruct  the  history  of  the  case.  The  patient  luul  been  sufToring 
from  a  single  gall-stone  in  the  common  duct.  The  passage  of  the  stone  put  an  end  to 
the  hepatic  colic,  but  the  symptoms  of  biliary  obstruction  still  persisted,  being  duo 
to  stcnosing  pancreatitis,  that  provcmtcd  the  j)assage  of  -Jie  biln.  Drainage  of  the 
lujpatio  duct  and  withdrawal  of  the  bile  externally  cured  tiie  paiu-n^atitis,  and  rendered 
the  common  duct  permeable. 


1034  TEXT-BOOK  OF  MEDICINE 

Other  Cases. — Before  studpng  as  a  whole  the  relations  between 
pancreatitis  and  gall-stones,  I  think  it  desirable  to  quote  several  cases. 

Riedel's  Case. — A  -woman  had  been  subject  to  hepatic  colic  for  a  long  while.  Six 
months  before,  severe  jaundice  appeared  after  an  attack  of  colic.  The  Uver  was  en- 
larged. Below  the  liver  a  tumour  as  hard  as  iron  and  as  large  as  the  fist  was  felt.  It 
was  thought  to  be  the  gall-bladder,  filled  with  calculi.  An  operation  was  performed. 
After  separation  of  the  adhesions  between  the  liver,  pylorus,  and  duodenum,  the 
gall-bladder  was  found  to  be  contracted  and  filled  with  calculi.  The  tumour, 
however,  was  formed  by  the  head  of  the  pancreas.  The  common  duct  was  as 
large  as  the  thumb  ;  it  contained  six  calcuh,  which  were  removed  through  an  incision. 
Cholecystectomy  and  drainage.  In  three  weeks  the  patient  was  cured ;  in  six  months 
the  pancreatic  tumour  had  diminished  in  size,  and  in  eighteen  months  it  could  no  longer 
be  felt. 

Mayo  Robson's  Case. — A  lady,  fifty  years  of  age,  had  suffered  for  several  years  from 
hepatic  coUc,  followed  by  jaundice.  For  some  months  the  attacks  had  been  more 
severe,  and  the  jaundice  had  become  permanent.  Vomiting  was  frequent.  The 
patient  had  become  very  thin  and  weak.  Fifteen  stones  were  removed  from  the  common 
and  cystic  ducts.  The  head  of  the  pancreas  was  invaded  by  a  large  nodular  mass.  The 
gall-bladder  was  anastomosed  with  the  duodenum.  Mayo  Robson  and  his  colleagues 
were  in  favour  of  cancer.  The  tumour  was,  however,  really  due  to  chronic  hypertrophic 
pancreatitis  associated  with  gall-stones.  Recovery  was  uneventful ;  ten  months  after 
the  operation  she  was  in  excellent  health. 

Qtjenu's  Case. — A  young  woman  had  suffered  for  five  years  with  hepatic  cohc,  fol- 
lowed by  jaundice.  For  three  months  the  jaundice  had  been  permanent,  and  the 
patient  had  lost  a  stone  in  weight.  Abdominal  palpation  was  negative.  Quenu  per- 
formed cholecystostomy.  The  gall-bladder  contained  two  large  calcuh,  but  the  common 
and  cystic  ducts  contained  none.  The  obstruction  to  the  flow  of  bile  was  caused  by 
induration  of  the  head  of  the  pancreas.  The  results  of  the  operation  were  normal ; 
after  a  month  the  bile  passed  into  the  intestine,  the  biUary  fistula  closed,  and  recovery 
was  complete  in  ten  weeks. 

Kehb's  Cases. — 1.  A  woman  had  suffered  for  fifteen  years  from  attacks  of  pain 
in  the  region  of  the  gall-bladder,  with  vomiting  and  jaundice.  In  the  last  two  years 
the  attacks  became  more  frequent ;  the  patient  had  lost  2  stone  in  weight  in  three 
months.  The  steps  of  the  operation  were  :  bayonet  incision  ;  removal  of  the  gall-bladder, 
which  was  small,  full  of  calcuh,  and  adherent  to  the  omentum.  The  head  of  the  pan- 
creas, affected  by  interstitial  pancreatitis,  was  as  hard  as  a  stone.  The  cystic  and 
common  ducts  were  free.  Kehr  drained  the  hepatic  duct.  The  pain  ceased,  and  the 
patient  recovered.  Examination  of  a  fragment  of  the  pancreas,  removed  at  the  opera- 
tion, showed  chronic  sclerous  pancreatitis. 

2.  A  patient  had  complained  for  some  years  of  hepatic  cohc.  The  last  few  attacks 
were  very  painful,  and  were  followed  by  severe  jaundice.  Kehr  diagnosed  obhtera- 
tion  of  the  common  duct  by  a  gall-stone.  The  steps  of  the  operation  were :  bayonet 
incision  ;  freeing  of  adhesions  between  the  gall-bladder  and  the  omentum.  The  pancreas 
was  enlarged  and  as  hard  as  a  stone.  A  calculus  fotmd  in  the  common  duct  was  pushed 
back  into  the  gaU-bladder.  Cholecystectomy.  Drainage  of  the  hepatic  duct.  Com- 
plete recovery  in  six  weeks. 

3.  A  woman  suffered  from  hepatic  cohc,  with  jaimdice  and  clay-coloured  stools. 
Examination  under  chloroform  revealed  near  the  umbihcus  an  indurated  tumour, 
which  appeared  to  be  the  head  of  the  pancreas.  Operation :  bayonet  incision.  The  gall- 
bladder was  chstended  and  adherent  to  the  pylorus  ;  several  stones  could  be  felt  in  the 
gall-bladder,  and  one  in  the  cystic  duct.  Removal  of  the  gaU-bladder.  No  calculi  in 
the  common  duct.     Examination  of  the  pancreas  showed  that  the  tumour  was  the 


DISEASES  OF  THE  PANCREAS  1035 

hard  and  thickened  head  of  that  organ.  The  hypertrophic  pancreatitis  had  obstructed 
the  flow  of  bile  through  the  common  duct.  Drainage  of  the  hepatic  duct.  Three 
months  later  the  patient  was  in  good  health. 

In  all  these  cases  the  pancreatitis  was  associated  with  the  presence  of 
gall-stones,  either  in  the  gall-bladder  or  in  the  ducts.  In  other  cases,  how- 
ever, the  pancreatitis  still  develops,  and  causes  obstruction  to  the  flow  of 
bile  through  the  common  duct,  although  the  calcuU  have  passed  through 
into  the  bowel. 

In  some  instances,  indeed,  we  can  follow  the  evolution  of  the  pan- 
creatitis both  in  the  calculous  and  in  the  non-calculous  stages.  This  feature 
was  well  shown  in  the  first  case  quoted.  The  pancreatitis  persisted  after 
the  expulsion  of  the  calculus,  until  the  patient  was  operated  upon. 

Korte  speaks  of  a  similar  case  : 

He  performed  cholecystectomy  in  a  woman  suffering  from  cholelithiasis.  As  the 
pain  and  jaundice  reappeared,  he  feared  that  ho  had  left  a  stone  in  the  ducts  and 
operated  a  second  time.  He  found  hypertrophic  pancreatitis,  preventing  the  flow  of 
bile  through  the  common  duct.     Drainage  of  the  hepatic  duct.     Complete  recovery. 

Mayo  Robson's  Case. — A  woman  was  suffering  from  hepatic  colic  and  jaundice. 
Under  chloroform,  a  hard  tumour  was  felt ;  it  had  irregular  edges,  and  was  situated 
between  the  umbilicus  and  the  costal  margin.  On  opening  the  abdomen,  adhesions  were 
found  between  the  stomach  and  the  liver.  The  pancreas  contained  a  tumour  of  maUg- 
nant  appearance  ;  the  prognosis,  therefore,  appeared  hopeless.  As  a  matter  of  fact,  it 
was  a  case  of  hypertrophic  sclerous  pancreatitis.  The  patient  ate  a  chop  three  days 
after  the  operation  ;  in  two  weeks  the  jaimdice  had  disappeared,  and  some  weeks  later 
the  patient  went  home  well.  Four  months  later  she  was  in  good  health  ;  i\\e  pancreatic 
tumour  had  disappeared. 

Pancreatico-Biliary  Syndrome-— Pancreatitis  Stenosans  and 
Pancreatitis  Exuberans. 

The  foregoing  cases  would  have  been  formerly  called  "  jaundice  from 
obliteration  of  the  bile-ducts  by  calculi."  The  pancreatitis  was  usually 
unnoticed,  or  called  cancer.  The  progress  made  in  the  surgery  of  the  bile- 
ducts  has  rendered  the  close  study  of  pancreatitis  possible,  giving  it  an  im- 
portant place  in  the  group  of  affections  due  to  gall-stones. 

In  1905  Quenu  and  Duval  collected  118  cases  of  pancreatitis  associated 
with  gall-stones.  To  these  figures  I  have  been  able  to  add  some  fifty  more 
cases.  Kehr,  from  a  systematic  exploration  of  the  pancreas  in  every 
operation  he  has  perfonued  on  the  bile-ducts,  says  that  pancreatitis  is  present 
in  3.']  per  cent.  These  figures  show  the  frequency  of  tlic  morbid  association, 
which  I  shall  call  the  "  pancreatico-biliary  syndrome." 

What  share  does  the  pancreas  take  in  this  association  ?  As  we  have 
seen  in  the  preceding  cases,  the  lesion  is  usually  limited  to  the  head  of  the 
pancreas,  the  remainder  of  the  organ  being  free.  The  head  is  cirrhosed,  and 
sometimes  as  hard  as  a  stone.     The  cirrhosis  has  in  most  cases  a  hyper- 


1036  TEXT-BOOK  OF  MEDICINE 

tropllic  tendency.  The  hypertrophy  is  at  times  so  marked  as  to  give  rise 
to  a  hard,  nodular,  and  ill- defined  tumour,  which  even  at  the  operation 
resembles  a  mahgnant  growth,  and  lends  itself  to  errors  in  diagnosis.  This 
morbid  process  demands  our  attention.  I  have  proposed  for  these  varieties 
of  pancreatitis  the  terms  "  pancreatitis  stenosans  and  pancreatitis  ex- 
uberans."  The  former  variety  surrounds  and  flattens  the  common  duct, 
and  in  some  cases  Wirsung's  canal  as  well,  preventing  the  flow  of  bile  and 
of  pancreatic  juice  into  the  intestine.  The  latter  variety  causes  stenosis,  but 
it  also  forms  a  tumour,  which  may  compress  the  duodenum. 

Histological  examination  shows  interstitial  and  parenchymatous  lesions. 
Opie  has  noted  the  following  varieties :  interstitial  pancreatitis,  inter- 
lobular cirrhosis,  and  peri-acinous  intralobular  cirrhosis.  The  remarkable 
feature  is  the  tendency  to  cause  stenosis  and  overgrowth.  The  head  of  the 
pancreas  may  be  three  or  four  times  its  normal  size.  The  hypertrophy, 
however,  does  not  go  on  indefinitely  ;  atrophy  may  occur  at  a  later  stage. 

What  is  the  explanation  of  the  occurrence  of  pancreatitis  in  the  course 
of  cholelithiasis  ?  Many  theories  have  heen  formulated.  We  know  that 
the  common  duct  lies  in  a  kind  of  gutter  on  the  posterior  surface  of  the 
pancreas,  and  also  that  the  common  bile  and  pancreatic  ducts  open  side  by 
side  at  the  ampulla  of  Vater.  One  theory  says  that  the  pancreatic  tissue 
is  infected  by  reason  of  its  close  proximity  to  the  common  duct ;  another 
theory  says  that  the  infection,  of  biliary  or  duodenal  origin,  passes  upwards 
through  Wirsung's  duct  into  the  pancreas. 

It  must  not  be  thought,  however,  that  the  development  of  chronic 
pancreatitis  is  favoured  only  by  calculi  in  the  common  duct  or  in  the  ampulla 
of  Vater.  In  Quenu  and  Duval's  statistics  we  find  that  pancreatitis  usually 
coexists  with  calculi  in  the  common  duct,  but  in  many  cases  the  common 
duct  and  the  ampulla  of  Vater  are  both  free,  the  calcuh  being  in  the  gall- 
bladder or  in  the  cystic  duct.  Sometimes  the  calculi  have  been  expelled, 
and  yet  the  pancreatitis  continues  to  develop.  In  short,  cholehthiasis  may, 
in  the  long-run,  cause  pancreatitis,  and  calculi  in  the  common  duct  are  most 
favourable  to  this  complication.  Moreover,  calcuh  are  not  the  only  factor, 
and  account  must  be  taken  of  the  more  or  less  septic  condition  of  the 
bile.  We  may  ask  if  infection  starting  from  the  intestine  may  not  be  the 
origin  of  ascending  hepato-pancreatitis,  causing,  on  the  one  hand,  lithiasis, 
and,  on  the  other,  pancreatitis  (Desjardins).  In  fact,  the  pathogenesis 
of  these  varieties  of  pancreatitis  is  not  yet  cleared  up. 

Symptoms  and  Diagnosis. — It  is  not  easy  to  state  the  symptoms  of 
pancreatitis.  The  first  point  is  that  the  mischief  only  occurs  in  persons 
who  have  suffered  for  a  long  time  from  cholelithiasis.  For  years  they  have 
had  hepatic  cohc  and  jaundice,  and  have  been  under  treatment  at  Vichy, 
Carlsbad,  Vittel,  or  Contrexeville.     Others  have  suffered  from  calculous 


DISEASES  OF  THE  PANCREAS  1037 

cholecystitis,  with  or  without  jaundice.  In  some  patients  with  pancreatitis 
the  s}Tnptoms  of  biHary  Uthiasis — pain,  hepatic  crises,  and  more  or  less  pro- 
longed jaundice — have  been  present  for  eighteen  or  nineteen  year*  Apart 
from  some  exceptions,  pancreatitis  only  supervenes  when  cholehthiasis  is 
of  long  standing. 

It  is  not  common  to  find  the  onset  of  pancreatitis  marked  by  acute  pain. 
The  condition  is  usually  insidious  in  its  development.  And  even  supposing 
that  pain  occurs ;  as  the  patient  has  already  suffered  from  gall-stone  coUc, 
it  is  difficult  to  know  how  much  of  the  pain  is  due  to  the  pancreatitis.  Even 
when  the  pain  is  most  marked  at  the  pancreatic  point  (2  inches  above  and 
external  to  the  umbihcus),  it  is  not  always  easy  to  say  whether  this  pain  is 
due  to  pancreatitis  or  to  calculi  in  the  common  duct. 

Obstructive  jaundice  does  not  help  in  making  a  pathogenic  diagnosis, 
because  it  may  be  caused  by  a  calculus  blocking  the  common  duct  or  Vater's 
ampulla,  in  the  absence  of  pancreatitis.  On  the  other  hand,  obstructive 
jaundice  may  arise  from  pancreatitis  stenosans,  even  though  no  calculus 
is  present  in  the  common  duct  or  at  Vater's  ampulla. 

Rapid  wasting  has  been  given  as  a  sign  of  stenosing  pancreatitis.  It  is 
said  to  be  due  to  the  fact  that  the  pancreatic  juice  cannot  pass  into  the  in- 
testine because  Wirsung's  duct  is  blocked.  The  statement  is  true  ;  but 
this  wasting  is  not  special  to  pancreatitis,  being  seen  in  cancer  of  the  head 
of  the  pancreas,  and  also  in  permanent  obhteration  of  the  common  duct 
by  a  calculus. 

Finally,  we  have  enlargement  of  the  head  of  the  pancreas.  The  tumour 
is  more  or  less  bulky,  painful,  and  indurated.  Its  situation  is  about  2  inches 
above  and  to  the  right  of  the  umbilicus.  It  appears  at  first  sight  that  this 
tumour  might  be  of  much  value  in  diagnosis,  and  yet,  as  we  have  already 
seen,  it  is  a  frequent  cause  of  error,  being  often  mistaken  for  cancer  of  the 
head  of  the  pancreas  or  for  calculous  cholecystitis. 

The  difficulties  in  diagnosis,  therefore,  are  evident.  How  can  we  say 
whether  a  patient  is  suffering  from  cholehthiasis  and  also  pancreatitis  ? 
Both  the  prognosis  and  the  treatment  are  concerned.  Much  has  been 
expected  from  the  analysis  of  the  urine  according  to  the  methods  of  Saiili 
and  of  Cammidge.  The  results  given  by  these  authorities  are,  however,  not 
conclusive  (Chauffard).     Glycosuria  is  exceedingly  rare. 

Chemical  and  microscopical  examinations  of  the  fajces  give  the  most 
valuable  information.  Stearrhoea,  from  deficiency  of  the  pancreatic  juice, 
is  a  marked  feature.  The  fatty  stools  vary  in  a])))earance.  "  Sometimes 
we  find  small  masses  of  fat,  as  large  as  a  pea  or  a  small  tuit;  at  other  times 
the  fat  fioats  on  the  surface,  fonning  oily  drops,  which  adhere  to  the  sides 
of  tlu;  chamber.  The  hard  masses  of  fjeces  are  coated  with  fat  on  their 
surface"  (Fran(;ais). 


1038  TEXT-BOOK  OF  MEDICINE 

Gaultier  has  shown  that  stearrhoea  is  of  the  highest  importance.  By 
quantitative  analysis  of  the  fat  contained  in  the  faeces,  he  has  found  that 
in  cases  •of  pancreatic  deficiency  the  utihzation  of  the  fat  (apart  from  the 
emulsified  fats)  is  lowered  to  the  extent  of  15  per  cent.  ;  and  he  has  demon- 
strated by  quahtative  analysis  that  the  saponification  of  the  fats  is  much 
decreased.  The  total  utilization  is  even  smaller  when  both  bihary  and 
pancreatic  deficiency  are  present. 

Gaultier  has  described  his  technique  ("  Precis  de  Coprologie  Clinique  "; 
Paris,  1907),  and  the  value  of  his  methods  has  been  repeatedly  proved  in 
my  clinic  at  the  Hotel-Dieu. 

Let  us  now  consider  the  question  of  prognosis.  The  association  of 
pancreatitis  with  bihary  Hthiasis  is  sometimes  serious,  from  the  progressive 
course  of  these  cases. 

Chronic  pancreatitis  affects  the  excretion  and  the  secretion  of  the  pan- 
creatic juice — the  excretion  by  blocking  Wirsung's  duct ;  the  secretion 
because  the  fibrosis  spreads  to  the  glandular  elements  throughout  the  organ. 
The  pancreatic  deficiency,  together  with  the  absence  of  the  bile,  fonns  the 
pancreatico-bihary  syndrome.  Permanent  jaundice  and  stearrhoea  are  the 
cardinal  symptoms.  We  find  also  gastro-intestinal  symptoms  :  anorexia, 
vomiting,  cohc,  and  offensive  diarrhoea ;  glycosuria  is  very  rare  ;  fever  is 
not  constant ;  haemorrhages  sometimes  occur.  The  patient  becomes 
cachectic,  and  the  case  resembles  cancer,  the  more  in  that  the  nature  of 
the  pancreatic  tumour  is  often  wrongly  diagnosed.  This  condition  ends 
in  death. 

The  tumour  formed  by  pancreatitis  exuberans  may  give  rise  to  comph- 
cations,  which  also  lead  to  errors  in  diagnosis.  Thus,  when  the  duodenum 
is  compressed,  the  symptoms  are  those  of  pyloric  stenosis. 

Treatment. — Surgical  intervention  is  the  only  effective  method  of 
deahng  with  these  cases.  A  patient  has  been  subject  for  a  variable  period 
to  attacks  of  cholecystitis,  hepatic  cohc,  and  jaundice.  In  spite  of  medical 
treatment,  the  symptoms  have  shown  no  improvement.  The  jaundice  is 
often  permanent,  the  wasting  is  marked,  the  stearrhoea  is  quite  evident, 
and  analysis  of  the  faeces  shows  pancreatic  deficiency.  In  such  a  case  early 
operation  is  advisable  ;  nothing  is  gained  by  delay.  To  wait  too  long  is  to 
expose  the  patient  to  the  risks  of  acute  pancreatitis  or  to  pancreatico- 
bihary  cachexia. 

The  operation  best  suited  to  these  cases  provides  for  the  removal  of 
the  gall-bladder,  in  which  gall-stones  are  formed  and  bihary  infection 
arises.  It  allows  the  exploration  of  the  large  ducts  and  the  removal  of 
the  calcuh  present  in  them,  and  renders  possible  free  drainage  of  the  hepatic 
duct,  and  diverts  the  bile.  After  some  weeks  this  diversion  of  the  poisonous 
bile  leads  to  remarkable  results. 


DISEASES  OF  THE  PANCREAS  1039 

The  common  duct  again  becomes  permeable,  so  that  the  bile  can  pass 
freely  into  the  bowel.  The  signs  of  bihary  and  pancreatic  retention  dis- 
appear. The  jaundice  fades  away,  the  urine  is  no  longer  loaded  with  bile 
pigments,  the  faeces  become  normal,  and  in  a  few  weeks  or  months  the 
patient  regains  the  weight  lost,  and  complete  recovery  is  assured.- 

The  fibrous  lesion  in  the  pancreas  retrocedes,  the  tumour  disappears,  and 
recovery  follows  when  free  drainage  is  given  for  the  poisonous  bile,  which 
is  capable  of  keeping  up  the  cirrhosis  of  the  pancreas. 

Cytosteatonecrosis — Pancreatico-Peritoneal  Haemorrhages. 

The  Pancreatic  Drama. — I  have  so  far  considered  chronic  pancreatitis 
associated  with  cholelithiasis,  and  ending  in  the  pancreatico-bihary 
syndrome.  Fatal  mischief  may,  however,  occur  suddenly  in  these  cases, 
even  during  an  apparently  quiet  stage,  and  in  the  absence  of  jaundice.  The 
patient  is  seized  Avith  acute  pain  in  the  umbihcal,  epigastric,  or  hypochondriac 
region.^.  The  suffering  is  terrible,  and  is  accompanied  by  vomiting,  pros- 
tration, and  syncope.  The  abdominal  hypersesthesia  is  general,  and  the 
constipation  is  absolute.  Under  these  circumstances  it  is  natural  to  think 
of  acute  peritonitis,  poisoning ;  perforation  of  the  stomach,  duodenum,  or 
gall-bladder ;  appendicitis,  or  intestinal  obstruction.  None  of  these  con- 
ditions are  the  cause  of  this  episode,  which  I  have  called  "  the  pancreatic 
drama,"  in  order  to  distinguish  it  from  other  conditions.  And,  either  at  the 
operation  or  at  the  autopsy,  we  find  none  of  the  lesions  above  mentioned, 
but  the  signs  of  this  pancreatic  drama  :  white  islets  (candle-grease  spots) 
of  fatty  necrosis,  which  are  often  associated  with  pancreatico-peritoneal 
hajmorrhages,  these  lesions  being  due  to  an  attack  of  acute  pancreatitis, 
which  is  almost  always  grafted  on  chronic  inflammation  of  the  pancreas. 

Cholelithiasis  is  not  indispensable  to  the  evolution  of  these  troubles,  but 
I  shall  in  this  section  limit  my  remarks  to  cases  in  which  biliary  infection 
due  to  calculi  and  pancreatitis  are  associated.  Before  describing  the  clinical 
features  of  the  pancreatic  drama,  it  will  be  well  to  study  the  chief  signs — 
cytosteatonecrosis  and  pancreatico-peritoneal  hajniorrhage. 

Cytosteatonecrosis. — We  always  find,  either  at  operation  or  autopsy, 
in  the  peritoneal  cavity  white  islets,  resembling  candle-grease  spots.  They 
project  slightly,  are  about  as  big  as  a  pin's  head,  and  may  be  discrete  or 
confluent.  At  the  post-mortem  examination  we  find  the  spots  in  the 
pancreas,  omentum,  mesentery,  appendices  epiploica;,  the  subperitoneal 
fat,  and  even  in  the  mediastinum.  The  appearance  of  these  white  spots  is 
most  characteristic. 

The  condition  is  due  to  necrosis  of  the  adi])Ose  tissue.  I  have  called  it 
"  cytosteatonecrosis,"  for  reasons  to  appear  later.     How  are  these  wliite 


1040  TEXT-BOOK  OF  MEDICINE 

spots  produced  ?  Ilallion  has  shown  that  two  stages  occur — steatolysis 
and  steatonecrosis.  The  former  consists  "  in  the  spHtting  up  of  the  fat 
droplet  in  the  adipose  cell,  either  into  fatty  acid  crystals  or  into  insoluble 
soaps."  The  fatty  acids  form,  in  the  cell,  crystals,  having  the  shape  of  fine- 
pointed  tufts,  or,  by  their  union  with  hme  salts,  an  insoluble  soap,  filling 
the  cells  in  a  homogeneous  mass. 

The  fat  of  the  cell,  then,  is  converted  into  crystals  of  fatty  acid  or  into 
insoluble  soap.  Another  feature,  just  as  important,  in  my  opinion,  is  the 
disappearance  of  the  cell  nucleus.  For  this  reason  I  have  proposed  the 
term  "  cytosteatonecrosis." 

Histological  sections  show  clearly  the  details  of  this  process.  They  are 
well  shown  in  the  following  figure  : 


Xh 


Fig.  61. — Cytosteatonbckosis. 

A,  Normal  intralobular  fat  cells ;  A',  norraal  peripancreatic  fat  cells ;  N,  necrotic  fat 
cells  ;  M,  zone  of  peri -adipose  necrosis  in  the  pancreatic  tissue  ;  P,  healthy  pancreatic 
acini.     (LetuUe.) 

The  steatolysis  and  cytosteatonecrosis  are  due  to  extravasation  of 
the  pancreatic  juice,  the  steapsin  having  the  power  of  splitting  up  the  fat 
into  fatty  acids  and  glycerin.  Both  these  processes  have  been  experi- 
mentally produced  in  animals  (Opie,  Langerhans). 

What  causes  this  diffusion  of  the  pancreatic  juice  into  the  peritoneal 
cavity  in  cases  of  pancreatitis  ?  How  does  the  juice  provoke  cj^tosteato- 
necrosis  in  the  deep  parts  of  the  tissues  ?  Why  does  the  cytosteatonecrosis 
affect  the  fat  in  the  thoracic  cavity  ?     An  answer  is  difficult. 

Upon  what  does  the  extreme  gravity  of  cytosteatonecrosis  depend  ? 
Death  is  not  due  to  the  fact  that  many  islets  are  scattered  through  the 
pancreas  and  the  peritoneal  fat.     On  the  other  hand,  death  is  not  due  to 


DISEASES  OF  THE  PANCREAS  1041 

peritonitis,  for  there  is  no  evidence  of  peritonitis,  and  we  do  not  find  poly- 
nuclear  cells  in  the  foci  of  cytosteatonecrosis.* 

The  cause  of  death  has  been  put  down  to  the  action  of  the  pancreatic 
juice  upon  the  solar  plexus.  Another  theory  is  that  death  is  due  to  absorp- 
tion of  the  diffused  trypsin.  At  all  events,  we  can  say,  from  the  chnical 
point  of  view,  that  the  finding  of  "  candle-spots  "  during  the  operation 
renders  the  prognosis  very  grave. 

Pancreatico-Peritonea!  Haemorrhage. — In  the  pancreatic  drama  cyto- 
steatonecrosis is  not  the  only  lesion.  We  also  find  haemorrhage  into  the 
pancreas  and  the  different  regions  of  the  peritoneal  cavity.  In  many  cases 
we  find  cHosteatonecrosis  alone,  but  pancreatico-peritoneal  haemorrhage 
is  always  accompanied  by  cytosteatonecrosis. 

On  opening  the  peritoneal  cavity,  bloody  fluid  often  flows  out.  Circum- 
scribed or  diffuse,  superficial  or  deep,  foci  of  haemorrhage  may  be  found  in 
the  pancreas,  the  subperitoneal  tissue,  the  omentum,  the  mesentery,  the 
fatty  capsule  of  the  Iddney,  etc.  The  condition  is  one  of  haematomata  in 
all  these  parts. 

I  have  called  these  haemorrhages  "  pancreatico-peritoneal "  in  order  to 
distinguish  them  from  certain  haemorrhages  in  the  pancreas,  associated  with 
suppuration,  gangrene,  or  calcuh;  and  described  under  the  general  term 
"  haemorrhagic  pancreatitis,"  which  includes  every  variety. 

What  is  the  explanation  of  these  haemorrhages  ?  They  are  not  due  to 
any  infective  process,  because  no  evidence  of  infection  is  found.  The  mis- 
chief arises  from  the  action  of  the  trypsin  in  dii-solving  the  proteids  and 
the  walls  of  the  vessels. 

The  result  is  that  the  steapsin  and  the  trypsin  pass  into  the  peritoneal 
cavity,  and  carry  on  a  pathological  digestio)i  of  the  fatty  tissue  and  the 
vessels  of  the  pancreas,  the  peritoneum,  and  its  adnexa.  The  noxious 
action  of  the  pancreatic  ferment  produces  necrosis  of  the  fat  cells  and  of 
the  vessel  walls,  whence  arise  the  cytosteatonecrosis  and  the  lupmorrhages. 

*  This  does  not  exclude  the  pcssibility  of  the  presence  of  infection  in  the  lesions 
under  discussion.  In  some  cases  we  find  suppurative  pancreatitis  and  abscesses, 
especially  in  the  head  of  the  pancreas.  In  Quenu  and  Duval's  paper  I  iiave 
found  12  cases  of  suppuration  in  114  cases  of  jmncreatitis  associated  with  biliary 
lithiasis.  The  calculi  were  situated  in  Vater's  ampulla,  the  gall-bladder,  and  the 
head  of  the  pancreas.  In  these  twelve  cases  the  suppuration  coincided  three  times 
with  cytosteatonecrosis  alone  and  three  times  with  luemorrhaj^e  and  cytosteato- 
necro.sia.  The  six  patients,  suffering  from  su])puration,  haemorrhage,  and  cytosteato- 
necrosis, died,  whether  they  were  or  were  not  operated  upon  ;  the  six  patients  who 
sulTered  from  cytosteatonecrosis  alone,  witli  suppuration,  were  operated  upon,  four 
recovering. 

(langrene  of  the  pancreas  is  very  grave.  The  death  of  tissue,  which  may  be  rapid 
and  extensive,  is  probably  due  to  the  action  of  anaerobic  micro-organisms,  (iangreno 
usually  complicates  the  suppurative  process. 

66 


1042  TEXT-BOOK  OF  MEDICINE 

The  real  cause  of  the  gravity  of  the  prognosis  and  of  death  is  not  absolutely 
cleared  up. 

Cases. — After  the  discussion  of  cytosteatonecrosis  and  haemorrhage — the 
two  anatomical  signs  of  the  pancreatic  drama — I  will  quote  cases  of  cyto- 
steatonecrosis, either  occurring  alone  or  in  association  with  haemorrhage. 
Wiener  has  collected  twenty-six  cases  in  which  cytosteatonecrosis  occurred 
without  haemorrhage. 

Thayer's  Case.— A  man  had  suffered  for  sixteen  months  from  hepatic  colic  -with 
jaundice,  when  acute  peritonitis  apparently  sxipervened.  Acute  pains  in  the  epigastrium 
and  left  hypochondrium  ;  collapse  and  death  in  thirty-four  hours.  Post-mortem  :  no 
peritonitis  ;  whitish  islets  of  fat  necrosis,  resembhng  spots  of  candle-grease.  Pancreas 
enlarged.  Over  one  hundred  calcuU  in  the  gall-bladder,  and  a  gall-stone  blocking  the 
terminal  portion  of  the  common  duct. 

Fraenkel's  Case. — A  woman  forty-eight  years  of  age,  who  had  suffered  from  hepatic 
colic  and  jaundice,  was  suddenly  taken  ill  with  acute  pain,  vomiting,  and  meteorism 
simulating  peritonitis  from  perforation.  Death  in  five  days.  Post-mortem :  no  peri- 
tonitis, but  whitish  islets  of  fat  necrosis  around  the  pancreas  and  in  the  omenta.  Stones 
in  the  gall-bladder,  and  one  at  the  ampulla  of  Vater. 

The  pancreatic  lesion,  accompanied  by  islets  of  steatonecrosis,  is  nearly  always 
fatal :  in  twenty-six  cases  collected  by  Wiener,  only  one  recovered,  thanks  to  operation. 
A  woman  was  suddenly  seized  with  acute  epigastric  pain,  radiating  into  the  hypo- 
chondriac regions  and  the  back.  Nausea,  but  no  vomiting ;  constipation.  Two 
days  later  the  pains  were  more  severe  ;  the  whole  abdomen  was  hypersesthetic  ;  the  face 
was  pale  and  anxious ;  the  pulse  was  125,  and  the  temperature  101-5°  F.  Peritonitis, 
cholecystitis,  and  appendicitis  were  all  thought  of  ;  the  operation  revealed  whitish  islets 
of  cytosteatonecrosis  in  the  omentum  ;  peritonitis  and  appendicitis  were  absent.  The 
pancreas  was  indurated.  Cholecystitis  was  found,  and  the  cystic  duct  was  blocked  by 
a  large  stone.  The  gall-bladder  was  removed  ;  the  bile-ducts  were  explored,  and  the 
hepatic  duct  was  drained.  The  symptoms  rapidly  improved,  and  the  patient  was  well 
in  eighteen  days. 

I  shall  now  give  a  summary  of  cases  in  which  pancreatico-peritoneal 
haemorrhage  was  associated  with  cytosteatonecrosis.  Most  of  these  cases 
are  labelled  "  acute  haemorrhagic  pancreatitis."  More  careful  inspection 
shows,  however,  that  the  acute  attack  supervened  in  the  course  of  chronic 

pancreatitis. 

Dobreauer's  First  Case. — A  man  with  shght  jaundice  was  seized  during  the  night 
with  very  acute  peri-umbihcal  pain,  followed  by  bilious  vomiting  and  complete  arrest 
of  faeces  and  flatus.  Pulse  small  and  irregular ;  temperature  normal.  Diagnosis : 
intestinal  obstruction.  Operation  :  no  obstruction  ;  haemorrhages  in  the  neighbourhood 
of  the  pancreas.  Death.  Post-mortem  :  whitish  islets  of  cytosteatonecrosis  in  the  sub- 
peritoneal tissue  ;  haemorrhages  in  the  pancreas  ;  gall-stones  in  the  gall-bladder  and  the 
common  duct. 

Dobreauer's  Second  Case. — A  man  had  acute  abdominal  pain,  most  marked  at 
the  umbihcus.  Vomiting  and  symptoms  of  intestinal  obstruction.  Operation :  no 
obstruction  ;  islets  of  cytosteatonecrosis  in  the  great  omentum  ;  pancreas  enlarged.  He 
died  next  day.  Post-mortem :  subperitoneal  haemorrhages  and  islets  of  cytosteato- 
necrosis ;  pancreas  enlarged,  hard,  and  infiltrated  with  foci  of  fat  necrosis ;  haemor- 
rhages aroimd  the  pancreas ;  gall-stones  in  the  gall-bladder  and  the  common  duct. 


DISEASES  OF  THE  PANCREAS  1043 

Dobreauer's  Third  Case. — A  man  was  taken  ill  with  violent  abdominal  pain  and 
repeated  attacks  of  vomiting.  Epigastrimn  distended  and  painful.  Pulse  quick ;. 
temperature  103°  F.  Diagnosis :  acute  hjemorrhagic  pancreatitis.  Operation : 
omentum  crammed  with  foci  of  cytosteatonecrosis  ;  pancreas  enlarged.  Death  from 
broncho-pneumonia.  Post-mortem  :  cytosteatonecrosis  in  the  great  omentum  and  the 
transverse  mesocolon  :  pancreas  surrounded  by  haemorrhage ;  a  hundred  small  stones 
in  the  gall-bladder.  . 

Hai^tead's  Case. — A  man  was  taken  ill  wth  acute  abdominal  pain  and  nausea. 
During  the  next  few  days  the  epigastrium  was  very  tender;  gall-stones  suspected. 
Operation  :  on  opening  the  belly,  blood-stained  fluid  flowed  out,  and  numerous  iilets  of 
cytosteatonecrosis  were  seen.  The  tissues  around  the  pancreas  were  infiltrated  with 
blood.  Patient  died.  The  autopsy  showed  haemorrhages  in  the  pancreas,  which  was 
enlarged.  Disseminated  islets  of  cytosteatonecrosis  in  the  fatt}^  tissue  of  the  peritoneal 
ca\'ity.     A  small  gall-stone  was  found  in  the  ampulla  of  Vater. 

BoRG  AXD  Ehrexpreis's  Case. — A  yoimg  woman  was  acbnitted  to  hospital  for 
appendicitis.  She  had  been  seized  on  the  previous  evening  with  acute  abdominal  pain 
and  vomiting.  Pulse  almost  imperceptible.  Marion  operated.  On  opening  the 
abdomen,  blood-stained  fluid  escaped.  Appendicitis  was  absent,  but  a  part  of  the 
omentum  covered  with  islets  was  revealed  by  the  incision.  Marion  then  diagnosed 
pancreatitis.  Death.  Post-mortem  :  white  islets  of  cytosteatonecrosis  present  in  the 
omentum,  the  mesentery,  and  even  in  the  subpleural  tissues.  The  head  of  the  pancreas, 
which  was  adherent  to  the  neighbouring  organs,  was  hard  and  much  enlarged  ;  the 
tail  of  the  organ  was  replaced  by  a  blackish  sanguinolent  pulp.  The  gall-bladder  con- 
tained six  calculi.  In  short,  acute  haemorrhage  and  c\'tosteatonecrosis  in  the  course 
of  chronic  pancreatitis. 

Bunting's  Case. — A  man  was  suddenly  taken  ill  Avith  acute  epigastric  pain  and 
ballooning  of  the  abdomen.  Collapse  soon  followed.  The  operation  showed  the  absence 
of  intestinal  obstruction,  which  had  been  suspected.  Death.  Post-mortem:  islets  of 
cytosteatonecrosis  in  the  base  of  the  mesentery  ;  pancreas  enlarged,  studded  Avith 
haemorrhages,  and  affected  -wnth  interstitial  sclerosis  ;  calculi  present  in  the  gall-bladder, 
the  cystic  duct,  and  the  ampulla  of  Vater. 

In  the  above  cases  the  patients  all  had  gall-stones.  These  cases  show 
the  gravity  of  pancreatitis  with  steatonecrosis  and  hasmorrhage. 

Out  of  thirty-.six  cases  in  Lenormand  and  Lecene's  paper  only  six  re- 
covered, thanks  to  early  operation.     I  give  a  resume  of  one  of  these  cases  : 

A  man  wlio  had  had  biliary  colic  some  years  before  was  suddenly  seized  with  acute 
abdominal  pain,  vomiting,  and  ab.solute  constipation.  The  l)elly  was  tym{)anitic  ; 
the  epigastric  region  was  distended  and  extremely  tender.  Diagnosis  :  necrosis  of  the 
pancreas,  or  perhaps  peritonitis  from  perforation  or  acute  intestinal  obstruction.  A 
Bupra-iimbilical  incision  gave  e.xit  to  abundant  bloody  fluid.  A  second  incision  below  the 
umbilicus  gave  exit  to  similar  fluid.  Numerous  islets  of  cytosteatonecrosis  were  present 
in  the  appendices  epiploica-,  the  mesentery,  and  the  parietal  peritoneum.  Drainage 
through  both  incisions.  Two  days  later  the  patient  had  a  stool,  the  pains  disappeared. 
and  recovery  followed. 

Symptoms  Diagnosis  Treatment.— I  shall  not  dwell  long  on  the 
syniptom.s  and  diagnosis  of  the  pancreatic  drama,  as  I  have  mentioned 
them  throughout  the  course  of  this  section.  At  first  sight  the  diagnosis 
surely  tends  to  the  hypothesis  of  acute  peritonitis,  with  or  without  perfora- 
tion, or  to  that  of  acute  obstruction.     The  sudden  and  acute  abdominal 

6G— 2 


1044  TEXT-BOOK  OF  MEDICINE 

pain,  the  vomiting,  and  the  collapse,  may  help  in  making  a  diagnosis.  We 
•must,  however,  bear  in  mind  pancreatitis,  carefully  inquiring  for  any  pre\dous 
history  of  gall-stones,  jaundice,  and  hepatic  colic.  We  must  also  define  the 
maximum  point  of  the  pain  and  muscular  rigidity,  which  in  pancreatitis 
is  a  little  above  and  to  the  right  of  the  umbilicus. 

Even  when  the  diagnosis  is  doubtful,  we  must  remember  early  surgical 
intervention.  We  risk,  it  is  true,  an  error  in  diagnosis  ;  but  what  does  an 
error  matter  if  the  patient's  life  is  saved  ?  And  even  if  we  have  wrongly 
suspected  peritonitis,  perforation  of  a  viscus,  appendicitis,  or  acute  obstruc- 
tion, the  mistake  will  not  harm  the  patient,  because  operation  is  indicated 
in  all  these  cases.  In  the  pancreatic  drama  the  patient's  only  hope  lies  in 
operation. 

Furthermore,  the  operation  at  once  gives  the  diagnosis.  The  bloody 
fluid  and  the  candle-grease  spots  in  the  omentum  or  elsewhere  show  that  the 
pancreas  is  affected.  It  is,  then,  necessary  to  drain  the  pancreas  and  the 
peritoneal  cavity.     Timely  operation  gives  an  excellent  chance  of  success. 


Eeflections  on  Cancer  of  the  Pancreas  and  of  Vater's  Ampulla 
AND  Pancreatic  Lithiasis. 

Whatever  may  be  the  part  played  by  biliary  lithiasis  and  the  part  played 
by  pancreatitis,  it  is  certain  that  the  association  of  these  two  factors  favours 
the  appearance  of  the  pancreatic  drama. 

I  have  asked  myself  whether  lesions  of  another  kind,  ending  in  retention 
of  bile  and  of  pancreatic  juice,  might  not  favour  the  pancreatic  drama. 
Take,  for  example,  cancer  of  the  head  of  the  pancreas.  The  almost  constant 
obliteration  of  the  common  duct,  the  fairly  frequent  obhteration  of  Wirsung's 
duct,  and  the  resulting  pancreatico-bihary  syndrome,  being  given,  it  is 
reasonable  to  suppose  that  such  setiological  conditions  might  be  propitious 
to  the  production  of  the  pancreatic  drama.  Nothing  of  the  kind  happens.  I 
have  collected  forty-five  cases  of  cancer  of  the  head  of  the  pancreas,  verified 
by  post-mortem  examination,  and  yet  the  pancreatic  drama  never  appeared. 

The  same  remark  apphes  to  cancer  of  Vater's  ampulla.  This  lesion  often 
provokes  obliteration  of  the  common  bile-duct  and  of  Wirsung's  canal,  in 
much  the  same  way  as  does  impaction  of  a  gall-stone.  In  both  cases  we  find 
retention  of  bile  and  pancreatic  juice  ;  in  both  cases  the  pancreatico-biliary 
syndrome  is  seen.  In  the  eleven  cases  of  cancer  I  have  collected,  post- 
mortem examination  did  not  show  cytosteatonecrosis  or  pancreatico- 
peritoneal  haemorrhages.  The  patients  died  from  the  cancer,  and  not  from 
the  pancreatic  drama.  In  these  cases  neither  stenosing  nor  hypertrophic 
pancreatitis  was  seen. 

As  regards  pancreatic  hthiasis,    I  have  been  somewhat  surprised  to 


DISEASES  OF  THE  PANCREAS  1045 

find  that  pancreatic  calculi,  obliterating  Wirsung's  duct,  and  causing  re- 
tention of  bile  and  of  pancreatic  juice,  produce  neither  hypertrophic  nor 
stenosing  pancreatitis.  Islets  of  cytosteatonecrosis  and  pancreatico- 
peritoneal  haemorrhages  do  not  occur  in  these  cases. 

Jaundice  is  mentioned  in  three  cases  of  pancreatic  calcuU.  In  Lazarus' 
case  a  calculus  was  found  in  the  ampulla  of  Vater.  In  Gould's  case  the 
operation  showed  calculi  in  the  head  of  the  pancreas  and  in  Vater's 
ampulla. 

In  some  cases  of  pancreatic  calcuh,  stearrhoea,  intact  muscular  fibres, 
and  crystals  of  fatty  acids  have  been  found  in  the  stools.  This  fact  merely 
shows  some  degree  of  pancreatic  insufficiency. 

In  a  case  of  pancreatic  lithiasis  reported  by  Von  Simpson,  the  symptoms  and  lesions 
of  the  jiancreatic  drama  are  mentioned.  The  patient  ■was  taken  ill  wth  violent  pain  in 
the  belly  and  constipation  ;  he  died  three  days  later.  The  autopsy  showed  pancreatic 
hthiasis  and  foci  of  cytosteatonecrosis  in  the  mesentery  and  the  appendices  epiploicae. 

The  interesting  point  is  that  tlie  gall-bladder  was  full  of  calcuh. 

In  all  the  cases  I  have  been  able  to  collect  of  cancer  of  the  head  of  the 
pancreas  or  Vater's  ampulla  and  of  pancreatic  calcuh,  I  have  only  found 
one  case  in  which  the  pancreatic  drama  appeared,  and  even  in  this  case 
gall-stones  were  found  in  the  gall-bladder. 


END   OF   VOL.    1. 


SailiUre,  TiitUall  <b  Cox,  b,  Uenrietta  tsliett,  C'oveiU  UnrJen. 


